Endocrinologia Japonica
Online ISSN : 2185-6370
Print ISSN : 0013-7219
ISSN-L : 0013-7219
Cholinergic and Serotonergic Neural Links and the Inhibitory Effects of Hippocampus, Lateral Amygdala and Central Gray Matter on Gonadotropin Release
MASAZUMI KAWAKAMIFUKUKO KIMURASHINNOSUKE KAWAGOE
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1976 Volume 23 Issue 1 Pages 11-21

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Abstract

Effects of electrical stimulation of the hippocampus (HPC), lateral amygdala (1-AMYG) and midbrain central gray matter (CG) on the release of ovulatory gonadotropin were examined using proestrous Wistar rats with or without pretreatment with reserpine, atropine or p-chlorophenylalanine (PCPA) at such dosage that had been confirmed not to block ovulation. Electrical stimulation of the HPC, 1-AMYG or CG under light ether anesthesia just before the critical period prevented a rise in serum LH, FSH and prolactin levels at 18:00. Pretreatment with atropine (200mg/kg body wt, sc) was effective to abolish this inhibitory effect of the HPC stimulation on the release of LH and FSH, whereas reserpine treatment (1mg/kg body wt, ip) did not affect the effect. The inhibitory effect of the 1-AMYG or CG stimulation on LH and FSH release was abolished by treatment with PCPA (150 mg/kg body wt, ip), while neither atropine nor reserpine had any effect. The inhibitory effect of the HPC stimulation on the release of these hormones was also blocked by PCPA treatment. In regard to the prolactin release, it was inhibited by the stimulation of the HPC, 1-AMYG or CG in both the non-treated rat and in the atropine or PCPA-treated one, while in the reserpine-treated rat it was not inhibited but rather was facilitated by these stimulations.
It was assumed that the normal maintenance of both cholinergic and serotonergic neural links for the expression of the HPC inhibition on ovulatory LH, FSH and prolactin secretion and that of serotonergic link for the expression of the 1-AMYG or CG inhibition are needed. The inhibitory action on prolactin release changed into facilitation under the depletion of monoamines, but the mechanism is unknown.

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© The Japan Endocrine Society
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