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PULSATILE LH SECRETION IN 0VARIECTOMIZED LACTATING RAT WITH HYPOTHALAMIC DEAFFERENTATION. HIROK0 TSUKAMURA t KEI-ICHIRO MAEDA & AKIRA YAROYAMA. School of A~riculture, Na$oya University, Nagoya 464-01, JAPAN.

We measured pulsatile luteinizing hormone (LH) secretion in ovariectomized lactating rats with complete (CC), anterior (AC), anterior-lateral (ALC), posterior (PC), or roof (RC) deafferentation of the hypothalamus. All lactating rats were ovariectomized on day 2 of lactation (day 0 = day of parturition) and deafferentation of nerve fibers to the medial basal hypothalamus (MBH) was performed under ether anesthesia on day 6 or 7 of lactation. About 24 h after the surgery, blood samples started to be withdrawn through the indwelling atrial catheter every 6 min for 3 h. LH and prolactin (PRL) in the plasma were measured by RIA. The typical pulsatile LH secretion was observed in all rats having CC, ALC and RC, but was suppressed in AC, PC and sham-deafferented animals. No significant difference was found in plasma PRL concentrations in all groups. These results suggest: i, the inhibiting information for activity of the GnRH pulse generator, which emanats from the teat by suckling stimulus, is transmitted to the MBH through the dorsal part of MBH; and 2, PRL does not mediate the suppressing effect on pulsatile LH secretion of the suckling stimulus in mid-lactation. The results also imply that the MBH is one of the sites where the GnRH pulse generator regulating oulsatile LH secretion is located.

INHIBITORY EFFECT OF THE Ca 2+ CHANNEL BLOCKER NIMODIPINE ON GROWTH HORMONE (GH) RELEASING FACTOR (GRF)-INDUCED GH SECRETION FROM RAT ANTERIOR PITUITARY CELLS. MASAKATSU KATO AND MITSUO SUZUKI, Department of Physiology, Institute of Endocrinology, Gunma University, Maebashi 371, Japan.

As a mechanism of GRF action in GH secretion, we proposed that GRF activates TTX insensitive Na + channels via cAMP, which in turn depolarizes the somatotrophs and activates voltage-sensitive Ca 2+

channels, thereby promoting Ca 2+ entry and GH secretion. To further characterize the involvement of voltage-sensitive Ca 2+ channels in GRF-stimulated GH secretion, we examined the effect of the L-type channel specific Ca 2+ antagonist nimodipine on GH secretion induced by several secretagogues in perifused dispersed rat anterior pituitary cells. 50 mM K+-induced GH secretion was the most effectively suppressed by nimodipine among those examined. The ID50 was between 10 -8 and 10 -7 M. One ~M nimodipine suppressed 1 nM GRF-induced GH secretion to 62.1% of the control and i0 ~M nimodipine further suppressed it to 33.4% of control. Dibutyryl cyclic AMP (DBcAMP)-induced GH secretion was less sensitive to inhibition by nimodipine. One mM DBcAMP-induced GH secretion was suppressed to 67.5% of control by i0 uM nimodipine. Since nimodipine preferentially blocks "open" state L-type Ca 2+ channels with a slow rate of onset, the maximum blockade by nimodipine would be achieved in a persistent depolarization. This explains why 50 mM K+-induced GH secretion was the most sensitive to inhibition by nimodipine. Potassium channel blocker, Cs + (20 mM), greatly augmented the sensitivity of GRF-induced GH secretion to inhibition by nimodipine. These results suggest that GRF-induced depolarization may trisger trains of action potentials or bursting activity, and that the nimodipine-sensitive Ca 2~ channels (L-type) play a major role in GRF-induced

GH secretion.

INTERLEUKIN-I STIMULATES ACTH RELEASE THROUGH AN INCREASE OF CORTICOTROPIN- RELEASING FACTOR ACTIVATED BY PROSTAGLANDIN. NAQTOSHI MURAKAMI, Department o_ff Physiology, Yamaguchi University School of Medicine, Ube, Yamaguchi 755, Japan.

Interleukin-i (IL-I) activates pituitary-adrenal axis to enhance secretion of adrenocorticotropic hormone (ACTH) into the circulation. We investigated whether intrahypothalamic prostaglandins (PGs) are involved in development of the ACTH response induced by IL-I. The results show that increased plasma concentration of ACTH induced by intravenous (i.v.) injection of IL-le (15 pg/kg) was inhibited by pre-treatment with a cyclooxygenase inhibitor, indomethacin. This indicates that the enhancement of plasma concentration of ACTH induced by i.v. injection of IL-I~ is processed by PGs. Furthermore, intrapreoptic injection of PGE 2 produced dose-dependent rises in plasma concentrations of ACTH, and this increase was inhibited by i.v. injection of anti-corticotropin-releasing factor (anti-CRF) antibody which neutralizes CRF in the portal vein. These results suggest that intrapreoptic PGE plays an important role in ACTH response by inducing CRF

release.