Upload
vuongkhue
View
217
Download
0
Embed Size (px)
Citation preview
d-AMPHETAMINE’S EFFECTS ON BEHAVIOR PUNISHED BY TIME-OUT FROM
POSITIVE REINFORCEMENT
Emily E. Guido
A Thesis Submitted to the
University of North Carolina Wilmington in Partial Fulfillment
of the Requirements for the Degree of
Master of Arts
Department of Psychology
University of North Carolina Wilmington
2010
Approved by
Advisory Committee
Raymond C. Pitts Anne Hungerford
Wendy Donlin Washington Christine E. Hughes
Chair
Accepted by
Dean, Graduate School
ii
TABLE OF CONTENTS
ABSTRACT ....................................................................................................................... iv
ACKNOWLEDGMENTS ...................................................................................................v
DEDICATION ................................................................................................................... vi
LIST OF TABLES ............................................................................................................ vii
LIST OF FIGURES ......................................................................................................... viii
INTRODUCTION ...............................................................................................................1
d-Amphetamine....................................................................................................................1
Time-Out and Stimulant Prevalence ....................................................................................1
Stimulants and Punished Behavior ......................................................................................3
Shock Punishment and Stimulants .......................................................................................4
Time-Out and Stimulants .....................................................................................................7
d-Amphetamine and Schedule-Induced Behavior ...............................................................9
d-Amphetamine and Schedule-Controlled Behavior Punished by Time-Out ....................15
Current Experiment ............................................................................................................16
METHOD ..........................................................................................................................17
Subjects ..............................................................................................................................17
Apparatus ...........................................................................................................................18
Behavioral Procedure .........................................................................................................19
Pharmacological Procedure ...............................................................................................20
Data Analysis .....................................................................................................................21
RESULTS ..........................................................................................................................22
DISCUSSION ....................................................................................................................33
iii
Time-Out and Punishment……………………………………………………………….33
d-Amphetamine’s Effects on Punished Schedule-Controlled Behavior…………………36
Rate-dependency, Timing, and d-Amphetamine………………………………………...39
Use of Time-Out and d-Amphetamine with Children…………………………………...43
REFERENCES ..................................................................................................................45
iv
ABSTRACT
Amphetamine’s effects on operant behavior punished by time-out have not been
examined. Examining amphetamine’s effects on operant behavior punished by time-out is
crucial to understanding how time-out affects children who are taking stimulant
medications. In the current study, a multiple random-interval (RI) 1-min RI 6-min
schedule of food presentation was arranged for pigeons’ key pecking. Once behavior was
stable under this schedule, a 20-s time-out was added to the RI 1-min component. The
timeout was presented according to a random ratio 3 (RR3) for 2 pigeons and an RR2 for
2 pigeons. Time-out decreased rates in the RI 1-min component for all 3 pigeons. For 1
pigeon, the RI 6-min component rates increased. d-Amphetamine had different effects
across the 3 pigeons. There were rate-dependent effects for 1 pigeon with increases in the
punished component and decreases in the unpunished component, a general decrease for
another in both components, and an increase at low doses followed by a general decrease
in response rates in both components for the other.
v
ACKNOWLEDGEMENTS
I would like to thank my mentor, Dr. Christine Hughes, for her support and
guidance throughout my time at UNCW. Her hard work, dedication, and attention to
detail have helped me tremendously, and for that I am truly grateful. I would also like to
thank my thesis committee, Drs. Raymond Pitts, Wendy Donlin Washington and Anne
Hungerford for their encouragement and comments throughout the completion of my
graduate degree. I would also like to thank animal care and everyone who helped to run
my animals.
vi
DEDICATION
I would like to dedicate this manuscript to my husband, Christopher Guido. His
support and encouragement mean more to me than I could ever express.
vii
LIST OF TABLES
Table Page
1. Summary of the research findings for d-amphetamine’s increasing or decreasing
effects on schedule-controlled behavior and schedule induced behavior with shock
and time-out .................................................................................................................14
2. The number of administrations of each dose to each subject ......................................21
3. Mean reinforcement rate (SR/min) in each component (RI 1-min & RI 6-min) during
prepunishment, the first 10 days of punishment, and the last 10 days of punishment
before saline was administered shown in Figure 1 for Pigeons 567, 863, and 838 with
the ranges in parentheses .............................................................................................25
4. Mean reinforcement rate including time spent in time-out (#R/(time-in duration + (#
TO x TO duration))) during the first 10 days of punishment and the last 10 days of
punishment shown in Figure 1 for Pigeons 567, 863, and 838 ....................................25
5. Mean time-out rate (TO/min) during the first 10 days of punishment and the last 10
days of punishment before saline was administered shown in Figure 1 for Pigeons
567, 863, and 838 where the ranges are in parentheses ...............................................26
6. Saline response rates in the RI 1-min and RI 6-min components for Pigeon’s 567,
863, and 838 can be found in table 6 where ranges are in parentheses .......................28
7. The mean time-out rate (TO/min) for Pigeon’s 567, 863, and 838 at control, saline,
and each dose of d-amphetamine (0.3, 1.0, 1.8, 3.0, and 5.6 mg/kg) are shown in table
7 where ranges are in parentheses ................................................................................28
8. Mean reinforcement rate (SR/min) for Pigeons 567, 863, and 838 at control, saline,
and each dose of d-amphetamine (0.3, 1.0, 1.8, 3.0, and 5.6 mg/kg) in each
component (RI 1-min and RI 6-min) where ranges are in parentheses .......................29
9. Mean reinforcement rate including time spent in time-out (#R/(time-in duration + (#
TO x TO duration))) for Pigeons 567, 863, and 838 at control, saline, and each dose
of d-amphetamine (0.3, 1.0, 1.8, 3.0, and 5.6 mg/kg) ................................................. 30
viii
LIST OF FIGURES
Figure Page
1. Overall response rate (R/min) across the last 10 days of the prepunishment
baseline, the first 10 days of the punishment baseline, and the last 10 days before
the first saline injection for Pigeons 567, 863, and 838 in the RI 1-min (open circles)
and the RI 6-min (filled circles) components. Note that the y-axes are different
ranges across pigeons and the gap in sessions for Pigeon 863 is because the
punishment schedule was changed from RR3 to RR2. .................................................24
2. Mean response rate (R/min) as a percentage of saline rates as a function of the dose of
d-amphetamine for Pigeons 567, 863, and 838 in the punished RI 1-min (open circles)
and the unpunished RI 6-min (filled circles) components. The error bars are ranges.
Note that the y-axes are different ranges across pigeons .............................................27
3. Mean response rates expressed as a percentage of saline rates as a function of the
dose of d-amphetamine for Pigeons 567, 863, and 838 in the punished RI 1-min (open
circles) and the unpunished RI 6-min (filled circles) components. The graphs on the
left show the data from the first presentation of the punished component and first
unpunished component in the session. The graphs on the right show the data from the
second presentation of the punished component and second unpunished component in
the session. The error bars are ranges ..........................................................................32
d-Amphetamine’s Effects On Behavior Punished By Time-Out from Positive
Reinforcement
d-Amphetamine
According to the National Institute of Drug Abuse (NIDA, 2009) d-amphetamine
is a stimulant and increases levels of dopamine in the brain. Dopamine is associated with
movement, pleasure, and attention. Taken in large doses, d-amphetamine can cause
euphoria and lead to abuse of the drug. Amphetamine has several other effects including
rapid breathing and heartbeat, high blood pressure, loss of appetite, dilated pupils,
increased focus, and decreased fatigue. When d-amphetamine is prescribed (e.g. for
attention-deficit hyperactivity disorder (ADHD)), it is given as infrequently as possible,
at the smallest dose required to achieve the desired effect of behavior change. If
necessary, it is gradually increased until the desired effect is reached. Doses are
individualized to the child and their needs, but the average dose is 20-30 mg a day.
Time-out and Stimulant Prevalence
In the field of applied behavior analysis, time-out usually refers to the withdrawal
of positive reinforcement, or the opportunity to earn positive reinforcement, contingent
on behavior. Time-out can be non-exclusionary, in which the participant is not
completely removed from the situation, or exclusionary, in which the participant is
removed completely from the environment for a period of time contingent upon his/her
unwanted behavior. Many teachers use the exclusionary technique by employing a
separate room, a hallway (i.e., the student sits in the hallway outside of the classroom), or
a partition (i.e., the student sits in the room, but his/her view is blocked). If the problem
behavior is positively reinforced, then placing the child in exclusionary time-out
2
presumably removes the opportunity for the positive reinforcement and the problem
behavior should decrease. Time-out is used often because of its ease of application,
acceptability with the public, and its rapid suppression of behavior (Cooper, Heron, &
Heward, 2007).
In addition to time-out and other behavioral management techniques, prescription
drugs have been used to manage children’s behavior. Stimulant medication, such as
Ritalin™ (methylphenidate) and Adderal™ (amphetamine) has been used to treat several
behavioral disorders, including ADHD. Zuvekas, Vitiello, and Norquist (2006) found that
Ritalin™ was prescribed to 2.7% and 2.9% of 0-18 year-old children in 1997 and 2002,
respectively. The 2.9% in 2002 equals 2.2 million users. Use was highest with 6-12 year-
olds (4.8% in 2002), next highest with 13-18 year-olds (3.2%), and lowest with children
under 6 years (0.3%). The use of these stimulant medications was more prevalent in
males (4.0% in 2001) than in females (1.7%) and in the White population (3.6%) than in
Black (2.2%) or Hispanic (1.4%) populations.
Stimulants also are reported to be used illegally among children and adults.
According to a 2009 NIDA study, 4.1% of 8th
graders, 7.1% of 10th
graders, and 6.6% of
12th
graders had abused amphetamine in the past year. NIDA also reported nonmedical
use of Ritalin by 1.8 % of 8th
graders, 3.6 % of 10th
graders, and 2.1 % of 12th
graders.
Nonmedical use of Adderall was reported by 2.0 % of 8th
graders, 5.7 % of 10th
graders,
and 5.4 % of 12th
graders. Methamphetamine also has been abused, but this has been
declining since 1999 by about two thirds to 1.2% in 8th
and 12th
graders and 1.5% in 10th
graders (Meyer & Serwach, 2008). Many children are prescribed stimulant drugs such as
amphetamine, and many are using stimulants illegally.
3
Children using these stimulants are also experiencing time-out in school and,
possibly, at home, which is why it is important to examine the effects of d-amphetamine
on behavior punished by time-out in controlled laboratory settings.
Stimulants and Punished Behavior
When examining punished behavior in a laboratory setting, a procedure known as
the conflict procedure (i.e., a conjoint schedule) has been developed by Geller and Seifter
(1960). In this procedure, responding usually first is maintained by positive
reinforcement, and the data obtained serve as the baseline. Then, punishment is added for
the same response that produces reinforcement. Thus, a conflict is created as the same
response produces both reinforcement and punishment. This schedule allows the
experimenter to compare the before-punishment baseline data to the data once
punishment is added.
In many studies (e.g., Branch, Nicholson, & Dworkin, 1977), a two-component
multiple schedule is used. The components alternate within the session, and each
component has its own schedule of positive reinforcement for a designated amount of
time. For example, in the Branch et al. study, two schedules were arranged: a random
interval (RI) 6-min schedule of food presentation and an RI 1-min schedule of food
presentation, and only one schedule was in effect at a time. Once responding is
established in each component, punishment, whether it is shock or time-out, is added to
one of the components (schedules) in the multiple schedule. Therefore, responding in the
punished component results in food presentation and either shock or time-out, and
responding in the unpunished component results only in food presentation. A benefit of
using a multiple schedule is that the effects of other variables, such as drugs, can be
4
examined on both punished and unpunished behavior in the same subject within the same
session.
Shock Punishment and Stimulants
In most of the research on punishment with nonhumans in laboratory settings,
shock has been used as the punisher. For example, McMillan (1973) conducted a study to
test the effects of different classes of drugs, including stimulants (d-amphetamine), on
punished behavior in four pigeons. The pigeons’ pecking was maintained by a multiple
fixed-interval (FI) 5-min FI 5-min schedule of food presentation. That is, in the presence
of either a red or green keylight (that alternated), a peck after 5 min resulted in 4-s access
to grain. Once this behavior was stable, punishment was added to one of the two FI 5-min
components. In the punished component, each response resulted in electric shock
(punisher). The intensity (2.5 mA to 5.2 mA) and duration (50-ms to 100-ms) were
manipulated across sessions until there was a moderate suppression of responding for
each pigeon. Ultimately, the rate of responding in the punished component was less than
half the baseline rates in the unpunished component.
McMillan (1973) then administered a range of doses of four classes of drugs:
sedatives (chlordiazepoxide, diazepam, oxazepam, meprobamate, pentobarbital, and
mescaline), major tranquilizers (chlorpromazine and tetrabenazine), narcotics (morphine,
delta 9 THC and delta 8 THC), and stimulants (d-amphetamine and imipramine). The
sedative class of drugs increased the rate of responding in the punished component at
doses that did not increase rates in the unpunished component. Rates of responding were
increased more by pentobarbital than any other sedative. The major tranquilizers
decreased the rate of responding in both the punished and unpunished components. Delta
5
9 and delta 8 THC decreased responding in both the punished and unpunished
components, as did imipramine at large doses. In contrast, morphine increased only the
rates of punished responding. d-Amphetamine only marginally increased rates of
punished responding beyond control ranges and only at the 1.0 mg/kg dose. This increase
was much less than the increase of unpunished responding, which was clearly increased
by 0.3 and 1.0 mg/kg.
Foree, Moretz, and McMillan (1973) performed a series of studies, as a follow-up
to McMillan’s study (1973), in which they examined the effects of different drugs on
punished responding. In Experiment 1, three pigeons key pecked under a multiple FI 5-
min fixed-ratio (FR) 30 schedule, with a limited hold (LH) of 60-s, of grain presentation.
That is, in the presence of a red key light, the first key peck after 5 min resulted in 4-s
access to grain, and in the presence of a blue key light the 30th key peck resulted in 4-s
access to grain. If 30 responses did not occur within 60 s in the presence of the blue key,
or if no response occurred within 60 s in the presence of the red key after the FI had
elapsed, then the schedule components alternated without grain presentation. The range
of baseline performance were 36-48 responses/min (R/min) in the FI schedule without
shock and were 120-180 R/min in the FR schedule. d-Amphetamine (0.3, 1.0, and 3.0
mg/kg) increased low rates of responding maintained by the FI schedule and decreased
high rates maintained by the FR schedule when there was no punishment. During the
punished condition, a 50-ms shock was presented according to an FR1 schedule during
each component. The shock intensity ranged across phases of the experiment from 2.5
mA to 5.2 mA. At the higher shock intensities, response rates were almost completely
eliminated, whereas at lower shock intensities the rates decreased to approximately 50%
6
in the FR and FI components compared to baseline rates. d-Amphetamine decreased
response rates at the 3.0 mg/kg dose in both components.
In Experiment 2, Foree et al. (1973) examined the frequency of punishment. Four
pigeons key pecked under a multiple FI 5-min, FI 5-min schedule of food presentation
with a LH of 40 s. After a stable baseline was obtained, a shock-presentation schedule
was added to both components. In the presence of the red key light, a shock was
delivered for each key peck (FR 1), and in the presence of the green key light a shock of
the same intensity and duration was delivered for every 30th key peck (FR 30). Response
rates were lower by around 45% more in the FR 1 component than in the FR 30
component. Overall, response rates decreased as doses of d-amphetamine increased in
both components.
d-Amphetamine’s effects on responding punished by shock also have been
examined in rats. In a study conducted by Evenden, Duncan, and Ko (1998), eight rats
responded on an FI 40-s schedule. Then, the experimenters used a light to signal
punishment, which was a 1-s, 0.6 mA electric shock delivered on an FR 20 schedule.
Punished and unpunished responding was intermixed within a session; response rates
decreased by up to 50% when punished compared to when unpunished. The effects of
psychotomimetics and anxiolytics on punished and unpunished responding then were
examined. The psychotomimetics they used were d-amphetamine and N-methyl-D-
aspartate antagonist (MK801), and a nonpsychomotor stimulant psychotomimetic 5-
HT2A/C agonist, DOI. The anxiolytics they used were chlordiazepoxide, NS2710,
pregabalin, citalopram, and yohimbine.
7
To examine the results, Evenden et al. (1998) divided each 40-s interval into 10,
4-s subintervals (bins). d-Amphetamine increased punished and unpunished responses at
each dose. In the unpunished component, 0.8 mg/kg and 1.6 mg/kg d-amphetamine
tripled response rates in certain bins (Bins 5, 6, and 7). All doses increased responses in
the punished component (by an average of 0.1 R/s which is a 15% increase from saline).
There was also an increase in overall rates for both the punished and unpunished
components especially at the 0.8 mg/kg and 1.6 mg/kg doses. There were decreased rates
at the 1.6 mg/kg dose in the later bins of the sessions. Evenden et al. also found that the
anxiolytics and psychotomimetics generally increased responding, although the increase
was much more noticeable in the unpunished component than in the punished
component. In general, Evenden et al. (1998) found that d-amphetamine slightly
increased overall punished response rates with shock. Overall, McMillan (1973) and
Evenden et al. (1998) found that d-amphetamine slightly increased behavior punished by
shock, whereas Foree et al. (1973) found d-amphetamine decreased behavior punished by
shock.
Time-Out and Stimulants
In a series of studies, McMillan (1967) compared the punishing effects of
response-dependent shock and response-dependent time-out. The first set of studies was
conducted to test the effects of shock and time-out on behavior. McMillan used squirrel
monkeys that pressed a lever on a variable interval (VI) schedule of food presentation
that was manipulated between subjects. He also manipulated the shock intensity.
Responding was maintained under a multiple VI 1-min VI 1-min schedule of food
presentation. In one of the components a 30-ms shock at 3.0 mA intensity was added, and
8
in the other component a 40-s time-out of total darkness was added. Each component was
presented twice within a session. Response-produced shock and response-produced time-
out suppressed the response rates to approximately the same degree, but there were some
differences in the suppression. In the shock-punishment component, the monkeys
responded more during the second presentation of the shock punishment, whereas in the
time-out component their rates remained suppressed during repeated presentations. That
is, the punishment effects of time-out were longer lasting than the punishment effects of
shock.
In the next study in this series of experiments, McMillan (1967) injected the
monkeys with pentobarbital twice a week to see the effects on punished responding. He
found that 1.0 mg/kg and 3.0 mg/kg pentobarbital increased response rates that were
previously suppressed by both electric shock and time-out. Responses punished by shock
were increased much more (about 8 times more) than those punished by time-out (50%
increase). Overall, McMillan showed that shock and time-out produce similar effects as
punishers and can therefore be used as a baseline for drug effects.
Van Haaren and Anderson (1997) examined the effects of chlordiazepoxide
(anxiolytic drug), buspirone (anti-anxiety agent), and cocaine on rats’ responding
punished by time-out. The experimenters used six rats. Responding was maintained under
a multiple RI 30 s RI 30 s schedule of food presentation. Then, in one of the RI 30-s
components a 10-s time-out, in which all stimuli were extinguished, which was signaled
by a Sonalert, was presented according to an RI 2 s schedule. The 5-min unpunished
component was presented 3 times in a session, and the 7.5-min punished component was
presented 2 times in a session. The rats were then injected with one of the three drugs.
9
Van Haaren and Anderson found that low doses of chlordiazepoxide (1.0 and 3.0 mg/kg)
increased response rates in the unpunished component by about 10% for three of the rats
and not by much for the other three rats. They also found that these doses increased
response rates in the punished component by about 20% for two of the rats and only
slightly for the other rats. There were dose-dependent decreases in the punished and
unpunished component at the larger doses (10.0 and 30.0 mg/kg) for all of the rats. They
also found that 1.7, 3.0, and 4.2 mg/kg buspirone decreased response rates in both
components and that the doses 0.1, 0.3, and 1.0 mg/kg did not change response rates.
They found that 17.0 and 30.0 mg/kg cocaine decreased rates in the unpunished
component and that no dose changed response rates in the punished component. Overall,
the results with cocaine were variable within and across rats and, therefore, inconclusive.
d-Amphetamine and Schedule-Induced Behavior
Schedule-induced drinking (Falk, 1961) is said to occur when there is an increase
in water intake based on the schedule of food presentation. In studies on schedule-
induced drinking, food and water first are available to the subject in its home cage. How
much water the subject drinks under these conditions is measured during this baseline.
Then the subject is placed in an experimental chamber, in which there is an intermittent
schedule of food presentation in effect (e.g. a fixed time [FT] schedule in all of the
following studies), and a water bottle is present. The amount of water drunk in the
session is measured and compared to the amount of water that was drunk in the home
cage when both food and water were constantly available. Schedule-induced drinking is
said to occur when the amount of water drunk during experimental sessions is greater
10
than that drunk in the home cage. In addition, schedule-induced drinking tends to occur
immediately after food delivery in the experimental chamber.
d-Amphetamine’s effects on schedule-induced drinking have been examined with
both shock and time-out as punishers. Pellon, Mas, and Blackman (1992) conducted a
study to examine the effects of d-amphetamine and diazepam on punished and
unpunished schedule-induced drinking in rats. They used six rats and a typical schedule-
induced drinking procedure as described above. In Phase 1 of the experiment, 60 food
pellets were presented according to an FT 1-min schedule when a 100-ml water bottle
was in the chamber. At the end of the session, they measured how many licks the rat
made and how much the rat drank. The mean water intake for each rat ranged from 4 to
4.5-ml while they had free access to water; whereas, their schedule-induced water intake
ranged from 17.2 to 26.0-ml.
In Phase 2, Pellon et al. (1992) separated the rats into two groups so that rats were
matched by the amount of schedule-induced drinking in Phase 1. The rats in the first
group were administered d-amphetamine (0.25, 0.5, 1.0, and 2.0 mg/kg), and rats in the
second group were administered diazepam (0.5, 1.0, 2.0 and 4.0 mg/kg). The
administration of drugs slightly decreased the amount of water consumed in the chamber,
but these slight changes in water consumption were within the range of variability of
baseline and, therefore, cannot be considered reliable.
After a return to baseline conditions, punishment was added, and the rats received
food every minute if they did not lick the water spout. If they licked the water spout,
there was a 10-s signaled delay (i.e., the houselight was turned off) until the next food
presentation. If the rat licked the water spout during the delay, the delay reset to 10 s (i.e.,
11
differential reinforcement of other behavior, DRO schedule was in effect). Pellon et al.
(1992) found that the punishment significantly decreased the mean amount of water that
the rats drank to about half of what they drank under the unpunished conditions. Under
the punishment baseline, d-amphetamine increased punished schedule-induced drinking,
but not unpunished schedule-induced drinking. The increase at the lower doses (0.25 and
0.5 mg/kg) for two of the rats was around 30% and within the range of control for the
other rat. The 1.0 mg/kg dose increased the amount of water drunk threefold for one of
the rats, increased it by almost double for another, and did not change it for the other. The
licking rate was increased slightly in two of the rats and fell within the baseline range for
the other at the 0.25 mg/kg dose. The licking rate for all of the rats was increased at the
0.5 mg/kg and 1.0 mg/kg doses. The 2.0 mg/kg dose decreased the licking rate for one of
the rats, increased it by almost triple for another and increased it by 20 times the control
rate for the other rat.
In contrast, diazepam increased the amount of water drunk when the schedule-
induced drinking was unpunished and did not affect the punished schedule-induced
drinking. Pellon et al. (1992) found that there was a dose-related effect, with small doses
producing increases in water consumption in unpunished licking, whereas larger doses
decreased water consumption and licking.
Similar to what Pellon et al. (1992) found, Perez-Padilla and Pellon (2003) found
that d-amphetamine increased water consumption that was reduced by negative
punishment procedures. They used 24 rats and a typical schedule-induced drinking
procedure. The 12 rats first were exposed to 30-min sessions with an FT 30-s schedule of
food presentation. The rats were divided into six pairs based on their licking rate and the
12
amount of water consumed during baseline. Perez-Padilla and Pellon selected one rat
from each pair to be the experimental rat for which every lick produced a response-
dependent unsignalled 10-s delay to the next food pellet. The other rat in the pair was the
control (yoked) rat and received the delay at the same time as its experimental
counterpart regardless of its behavior (response-independent). The first group of 12 rats
was the maintenance group in which the delay was added after polydipsia (excessive
water intake) was induced, and the second group of 12 rats was the acquisition group, in
which the delay was present from the outset of the experiment. After 30 sessions, the
animals were injected with d-amphetamine (0.1-3.0 mg/kg). In the experimental rats in
the maintenance group, 1.0 mg/kg d-amphetamine increased licks per minute by 200%
and water intake by 100%; the 3.0 mg/kg dose decreased rates. In contrast, d-
amphetamine dose-dependently decreased licks per minute and water intake in the yoked-
control rats. That is, the effects of d-amphetamine depended on the punishment
contingency. In both the experimental and yoked-control rats in the acquisition group, d-
amphetamine dose-dependently decreased licks per minute and water intake for both the
experimental and yoked control rats. The 1.0 mg/kg dose decreased rates the most with
the licking rate decreasing by almost 100% and the water intake decreasing by about
20%. The differential drug effects in the two groups of rats show that when punishment is
introduced, after schedule-induced drinking was established (maintenance group) or
during acquisition (acquisition group), affects the data.
Perez-Padilla and Pellon (2006) examined the effects of d-amphetamine on
punished and unpunished behavior at the same time. They used 16 rats and a typical
schedule-induced drinking procedure to examine if the level of response suppression is an
13
important determinant of d-amphetamine’s effects. The rats were divided into two groups
by Perez-Padilla and Pellon to examine the level of response suppression. The first group
was exposed to a multiple FT 30-s FT 45-s schedule, and the second group was exposed
to a multiple FT 30-s FT 90-s schedule. A lick-contingent signaled delay was added to
the FT 30-s component. Similar to Pellon et al. (1992), and Perez-Padilla and Pellon
(2003), Perez-Padilla and Pellon (2006) also found that d-amphetamine (0.1- 3.0 mg/kg)
dose-dependently increased (until the 3.0 mg/kg dose) punished schedule-induced
drinking in both groups. However, there was also an increase in the unpunished rate (FT
90-s) at the 1.0 mg/kg dose. The baseline rates in the FT 45-s FT 90-s group, however,
were very low. These data suggest that there may be an interaction between baseline
levels of schedule-induced drinking and the effects of d-amphetamine, showing that the
level of response suppression is an important determinant for the effects of d-
amphetamine. d-Amphetamine increased punished licking the most when it was the most
reduced (FT 30s with delay and FT 90s). Therefore, the greater the decrease in the licking
rate, the greater the effect of d-amphetamine.
d-Amphetamine has also been examined using shock as a punisher with schedule-
induced drinking with different results than those found with time-out as a punisher.
Flores and Pellon (1998) found that d-amphetamine dose-dependently decreased the licks
per minute with schedule-induced drinking punished by shock. In a subsequent study,
Perez-Padilla and Pellon (2007) found within the same session that d-amphetamine
decreased schedule-induced drinking when punished by shock and increased schedule-
induced drinking when punished by time-out. Therefore, when shock was used instead of
14
time-out to punish schedule-induced drinking, d-amphetamine decreased rates whether
examined across phases or within the same session.
Table 1 shows a summary of the research findings for d-amphetamine’s
increasing or decreasing effects on schedule-controlled behavior and schedule induced
behavior with shock and time-out.
Table 1 Summary of Findings Presented
Shock Time-Out
Increased Decreased Increased Decreased
Schedule-
Controlled
Foree et al.
1973
McMillan 1973
Evenden et al.
1998
Schedule-
Induced
Flores, Pellon
1998
Perez-Padilla &
Pellon 2007
Perez-Padilla &
Pellon 2003
(Acquisition)
Perez-Padilla &
Pellon 2003
(Maintenance)
Perez-Padilla &
Pellon 2006
Pellon et al.
1992
Perez-Padilla &
Pellon 2007
15
d-Amphetamine and Schedule-Controlled Behavior Punished by Time-Out
Different effects of d-amphetamine on rates of behavior have been found as a
function of the type of punisher; that is, shock and time-out. d-Amphetamine increased
rates of schedule-induced drinking punished by time-out (Perez-Padilla & Pellon, 2007),
but decreased rates of schedule-induced drinking punished by shock (Flores and Pellon,
1998). d-Amphetamine generally decreased schedule-controlled response rates punished
by shock (e.g., Foree et al., 1973). The effects of d-amphetamine on schedule-controlled
behavior punished by time-out have not been examined.
The present study replicated Branch et al. (1977) with time-out as the punisher
and d-amphetamine as the drug. In their study, pigeons’ key pecking was maintained by a
multiple RI 6-min RI 1-min schedule of mixed-grain presentation. Then a random ratio
(RR) 3 schedule of 20-s time-outs was added to the RI 1-min component. In a subsequent
phase, they punished responding in the RI 1-min component with shock presentation.
Branch et al. showed that pentobarbital had different effects on schedule-controlled
responding in pigeons dependent on the type of punisher. That is, response rates that were
suppressed by time-out presentation were not increased by pentobarbital; in contrast
response rates punished by shock were reliably increased (Branch et al., 1977). Similar to
studies by Perez-Padilla and Pellon (2007), these results indicate that effects of drugs on
punished behavior may depend on the type of punishment. In the present experiment, the
effects of d-amphetamine on schedule-controlled response rates punished by time-out
were examined. The procedure in the Branch et al. study was used so that effects of d-
amphetamine could be examined on punished and unpunished behavior within the same
session.
16
Current Experiment
Responding was maintained in four pigeons using a multiple RI 6-min, RI 1-min
schedule of food presentation with 20-s time-outs added to the RI 1-min component
presented with a RR2 schedule for two of the pigeons and a RR3 schedule for the other
two pigeons. The schedules were adjusted so that response rates in the punished
component were approximately half of the previously unpunished rates. There were two
components (RI 1-min and RI 6-min) with 3 presentations of each component, each 5
min long excluding time spent in time-out. There were no time-outs between
components. The effects of d-amphetamine (0.3, 1.0, 1.8, 3.0, and 5.6 mg/kg) were
examined.
Based on the literature, d-amphetamine could decrease rates in the punished
component and not decrease rates in the unpunished component. These differential
effects also are predicted by data that show that d-amphetamine affects timing (Odum,
Lieving, & Schall, 2002). That is, d-amphetamine would make it seem as though more
time has passed while the pigeon is in time-out than has actually passed, therefore the
time-out would seem longer and, therefore, the time-out would be more punishing.
d-Amphetamine could increase the rates of punished behavior and not change or
decrease unpunished rates. This differential effect is predicted by a rate-dependency
notion of amphetamine’s effects. That is, the low punished rates are increased by d-
amphetamine; whereas, the higher unpunished rates are not changed or decreased like the
results found by Pellon, et al. (1992) and discussed by Odum, Lieving, and Schall (2002).
These results would show that with schedule-controlled behavior, d-amphetamine
produced effects dependent on type of punisher and consistent with the schedule-induced
17
literature results found by Pellon et al. (1992) and Perez-Padilla and Pellon (2007). Time-
out would not seem as long and therefore would not be very effective in reducing the
given behavior. Therefore, this also suggests that time-out may not be effective as a
punisher if a child is taking a stimulant medication than if a child is not taking a stimulant
medication.
d-Amphetamine could decrease both punished and unpunished response rates.
This would show that d-amphetamine decreases schedule-controlled behavior with shock
and with time-out, suggesting that time-out and shock are equitable punishers with
schedule-controlled behavior like McMillan found in 1967.
d-Amphetamine could also increase both punished and unpunished response rates.
This would show that d-amphetamine has different effects on schedule-controlled
behavior based on the punisher suggesting that time-out and shock are not equitable
punishers, like the results found by Perez-Padilla and Pellon in 2007. These results may
reflect an overall stimulant effect in which behavior in general is increased.
METHOD
Subjects
Four racing homer pigeons were used; one of which was experimentally naïve
(Pigeon 190). The other three pigeons had responded under RI schedules and had a
previous history of being injected with d-amphetamine, but had not received d-
amphetamine for at least 6 months before the beginning of this study. Before training, the
birds were reduced to 80% of their free-feeding weight. They were weighed each day
before the session and again after the session and given the appropriate amount of Purina
Checkers after the session to maintain 80% of their free feeding weight. Water and health
18
grit were continuously available in their individual home cages in a colony room in which
humidity, light cycle (12 hr light/dark cycle, lights on at 7 a.m.), and temperature (69 to
71 degrees F) were controlled.
Apparatus
Four identical chambers were used in this experiment (BRS/LVE, Inc. model
SEC-002). The chambers opened on the side; the keys were on the right side of the
chamber when the door opened. The interior chamber was 35.0 cm by 30.5 cm by 36 cm.
There were three, 2.5-cm diameter, response keys equidistant from one another on the
right side of the chamber. The side keys were 9.0 cm from the corresponding side wall,
and each key was 8.5 cm apart (center to center) from the next key in a horizontal line.
The keys were 26 cm from the floor of the chamber. It took 0.25 N of force to be
considered a key peck. The three keys could be transilluminated red, yellow, and green,
though only the center key was used in this study. The food hopper, which was centered
11 cm below the center key, and the opening for the hopper was 5 cm by 6 cm. Three 1.2-
W houselights were located 6.5 cm directly above the center key in a row. The
houselights were red, white, and green; only the white light was used in this study. Each
chamber had a ventilation fan that ran throughout the session and there was white noise
white noise in the running room to mask any outside noises. The experiment was
programmed and the data were collected by using Med Associates® (Georgia, VT)
interfacing and software on a Windows computer. The computer was in an adjacent room
where interface equipment operated at 0.01-s resolution.
19
Behavioral Procedure
Following magazine training, key pecking was shaped for 1 pigeon through
differential reinforcement of successive approximations on the center key in the presence
of a yellow keylight. The other three pigeons were already key pecking. Food
presentation consisted of 3-s access to milo. The white houselight was illuminated
whenever the keylight was on. A light illuminated the hopper when food was made
available and the key lights and house light were no longer illuminated. Key pecking was
then reinforced according to an FR 1 schedule for one session, each session in the
presence of a red and a yellow keylight with 40 reinforcers. Then a multiple schedule of
RI 10-s RI 10-s was introduced in which only one schedule was in effect at a time, and
each was associated with either a red or yellow key light. Each component lasted for 10 s,
and the other schedule was in effect for 10 s; each component was presented 3 times.
There were no time-outs between components, and the only signal was the change of the
key light to designate the different component. Over several days, the RI values and
component lengths were gradually increased to a multiple RI 1-min RI 6-min schedule of
food presentation with 2 components presented 3 times each within a session, each
component lasted for 5 min. For Pigeons 838 and 863, the RI 1-min component was
associated with the red key light, and the RI 6-min component was associated with the
yellow key light. For Pigeons 190 and 567, the RI 1-min component was associated with
the yellow light, and the RI 6-min component was associated with the red key light. One
of the two components (RI 1-min or RI 6-min) was chosen at random to start the session
every day. There was a 2-hr time limit in place for all six components, so if the session
was not completed in 2 hr the session was terminated.
20
To determine whether the data were stable, the average response rates over the
last 10 days were compared to the rates of the first 5 and last 5 days of those 10 days in
each component. Each average from the 5-day blocks had to be within 10% of the
average for the 10 days for response rates to be considered stable. Once response rates
(R/min) were stable based on the criteria above under the baseline schedule, an RR
schedule of time-out (houselight and keylight were extinguished and key pecks did not
produce food) presentation was added to the RI 1-min component. Initially, the time-outs
were 20 s in duration and followed responses immediately with a probability of .33.
Because of lack of a clear punishment effect with Pigeons 863 and 190, the frequency of
timeouts was increased. Therefore, the schedule of timeout presentation was an RR3 for
Pigeons 838 and 567 and an RR2 for Pigeons 863 and 190. A peck that resulted in food
presentation could not also produce a time-out. If food and a time-out are scheduled at the
same time, the food is presented and the time-out is cancelled. The component length was
the same during the non-time-out component as during the time-out component exclusive
of the time spent in time-out (so time-in time was the same for the punished and
unpunished components).
Pharmacological Procedure
d-Amphetamine sulfate was dissolved in saline (0.9% sodium chloride) and
injected 15 min prior to selected sessions. Injections were given into the breast muscle
(i.m.) on alternating sides using a solution volume of 1.0 ml/kg. Injections were given no
more than twice a week. Before the administration of drugs was given, two saline
injections were administered and examined to ensure that there were no effects of the
injection. If the response rates were outside of the control range when saline was
21
administered, then that pigeon was injected with saline again until there were two saline
injections without a reaction. Then doses of 0.3, 1.0, 1.8 and 3.0 mg/kg were given two
times each, and more determinations were given to certain pigeons based on the data.
Each dose was given once before a dose was repeated. The 5.6 mg/kg dose was only
given once to Pigeon’s 863 and 567 because they stopped responding. Pigeon 863 had
lasting effects from the dose where he did not respond the day following the injection as
well as the day he was injected and ate no food for two days. The order of doses was
random within each round of doses. Pigeon 190 never received a saline or drug
administration. The number of administrations of each dose to each subject are presented
in Table 2.
Table 2 Number of administrations of saline and d-amphetamine.
Pigeon
Dose 838 863 567
Saline 7 6 6
0.3 mg/kg 3 2 2
1.0 mg/kg 4 4 3
1.8 mg/kg 4 3 3
3.0 mg/kg 3 3 3
5.6 mg/kg 3 1 1
Data Analysis
Only the first four components were used in data analysis because Pigeon 567 and
Pigeon 863 regularly did not finish the session once punishment was added to the RI 1-
min component. These two pigeons completed the first four components during baseline
every day so those components were used for all subjects. Only three subject’s data were
used because Pigeon 190 showed no punishment effect. The time-out duration and
22
frequency were manipulated with this pigeon; however, timeout never punished his
response rates. Because of this, he was never injected with d-amphetamine, and his data
were not used in the current analyses.
For the other three pigeons, the response rates were examined during the baseline
period for both the RI 1-min and the RI 6-min components. That is, how often each
pigeon responded in each of the components was calculated by dividing the number of
responses by the time available for responding. Reinforcement time was not included in
these calculations. Then the effect of time-out on these rates was examined. The time
during punishment (time-outs) was not included in the denominator. The reinforcement
rate also was calculated in both the RI 1-min and RI 6-min components, by dividing the
number of reinforcers earned in a component by the time spent in the component,
exclusive of time-out and reinforcement. Reinforcement rate also was calculated by
dividing the number of reinforcers earned in a component by the time spent in the
component inclusive of time-out #R/(time-in duration + (# TO x TO duration)) . Time-
out rate was calculated by taking the number of time-outs divided by time (minutes). The
effects of d-amphetamine on response rates were examined by constructing dose-effect
curves. Response rates were reported as percentage of saline. That is, the mean response
rate following injections at a particular dose was divided by the mean response rate
following saline injections. These calculations were conducted for all doses in each
component.
RESULTS
Figure 1 shows that during the prepunishment baseline, response rates were
higher in the RI 1-min component than in the RI 6-min component for each pigeon. Rates
23
were 30, 45, and 30 R/min higher in the RI 1-min component than in the RI 6-min
component for Pigeons 567, 863, and 838, respectively, during the prepunishment phase.
When timeouts were added to the RI 1-min component, there was a clear punishment
effect for each pigeon. That is, response rates decreased by 58.40, 17.29, and 61.41
R/min for Pigeons 567, 863, and 838, respectively. For Pigeons 838 and 567, response
rates in the RI 6-min component did not change when punishment was added to the RI 1-
min component. In contrast, for Pigeon 863, response rate in the RI 6-min component
increased from 18.07 to 44.78 R/min, such that response rates in both components were
approximately equal during the punishment baseline. For all of the pigeons, response
rates in the first 10 days of punishment generally were similar to rates in the last 10 days
of punishment before saline was administered. Pigeon 838 showed a decreasing trend in
rates in the RI 1-min component, as did Pigeon 567, though less of a decrease. Both
Pigeon 567’s and Pigeon 838’s rates in the RI 1-min component remained at the lower
rates shown in the last 10 days of punishment (to the first 10 days of punishment)
throughout the drug administration.
Mean reinforcement rate (SR/min) in each component (RI 1-min & RI 6-min)
during prepunishment, the first 10 days of punishment, and the last 10 days of
punishment before saline was administered for Pigeons 567, 863, and 838 can be seen in
Table 3 (ranges in parentheses). Mean reinforcement rate did not vary greatly from
prepunishment to punishment. For Pigeon 567, reinforcement rate in the RI 1-min
component increased slightly, and for Pigeon 863 reinforcement rate in the RI 6-min
component almost doubled. For these two pigeons, however, the range of reinforcement
rates across phases overlapped.
24
Figure 1. Overall response rate (R/min) across the last 10 days of the prepunishment
baseline, the first 10 days of the punishment baseline, and the last 10 days before the first
saline injection for Pigeons 567, 863, and 838 in the RI 1-min (open circles) and the RI 6-
min (filled circles) components. Note that the y-axes are different ranges across pigeons
and the gap in sessions for Pigeon 863 is because the punishment schedule was changed
from RR3 to RR2.
567
165 167 169 171 173 174 175 177 179 181 183 213 215 217 219 222 0
20
40
60
80
100
120
140
160
863
155 157 159 161 163 164 200 202 204 206 208 215 217 220 222 224 0
10
20
30
40
50
60
70
838
Session
156 158 160 162 164 165 168 170 172 174 176 192 194 196 198 201 0
20
40
60
80
100
120
140
160
180
200
RI 6 min RI 1 min
Res
po
nse
s/m
in
25
Table 3
Mean reinforcement rate (reinforcers/min of time in) with ranges in parentheses
Prepunishment 1st 10 punishment Last 10 punishment
Pigeon RI 1-min RI 6-min RI 1-min RI 6-min RI-1 min RI-6 min
567 0.89
(.50-1.30)
0.16
(0-0.40)
1.05
(0.50-
1.88)
0.26
(0.10-
0.50)
1.14
(0.60-1.50)
0.13
(0-0.30)
863 0.98
(0.40-
1.50)
0.13
(0-0.30)
0.92
(0.50 -
1.30)
0.22
(0-0.60)
1.02
(0.50 -
1.50)
0.25
(0.01-
0.40)
838 1.09
(0.60-
1.70)
0.18
(0-0.30)
0.90
(0.60 -
1.30)
0.16
(0-0.40)
1.03
(0.30-1.40)
0.22
(0-0.50)
Table 4
Reinforcement Rate (Reinforcers per minute including time-outs)
Pigeon 1st 10 punishment Last 10 punishment
567 0.11
(0.06-0.17)
0.13
(0.08-0.17)
863 0.13
(0.06-0.19)
0.14
(0.08-0.25)
838 0.13
(0.07-0.24)
0.19
(0.05-0.26)
Table 4 shows the mean reinforcement rate including time spent in time-out
during the first 10 days of punishment and the last 10 days of punishment for Pigeons
567, 863, and 838. When reinforcement rate was calculated this way, the mean
reinforcement rates in both components were more similar (compare Tables 3 and 4).
Reinforcement rate decreased substantially (up to 90%) when time spent in time-out was
included compared to when reinforcement rate was calculated without time spent in time-
out for all three pigeons.
26
Table 5 shows the mean time-out rate (TO/min) during the first 10 days of
punishment and the last 10 days of punishment before saline was administered for
Pigeons 567, 863, and 838 (ranges in parentheses). Mean time-out rate stayed
approximately the same for Pigeons 567 and 863 from the first 10 days of punishment to
the last 10 days of punishment with only slight decreases. Time-out rate decreased from
the first 10 days of punishment to the last 10 days of punishment the most for Pigeon 838.
Table 5
Time-out Rate (number of timeouts per minute)
Pigeon 1st 10 punishment Last 10 punishment
567 22.88 (16.25 – 25.91)
22.79 (19.44 – 24.52)
863 19.85 (17.44 – 22.53) 18.69 (11.76 – 21.93)
838 18.02 (11.66 – 26.31) 13.26 (11.26 – 15.15)
Figure 2 shows that for Pigeons 567 and 863, d-amphetamine tended to have
dose-dependent decreases in response rates. d-Amphetamine decreased response rates for
Pigeon 567 at all doses in both components with no differential effects. For Pigeon 863,
there were differential effects at the 1.0 mg/kg dose with increases in the unpunished
component and decreases in the punished component. There were also slight differential
effects at the 0.3 mg/kg dose with increases in both the punished and unpunished
components, but with the unpunished component increasing more than the unpunished
component. For Pigeon 838, there were differential effects at all doses with increases in
the punished components at all doses (except 5.6 mg/kg), and decreases in the
unpunished component at all doses. Saline response rates in the RI 1-min and RI 6-min
27
Figure 2. Mean response rate (R/min) as a percentage of saline rates as a function of the
dose of d-amphetamine for Pigeons 567, 863, and 838 in the punished RI 1-min (open
circles) and the unpunished RI 6-min (filled circles) components. The error bars are
ranges. Note that the y-axes are different ranges across pigeons.
Dose Effect Curves
0.3 1.0 3.0 5.6 0
20
40
60
80
100
120
567
863
0.3 1.0 3.0 5.6
Pe
rcen
tag
e o
f S
alin
e R
ate
s
Rate
s
0
50
100
150
200
250
838
d -Amphetamine (mg/kg)
0.3 1.0 3.0 5.6 0
20
40
60
80
100
120
140
Unpunished Punished
28
components for Pigeon’s 567, 863, and 838 can be found in Table 6 where ranges are in
parentheses.
Table 6
Response rates (R/min) from sessions before which saline was administered with ranges
in parentheses.
Pigeon RI 1-min RI 6-min
567 66.53 (48.54 – 85.21) 103.26 (86.11 - 110.83)
863 41.03 (33.69 – 45.95) 28.01 (19.04 – 44.15)
838 32.05 (27.61 – 38.77) 90.11 (82.43 - 101.86)
Table 7
Time-Out Rate (timeouts per minute) during the RI 1-min component during sessions
before which no injection (control), saline, or a dose of d-amphetamine was given with
ranges in parentheses.
Dose 567 863 838
Control 21.02 (15.15 – 27.31) 18.44 (10.17 – 25.52) 8.88 (3.99 – 11.36)
Saline 21.88 (15.35 – 28.70) 20.22 (15.55 – 23.52) 10.14 (8.57 – 11.76)
0.3 mg/kg 24.42 (22.72 – 27.11) 22.58 (16.55 – 28.31) 9.97 (7.38 – 12.16)
1.0 mg/kg 20.17 (17.14 – 22.92) 16.20 (1.60 – 27.31) 12.33 (9.57 – 17.34)
1.8 mg/kg 14.85 (12.36 – 17.14) 4.65 (0 - 19.54) 13.11 (7.97 – 16.15)
3.0 mg/kg 11.66 (7.38 – 14.35) 3.79 (0 – 13.36) 13.16 (10.37 – 16.35)
5.6 mg/kg 3.19 (1.40 – 4.98)
0 7.51 (2.59 – 10.37)
29
Table 7 shows the mean time-out rate (TO/min) for Pigeons 567, 863, and 838
from control sessions and session before which saline and doses of d-amphetamine were
administered (ranges in parentheses). The mean time-out rate decreased as a function of
an increasing dose of d-amphetamine for Pigeons 567 and 863. Relative to the time-out
rate when saline was administered, Pigeon 838’s time-out rate increased at 1.0, 1.8, and
3.0 mg/kg.
Table 8
Reinforcement Rate (R/min) during sessions before which no injection (control), saline,
or a dose of d-amphetamine was given with ranges in parentheses.
567 863 838
Dose RI 1-min RI 6-min RI 1-min RI 6-min RI 1-min RI 6-min
Control 0.94
(.50 -
1.70)
0.15
(0 - 0.40)
1.09
(0.60 –
2.30)
0.16
(0 – 0.04)
0.96
(0.50 -
2.40)
0.17
(0 - 0.60)
Saline 1.10
(0.70 -
1.50)
0.25
(0 - 0.40)
0.93
(0.30 –
1.60)
0.17
(0.10 –
0.30)
0.80
(0.40 -
1.10)
0.14
(0 - 0.30)
0.3 mg/kg 1.10
(1.00 -
1.20)
0.30 1.10
(0.60 –
1.60)
0.25
(0.20 –
0.30)
0.80 0.30
(0.10 -
0.60)
1.0 mg/kg 0.80
(0.70 -
0.90)
0 0.82
(0.50 –
1.10)
0.07
(0 – 0.30)
1.12
(0.90 –
1.50)
0.25
(0.10 –
0.50)
1.8 mg/kg 1.00
(0.90 -
1.10)
0.33
(0.20 -
0.50)
0.63
(0.30 –
1.10)
0.13
(0.10 –
0.20)
0.90
(0.50 –
1.30)
0.12
(0 – 0.30)
3.0 mg/kg 1.13
(0.90 -
1.30)
0.27
(0.20 -
0.40)
0.33
(0.10 –
0.70)
0 0.90
(0.80 –
1.00)
0.10
(0 – 0.20)
5.6 mg/kg 0.7975
0 0 0 0.83
(0.70 –
0.90)
0.03
(0 – 0.10)
30
Table 9
Reinforcement Rate with d-Amphetamine Including Time-out
Dose 567 863 838
Control 0.12
(0.06-0.17)
0.15
(0.09-0.29)
0.24
(0.13-0.47)
Saline 0.13
(0.09-0.24)
0.12
(0.04-0.19)
0.18
(0.10-0.27)
0.3 mg/kg 0.12
(0.11-0.13)
0.13
(0.07-0.19)
0.19
(0.16-0.21)
1.0 mg/kg 0.10
(0.09-0.13)
0.13
(0.07-0.27)
0.22
(0.15-0.33)
1.8 mg/kg 0.17
(0.15-0.20)
0.25
(0.21-0.44)
0.17
(0.08-0.23)
3.0 mg/kg 0.23
(0.22-0.25)
0.15
(0.09-0.16)
0.17
(0.16-0.19)
5.6 mg/kg 0.39 0 0.24
(0.18-0.34)
Tables 8 and 9 shows the mean reinforcement rate excluding (Table 8) and
including (Table 9) time spent in time-out for Pigeons 567, 863, and 838 from control
sessions and from sessions before which saline and doses of d-amphetamine were
administered (ranges in parentheses). Mean reinforcement rate was fairly consistent in the
RI 1-min component for all of the pigeons until the larger doses where the reinforcement
rate decreased. In the RI 1-min component there were increases in reinforcement rate at
the 0.3 mg/kg dose for Pigeon’s 863 and 838 and 1.0 mg/kg for Pigeon 838, but
decreases for Pigeon 567 at those two doses. Pigeons 567’s and 838’s reinforcement rate
increased at the highest dose while Pigeon 863’s dropped to 0.
31
In order to determine whether there were time-course effects of d-amphetamine,
dose-effect curves were constructed based on response rates in the first and second
presentations of the RI-1 min (punished) and RI 6-min (unpunished) components. Figure
3 shows these dose-effect curves; data from the first two presentations of each component
are displayed in the left panel, and data from the second two presentations of each
component are displayed on the right. Pigeons 567 and 838 show similar effects across
the presentations. There is not much difference between punished and unpunished rates
early in the session (first presentations), but there appear to be larger decreases in the
unpunished component at the 1.8, and 3.0 mg/kg dose later in the session (second
presentations) as compared to earlier in the session, though the error bars overlap.
Therefore, Pigeon 567’s rates are similar across all the presentations of the components.
For Pigeon 863, d-amphetamine’s effects also were slightly different across the
session. Early in the session (first presentations) for Pigeon 838, d-amphetamine
produced differential effects on punished and unpunished key pecking. At 0.3 and 1.0
mg/kg, response rates in the unpunished component were substantially increased (e.g.,
61.94% from saline at the 1.0 mg/kg). Rates differed between the components at the 1.0,
1.8, and 3.0 mg/kg doses (e.g., at the 1.0 mg/kg dose unpunished rates increased 61.94%
while punished rates increased 3.14% from saline). In the second presentations of the
session, his rates differed at the 1.0, 1.8, and 3.0 mg/kg doses (e.g., at the 1.0 mg/kg dose
d-amphetamine decreased response rates 11.61% in the unpunished component and
decreased 38.98% in the punished component).
For Pigeon 838, d-amphetamine produced similar effects in each component
across the session; that is, rates in the RI 1-min (punished) component were increased
32
Figure 3. Mean response rates expressed as a percentage of saline rates as a function of
the dose of d-amphetamine for Pigeons 567, 863, and 838 in the punished RI 1-min (open
circles) and the unpunished RI 6-min (filled circles) components. The graphs on the left
show the data from the first presentation of the punished component and first unpunished
component in the session. The graphs on the right show the data from the second
presentation of the punished component and second unpunished component in the
session. The error bars are ranges.
Presentation 1
0.3 1.0 3.0 10.0 0
50
100
Presentation 2
0.3 1.0 3.0 10.0 0
20
40
60
80
100
120
863
0.3 1.0 3.0 10.0
Pe
rcen
t Sa
line
0
50
100
150
200 863
0.3 1.0 3.0 10.0 0
50
100
150
200
838
Dose d -Amphetamine mg/kg
0.3 1.0 3.0 10.0 0
20
40
60
80
100
120
140
160
Dose d -Amphetamine mg/kg
10.0
838
0.3 1.0 3.0 0
20
40
60
80
100
120
140
160
567 567
Unpunished Punished
33
above saline rates, and rates in the RI 6-min (unpunished) component were dose-
dependently decreased. The differential effects were more pronounced later in the session
(e.g., at the 1.8 mg/kg dose in the first presentations d-amphetamine increased punished
rates 18.09% and decreased unpunished rates 36.37% from saline while in the second
presentations, d-amphetamine increased punished rates 31.92% and decreased
unpunished rates 46.66% from saline). Overall, all three pigeon’s rates were fairly
consistent across presentations within each subject.
DISCUSSION
In this experiment, there were three goals: to replicate the Branch et al. (1977)
study with respect to a punishment baseline, to examine d-amphetamine’s effects on
punished and unpunished schedule-controlled behavior, and to interpret those effects in
terms of children who are placed in time-out and are on a stimulant medication.
Timeout Punishment
Figure 1 shows that response-contingent presentation of time-out punished
response rates. Although time-out punished response rates, there were two different
punishment effects. Pigeon 863 showed the punishment effect that was desired, and
which replicated the punishment effect found in the Branch et al. (1977) study; that is,
response rates in each component were approximately equal after punishment was added,
with response rates decreasing in the RI 1-min component and increasing in the RI 6-min
component. Pigeon’s 567 and 838’s response rates decreased in the RI 1-min component
without affecting response rates in the RI 6-min component so that their response rates
were not equal in the two components. Thus, the different punishment effects with these
pigeons may have been a function of the baseline rates. That is; Pigeons 567 and 838’s
34
response rates in both components were high (compared to Pigeon 863) and very similar
before punishment was added (113.31 R/min in the RI 6-min and 138.53 R/min in the RI
1-min and 95.60 R/min in the RI 6-min component and 118.40 R/min in the RI 1-min
component, respectively). Thus, when their RI 1-min rates were punished, their RI 1-min
rates dropped below those found in the RI 6-min component. In contrast, Pigeon 863’s
rates in the RI 6-min component were very low during prepunishment (18.07 R/min), and
this pigeon showed the biggest difference between baseline rates in the two components
(RI 1-min rates were 58.19 R/min). When punishment was added, his RI 1-min rates
decreased, and his RI 6-min rates increased to match the punished RI 1-min rates. It may
be possible to obtain more consistent results if prepunishment rates were more
differentiated (like those found in Pigeon 863) so that all three pigeons would have the
same punishment effect; that is, having separate rates during prepunishment and
comparable rates during punishment.
A possible way to arrange more disparate rates in the two components during
baseline would be to increase the RI value from 6 min to a higher value (e.g., 9 min). A
longer RI should result in lower response rates. Branch et al. (1977) had shorter
component lengths than in the current study (3 min instead of 5 min) and had more
presentations of the components per session (4 instead of 3). Perhaps having more
presentations for a shorter duration might help to differentiate the rates between the
components. With shorter components (3 min), it is less likely that the pigeon will
receive any reinforcers in the RI 6-min component than it is if the components are longer
(5 min); fewer reinforcers could produce lower rates. So, perhaps shorter component
35
lengths or increasing the interval value would create more differentiated baseline rates in
the two components.
Another plausible reason for undifferentiated rates between the components was
poor stimulus control over behavior in the multiple schedule. One reason for this could be
the lack of a time-out between each component. Having a black-out between components
would help the discriminative stimuli in the components establish better stimulus control
over response rates. Using a black-out in this experiment was not feasible, however,
because time-out was the punisher being used, and a time-out between components
would serve as a response-independent time-out and could alter punishment effects
within components. Therefore, a time-out between components is not a way to obtain
more differentiated response rates prior to punishment unless a different type of time-out
was used. If a different stimulus, for example, a different keylight color that was
associated with extinction, was used as the time-out signal, then black-outs could be used
between components. This might allow for more differentiated response rates prior to
punishment.
Various parameters could be manipulated in an attempt to produce differentiated
rates prior to punishment. For example, the RI 6-min schedule could be increased to an
RI 15-min for Pigeon 838 and the number of component presentations could be altered to
obtain more differentiated rates prior to punishment. Attempts could also be made to
produce equal rates during punishment by altering the duration and frequency of the
time-out.
Branch el al. (1977) did not say how long it took them to obtain their stable
baseline or how they determined that RI 6-min and RI 1-min were the schedule values to
36
use. The pigeon’s rates when punished were equal or near equal for all of their subjects. It
was not stated whether this took them considerable time and effort to achieve, or whether
it happened on the first attempt. With the four subjects used in this study, only one had
punished rates that were equivalent to the unpunished rates. It would be useful to know
how long it took Branch et al. to achieve the punished response rates that they did with all
of their subjects and why they chose the parameters that they did.
d-Amphetamine’s Effects on Punished Schedule-Controlled Behavior
In this study, d-amphetamine’s effects on schedule-controlled behavior were
inconsistent across subjects, as shown in Figures 2 and 3. Pigeon 567 showed a general
decrease in both components at all doses. Pigeon 838 showed increases in the punished
component and decreases in the unpunished component. Pigeon 863 showed increases in
both components at the 0.3 mg/kg dose and increases in the unpunished component only
at the 1.0 mg/kg dose. He then showed a decrease in both components at all remaining
doses. Pigeon 863 may needed more lower doses to show a different effect.
d-Amphetamine’s general decrease in response rates for Pigeons 567 and 863
(with some differential effects for Pigeon 863) replicates other data that show decreases
in responding when shock is used as a punisher (Foree et al., 1973; Flores & Pellon,
1998; Perez-Padilla & Pellon, 2007). Thus, these subjects’ data suggest that time-out
(negative punishment) and shock (positive reinforcement) are functionally similar
punishers. These decreases might be seen because d-amphetamine is a motivating
operation and changes the efficacy of food; that is, food may not be serving as a strong
reinforcer any more (as it was previously before drugs were administered). d-
37
Amphetamine could also have motoric effects, so the pigeon might be less able to peck
the key.
The rate-decreasing effects of d-amphetamine on punished behavior seen with
Pigeon 567 and 863 are in conflict with the findings of Pellon et al. (1992), Perez-Padilla
and Pellon (2003), and Perez-Padilla and Pellon (2006) with schedule-induced behavior.
A possible explanation for this discrepancy is the type of behavior being punished. That
is, with the schedule-induced behavior, the rat received food if it did not lick the water
tube (Pellon et al.), whereas in the current experiment the pigeon had to key peck in order
to receive food even though this same response also occasionally produced a time-out.
Thus, in the studies in which schedule-induced behavior was punished, the responses that
produced food (i.e., doing something else other than licking) and that produced timeout
(i.e., licking) were incompatible; whereas, in the current experiment, the responses (key
pecking) were the same response. Also, Foree et al. (1973) showed that d-amphetamine
had different drug effects based on the schedule that was in effect (FR or FI). An FT
schedule of food delivery was used in the schedule-induced drinking procedures, and an
RI schedule was used in the current experiment, the different drug effects found may be
due to these different schedules.
For Pigeon 863, the lowest dose (0.3 mg/kg) here increased response rates in both
components during both presentations. In the first presentation, the first two doses
increased response rates in both the RI 1-min and the RI 6-min components. Higher doses
produced differential effects on rate with increases in the unpunished component and
decreases in the punished component until the 3.0 mg/kg dose in the first presentation. In
the second presentation, the lowest dose (0.3 mg/kg) had increases in both components,
38
while the 1.0 mg.kg dose had decreases in the punished component. In the second
presentation, his response rates were almost completely suppressed at the 1.8 mg/kg dose,
especially in the unpunished component. It is unclear whether 1.8 mg/kg was a large dose
for him based on the discrepancy between the results from the first presentation and the
second presentation. Similar effects to those seen during the first presentation at the first
two doses (increases) may have been observed if smaller doses of the drug had been
administered. The dose-dependent effects, that is the larger doses of the drug decreasing
rates and the smaller doses increasing rates, are consistent with Foree et al. (1973) in the
FR component as well as Perez-Padilla and Pellon (2003), and Perez-Padilla and Pellon
(2006). The increase in both punished and unpunished response rates at lower doses
generally are not seen when shock is administered, therefore, these data suggest that
time-out and shock might not be equitable punishers. These rate increases might also be a
typical stimulant effect; that is, an overall increase in behavior.
In contrast to the other two pigeons, for Pigeon 838, d-amphetamine increased
punished behavior at doses that decreased unpunished responding, replicating the data of
Pellon and Blackman (1992), Perez-Padilla and Pellon (2003) with the maintenance
group, and Perez-Padilla and Pellon (2006) in which d-amphetamine increased schedule-
induced behavior punished by time-out. This pigeon had low punished rates (39.32
R/min) relative to his unpunished rates (86.86 R/min) as seen in Figure 1. The differential
drug effects on punished and unpunished responding could be described as rate-
dependent effects, that is, low rates of behavior were increased and high rates of behavior
were decreased. It is important to note that the difference is not in absolute rates,
otherwise, Pigeon 863’s decrease in rates in the RI 1-min component and increase in rates
39
in the RI 6-min component from pre-punishment to punishment during baseline would be
described as rate dependent. Pigeon 863’s rates would not be described as rate dependent
because it is not just absolute rates but in the contrast between the rates as seen in Pigeon
838. d-Amphetamine’s effects on schedule-controlled behavior have been described as
rate-dependent across many procedures (Dews & Wenger, 1977; Kelleher & Morse,
1968; McKearney & Barrett, 1978, Evenden et al., 1998).
Rate-dependency, Timing, and d-Amphetamine
Because punishment in this experiment involved presentation of a duration of
time-out and d-amphetamine has been shown to have effects on timing (Odum et al.,
2002), the effects in this experiment may have been a product of d-amphetamine’s effects
on timing. The scalar expectancy theory (SET) or temporal overestimation, is an
information processing model of timing with three stages; clock, memory, and decision.
Meck (1996) proposed that there is a clock that acts like a pacemaker keeping time for
the animal and dopamine levels affect the rate of the pacemaker and, therefore, the
perception of the passage of time. So, the more dopamine there is in the system, the faster
the clock ticks. Administrations of d-amphetamine would increase dopamine and
purportedly increase the clock and produce an overestimation of time. That is, it would
seem to the animal as though more time had passed than the time that had actually
passed. If this were the case in the current experiment, then the time-out would seem
longer, and there would be a decrease in response rates in the punished component. The
general response-rate decreasing effects of d-amphetamine seen with Pigeons 567 and
863 appear to support this view. However, Pigeon 567 also had decreases in his
40
unpunished component where there was no time-out. This does not support the timing
hypothesis.
For Pigeon 863, there were larger decreases in the punished component than in
the unpunished component, making a given duration of time seem longer so time-out is
more aversive. This supports the timing hypothesis that the clock ticks faster so the
subject overestimates the passage of time.
Odum et al. (2002) examined time discrimination in pigeons to differentiate
between rate dependency and SET or temporal overestimation. The procedure used by
Odum et al. was a multiple schedule version of the timing procedure of Reynolds and
Catania (1962). The pigeons were trained using two duration samples of the houselight lit
for either 5 s or 30 s. Then the houselight was turned off and the key was lit either blue or
green. If the keylight was blue and the houselight was on for 5 s, then pecking was
reinforced according to a VI 20-s schedule. If the keylight was green and the houselight
was on for 5 s, then pecking was not reinforced. If the keylight was green and the
houselight was on for 30 s, then key pecks were reinforced on a VI 20 s schedule and if
the houselight was on for 30 s and the keylight was blue, then key pecks were not
reinforced. Once the pigeons were responding reliably, they added intermediate sample
durations (10, 15, 20, and 25 s), but key pecking was not reinforced after these
intermediate sample durations. The highest rate on the blue key occurred when the 5-s
sample occurred, and rates decreased on the blue key as a function of the increasing
sample duration. The highest rate on the green key occurred when the 30-s sample
occurred, and rates decreased on the green key as a function of decreasing sample
41
duration. The two functions crossed at an intermediate sample duration; the point at
which the functions cross is the point of subjective equality (PSE).
Then d-amphetamine (0.1, 0.3, 1.0, and 3.0 mg/kg) was administered. If the clock
theory was correct and amphetamine produced an overestimation of time, then the
functions would be shifted to the left and the PSE would be reduced. Underestimation of
time would shift the functions to the right and the PSE would be increased. If the effect of
amphetamine was rate dependency, then the PSE should stay the same and low rates of
responding should increase and higher rates of responding should decrease. That is, the
functions should flatten.
Odum et al. (2002) found in all four pigeons that behavior showed discriminative
control by time without drugs and temporal discrimination based on the duration (longest
and shortest duration). That is, during the short component, mean rates of responding
decreased as a function of sample duration, and during the long component, mean rates of
responding increased as a function of sample duration. They found that d-amphetamine
did not shift the PSE. Rather, they found that the function was flattened (high rates being
decreased and low rates being increased). Therefore, their data do not support a timing
theory of d-amphetamine’s effects, rather, their data support rate dependency.
In the current experiment, the data with Pigeon 838 also support rate dependency
and do not support the overestimation of timing hypothesis of d-amphetamine’s effects.
Indeed, Pigeon 838’s data suggest that there was an underestimation of time. That is, it
would seem to the animal as though less time had passed than the time that had actually
passed. Therefore, the time-out would seem shorter, and there would be an increase in
responding in the punished component. These effects also support the delay discounting
42
literature, Pitts and McKinney (2005) concerning d-amphetamine and sensitivity to delay.
In a typical delay-discounting procedure, choices for a larger reinforcer decrease as delay
to it increases. Stimulants tend to increase choices of the larger more delayed reinforcer
(Pitts & Febbo, 2004; Pitts & McKinney). Pitts and Febbo trained pigeons under a
concurrent-chains schedule. In the initial link, two key lights were transilluminated in the
chamber. The pigeon responded on the keys in the initial link in order to reach the
terminal link, in which food reinforcement was available. The initial link ran on an RI 1-
min schedule. The first response on the selected key after the interval elapsed produced
the terminal link associated with that key. In the terminal link, one key was associated
with the smaller, sooner reinforcer, 1-s access to grain after a 2-s delay. The other key
was associated with the larger, more delayed reinforcer, a 4-s access to grain after a delay
that ranged from 2s to 40s. The delays associated with the larger reinforcer increased
systematically across blocks of the session. During baseline, rates maintained by the
larger reinforcer decreased while rates maintained by the smaller reinforcer increased as
the delay to the larger reinforcer increased. Pitts and Febbo found that methamphetamine
increased preference for the larger reinforcer when it was delayed relative to preference
seen in control sessions. They analyzed the data quantitatively and found that
methamphetamine decreased the pigeon’s sensitivity to reinforcement delay. These
results suggest that a behavioral mechanism of stimulants’ effects is a decrease in the
discounting effects of reinforcement delay. TA, Pitts, Hughes, McLean, and Grace (2008)
also maintained responding of 8 pigeons using a concurrent-chains procedure. This
procedure is similar to the procedure used by Pitts and Febbo. There were initial links
that lead to terminal links. The initial links ran on a VI 10-s schedule. One of the terminal
43
links was associated with an FI 8-s schedule consistently throughout the study. The
schedule that was in effect in the other terminal link changed between an FI 4-s schedule
and an FI 16-s schedule unpredictably across sessions. Responding under this schedule
was stable with the pigeon’s allocating their responses to the FI 4-s schedule when the FI
4-s and FI 8-s schedules were the available options, and chose the FI 8-s schedule when
the FI 8-s and FI 16-s schedules were the available options. TA et al. examined d-
amphetamine’s effects on reinforcement delay. They found that d-amphetamine
decreased response allocation for the shorter delay; that is, responding on the FI 4-s
schedule (when the FI 4-s and FI 8-s schedules were in effect) and FI 8-s schedule (when
the FI 8-s and FI 16-s schedules were in effect) was decreased so that the response
allocation to the two options were closer together (responding trended toward
indifference). Similar to Pitts and Febbo, they found that d-amphetamine reduced
sensitivity to reinforcement delay. For Pigeon 838, there were increases in response rates
in the punished component with d-amphetamine, suggesting that time-outs seemed
shorter. Therefore, based on previous data, if sensitivity to delay is decreased then delay
would have less of an effect and responding would increase, as seen with Pigeon 838’s
increase in punished responding with d-amphetamine.
Use of Time-Out and d-Amphetamine with Children
In the current study, different effects of d-amphetamine were found on behavior
punished by time-out. One effect with Pigeon 838 suggests that d-amphetamine increases
rates of behavior punished by time-out, which would not be beneficial and actually make
the targeted behavior increase (instead of the goal of decreasing the behavior with time-
out). Another effect is with the decreasing effects, specifically with a larger decrease in
44
the punished component than in the unpunished component, found with Pigeon 863 at
one dose, suggest that in some cases d-amphetamine may make time-out more aversive,
which would be beneficial. Understanding the conditions that predict the effects of d-
amphetamine is essential. Those conditions most likely were not baseline reinforcement
rate because, although it was slightly higher with Pigeon 838 than the other two pigeons
(see Table 3), it was not that different across the three pigeons. The different effects seen
may have to do with the overall rate of punished behavior. If the overall rate of the
punished behavior is low (e.g., Pigeon 838), then d-amphetamine shows rate-dependent
effects; that is, it increases these low rates of punished behavior. When the punished rates
were not low (e.g., Pigeon 567) a decrease was shown, and when the punished rates were
equal with the unpunished rates (Pigeon 863) there was a general decrease in both
components (with a larger decrease in the punished component).
More work needs to be done to manipulate the schedule, time-out duration, and
time-out frequency until punished responding is equal to unpunished responding. Once
this punished baseline is achieved, d-amphetamine should be readministered and its
effects examined, hopefully yielding consistent results.
45
References
Branch, M. N., Nicholson, G., & Dworkin, S. I. (1977). Punishment-specific effects of
pentobarbital: dependency on the type of punisher. Journal of the Experimental
Analysis of Behavior, 28, 285-293.
Catania, A. C., & Reynolds, G. S. (1968). A quantitative analysis of the responding
maintained by interval schedules of reinforcement. Journal of the Experimental
Analysis of Behavior, 11, 327-383.
Cooper, J. O., Heron, T. E., & Heward, W. L. (2007). Applied behavior analysis (2nd
ed.).
New Jersey: Pearson Prentice Hall.
Dews, P. B., & Wenger, G. R. (1977). Rate-dependency of the behavioral effects of
amphetamine. Advances in Behavioral Pharmacology, 1, 167-227.
Evenden, J., Duncan, B., & Ko, T. (1998). A comparison of the effects of
psychotomimetics and anxiolytics on punished and unpunished responding
maintained by fixed interval schedules of food reinforcement in the rat.
Behavioural Pharmacology, 9 (2), 127-135.
Falk, J. L. (1961). Production of polydipsia in normal rats by an intermittent food
schedule. Science, 133, 195-196.
Flores, P., & Pellon, R. (1998). Effects of d-amphetamine, diazepam and buspirone on
schedule-induced polydipsia suppressed by response-dependent and response-
independent shock. Behavioural Pharmacology, 9, 127-135.
Foree, D. D., Moretz, F. H., & McMillan, D. E. (1973). Drugs and punished responding
II: d-Amphetamine induced increases in punished responding. Journal of the
Experimental Analysis of Behavior, 20 (2), 291-300.
46
Geller, I., Seifter, J. (1960). The effect of meprobamate, barbiturates, d-amphetamine and
promazine on experimentally induced conflict in the rat. Psychopharmacology, 1,
482–492.
Kelleher, R. T., & Morse, W. H. (1968). Determinants of the specificity of the behavioral
effects of drugs. Ergebnisse der Physiologie, 60, 1-56.
McKearney, J. W., & Barrett, J. E. (1978). Schedule-controlled behavior and the effects
of drugs. Contemporary Research in Behavioral Pharmacology, 1-68.
McMillian, D. E. (1967). A comparison of the punishing effects of response-produced
shock and response-produced time out. Journal of the Experimental Analysis of
Behavior, 10, 439-449.
McMillan, D. E. (1973). Drugs and punished responding I: rate-dependent effects under
multiple schedules. Journal of the Experimental Analysis of Behavior, 19, 133-
145.
Meck, W. H. (1996). Neuropharmacology of timing and time perception. Cognitive Brain
Research, 3, 227-242.
Myer, P., & Serwach, J. (2008). Various stimulant drugs show continuing gradual
declines among teens in 2008, most illicit drugs hold steady. Retrieved July 30,
2009 from www.monitoringthefuture.org
National Institute of Drug Abuse (2009). The science of drug abuse and addiction.
Retrieved September 23, 2009 from http://www.drugabuse.gov/NIDAHome.html
Odum, A. L., Lieving, L. M., & Schaal, D. W. (2002). Effects of d-amphetamine in a
temporal discrimination procedure: Selective changes in timing or rate
dependency? Journal of the Experimental Analysis of Behavior, 78, 195-214.
47
Pellon, R., Mas, B. & Blackman, D. E. (1992). Effects of d-amphetamine and of
diazepam on non-punished and punished schedule-induced drinking in rats.
Behavioural Pharmacology, 3, 75-81.
Perez-Padilla, A., & Pellon, R. (2003). Amphetamine increases schedule-induced
drinking reduced by negative punishment procedures. Psychopharmacology, 167,
123-129.
Perez-Padilla, A., & Pellon, R. (2006). Level of response suppression and amphetamine
effects on negatively punished adjunctive licking. Behavioural Pharmacology, 17,
43-49.
Perez-Padilla, A., & Pellon, R. (2007). Behavioural and pharmacological specificity of
the effects of drugs on punished schedule-induced polydipsia. Behavioural
Pharmacology, 18, 681-689.
Pitts, R. C., & Febbo, S. M. (2004). Quantitative analyses of methamphetamine’s effects
on self-control choices: Implications for elucidating behavioral mechanisms of
drug action. Behavioral Processes, 66, 213-233.
Pitts, R. C., & McKinney, A. P. (2005). Effects of methylphenidate and morphine on
delay-discount functions obtained within sessions. Journal of the Experimental
Analysis of Behavior, 83, 297-314.
TA, W.M., Pitts, R. C., Hughes, C. E., McLean, A. P., & Grace, R. C. (2008). Rapid
acquisition of preference in concurrent chains: Effects of d-amphetamine on
sensitivity to reinforcement delay. Journal of the Experimental Analysis of
Behavior, 89, 71-91.
48
van Haaren, F., & Anderson, K. G. (1997). Effects of chlordiazepoxide, buspirone and
cocaine on behavior suppressed by timeout presentation. Behavioural
Pharmacology, 8, 174-182.
Zuvekas, S. H., Vitiello, B., Norquist, G. S. (2006). Recent trends in stimulant medication
use among U. S. children. American Journal of Psychiatry, 163, 579-585.