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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

d-AMPHETAMINE’S EFFECTS ON BEHAVIOR PUNISHED BY …dl.uncw.edu/Etd/2010-3/guidoe/emilyguido.pdf · Emily E. Guido A Thesis Submitted to the University of North Carolina Wilmington

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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

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