ADRENERGIC INPUTS TO THE AMYGDALA AND THE CONTROL OF GONADOTROPHIN RELEASE

1979 ◽  
Vol 90 (3) ◽  
pp. 385-393 ◽  
Author(s):  
José Borrell ◽  
Flavio Piva ◽  
Luciano Martini

ABSTRACT Drugs able to mimic or to antagonize the action of catecholamines have been implanted bilaterally into the basomedial region of the amygdala of adult castrated female rats. The animals were killed at different intervals after the implantation of the different drugs, and serum levels of LH and FSH were measured by radioimmunoassay. The results have shown that the intra-amygdalar implantation of the alpha-adrenergic blocker phenoxybenzamine induces a significant increase of the release both of LH and FSH. The implantation of the beta-adrenergic blocker propranolol brings about a rise of LH only. The dopamine receptor blocker pimozide stimulates the release of LH and exerts a biphasic effect (stimulation followed by inhibition) of FSH secretion. The alpha-receptor stimulant clonidine and the dopaminergic drug 2-Br-alpha-ergocryptine were without significant effects. From these observations it is suggested that the adrenergic signals reaching the basomedial area of the amygdala (possibly from the brain stem) may be involved in the modulation of gonadotrophin secretion.

1979 ◽  
Vol 83 (1) ◽  
pp. 113-118 ◽  
Author(s):  
E. L. BITTMAN ◽  
B. D. GOLDMAN

SUMMARY Female hamsters rendered acyclic by exposure to short photoperiods (10 h light: 14 h darkness) showed diurnal surges of both LH and FSH which persisted after removal of the ovaries and adrenal glands. The reduced increase in gonadotrophin secretion after ovariectomy, typical of hamsters exposed to short days, was also not contingent upon the presence of the adrenal glands. The results demonstrate that 'supersensitivity' of the neuroendocrine axis to feedback of ovarian or adrenal steroids cannot fully account for either the daily surges of gonadotrophins or the diminished response of LH and FSH to ovariectomy in hamsters maintained on short days. It is suggested that these changes result instead from other pineal-mediated actions of short photoperiods upon the brain.


1984 ◽  
Vol 105 (3) ◽  
pp. 308-313 ◽  
Author(s):  
David R. Mann ◽  
Michael S. Blank ◽  
R. Sridaran ◽  
V. Daniel Castracane ◽  
Charles Eldridge ◽  
...  

Abstract. The objective of this study was to determine whether anti-oestrogens (nafoxidine, MER-25) would block the suppressive effects of ACTH on gonadotrophin secretion in immature rats. Female rats were castrated at 25–26 days of age, and an Alzet osmotic minipump containing ACTH (1–24) or saline was implanted in each animal. ACTH was administered at a rate of 1 IU/day by constant infusion. Beginning on the day of surgery, animals were injected daily for 5 days with 0.25, 5 or 25 μg/100 g body weight of nafoxidine or 5 mg MER-25 and sacrificed on the sixth day following castration. ACTH lowered serum LH concentrations and increased pituitary LH levels. Serum androstenedione concentrations were more than two times greater in ACTH-infused than in control rats, but serum oestrone levels were not affected. Serum testosterone and oestradiol concentrations in ACTH-infused rats remained below levels of detection. Administration of 0.25 μg of nafoxidine prevented the suppressive effects of ACTH on serum LH. Serum levels of LH in these animals were comparable to saline-treated controls (418 ± 94 vs 443 ± 73 ng/ml). The two higher doses of nafoxidine and MER-25 were ineffective in suppressing the actions of ACTH on serum LH. MER-25 reduced serum LH values in both controls and ACTH-infused rats. Serum FSH concentrations were not altered by ACTH or nafoxidine treatment. MER-25 elevated pituitary FSH concentrations in both control and ACTH-infused rats. These data suggest that the inhibitory effect of ACTH on LH secretion in immature rats is mediated by an oestrogenic steroid, since this action can be blocked by simultaneous treatment with a low dose of the anti-oestrogen, nafoxidine.


2015 ◽  
Vol 113 (1) ◽  
pp. 380-389 ◽  
Author(s):  
Olga Dergacheva

Patients with sleep-related disorders, including obstructive sleep apnea (OSA), have an increased risk of cardiovascular diseases. OSA events are more severe in rapid eye movement (REM) sleep. REM sleep further increases the risk of adverse cardiovascular events by diminishing cardioprotective parasympathetic activity. The mechanisms underlying REM sleep-related reduction in parasympathetic activity likely include activation of inhibitory input to cardiac vagal neurons (CVNs) in the brain stem originating from the lateral paragigantocellular nucleus (LPGi), a nucleus that plays a role in REM sleep control. This study tests the hypothesis that chronic intermittent hypoxia and hypercapnia (CIHH), an animal model of OSA, inhibits CVNs because of exaggeration of the GABAergic pathway from the LPGi to CVNs. GABAergic neurotransmission to CVNs evoked by electrical stimulation of the LPGi was examined with whole cell patch-clamp recordings in an in vitro brain slice preparation in rats exposed to CIHH and control rats. GABAergic synaptic events were enhanced after 4-wk CIHH in both male and female rats, to a greater degree in males. Acute hypoxia and hypercapnia (H/H) reversibly diminished the LPGi-evoked GABAergic neurotransmission to CVNs. However, GABAergic synaptic events were enhanced after acute H/H in CIHH male animals. Orexin-A elicited a reversible inhibition of LPGi-evoked GABAergic currents in control animals but evoked no significant changes in CIHH male rats. In conclusion, exaggerated inhibitory neurotransmission from the LPGi to CVNs in CIHH animals would reduce cardioprotective parasympathetic activity and enhance the risk of adverse cardiovascular events.


1980 ◽  
Vol 93 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Flavio Piva ◽  
José Borrell ◽  
Patrizia Limonta ◽  
Gilberto Gavazzi ◽  
Luciano Martini

Abstract. Adult female rats castrated 4 weeks before were implanted bilaterally into the basomedial area of the amygdala with drugs known to mimic or to counteract the actions of acetylcholine. The animals were sacrificed at different time intervals after the implantation of the different compounds, and serum levels of LH and FSH were measured by radioimmunoasay. The data obtained indicate that the intra-amygdalar implantation of the muscarinic blocker atropine induces a significant increase of the release of LH without altering FSH secretion. The implantation of two cholinomimetic drugs, pilocarpine, an almost pure muscarinic agonist, and carbachol, which possesses both muscarinic and nicotinic properties, exerted an inhibitory effect only on LH release. On the contrary, the intra-amygdalar placement of the nicotinic blocker mecamylamine was followed by an increase of FSH with no changes in LH. These observations may suggest that cholinergic signals reaching the amygdala may be of some relevance in the mechanisms controlling gonadotrophin secretion. Muscarinic receptors seem to play an inhibitory role in the regulation of LH secretion, while nicotinic receptors seem to modulate in an inhibitory way FSH release.


1989 ◽  
Vol 120 (2) ◽  
pp. 261-268 ◽  
Author(s):  
A. Kooy ◽  
R. F. A. Weber ◽  
M. P. Ooms ◽  
J. T. M. Vreeburg

ABSTRACT The effects of the transplantable purely prolactin-secreting tumour 7315b on serum gonadotrophins were studied in adult rats. Possible contributions of the adrenals to the tumour-induced inhibition of serum LH and FSH were evaluated. The suppressive actions of tumour 7315b on serum gonadotrophins in gonadectomized plus adrenalectomized male and female rats were compared. Within 4 weeks after inoculation of tumour 7315b in intact male rats very high levels of prolactin and decreased serum levels of gonadotrophins and testosterone were recorded. At autopsy reduced weights of testes and accessory sex organs and slightly increased adrenal weights were found. In addition, in animals treated with a small testosterone-filled capsule after castration, tumour 7315b reduced serum concentrations of LH and FSH. Adrenalectomy did not prevent this suppressive action of the tumour on the post-castration rise of serum gonadotrophins. Suppression of serum gonadotrophins during hyperprolactinaemia was greater in gonadectomized plus adrenalectomized female rats than in male rats, indicating that the degree of the tumour-induced suppression of LH and FSH after castration is determined to a large extent by the sex of the animal. The purely prolactin-secreting tumour 7315b has therefore been shown to be a suitable model for studying the effects of severe hyperprolactinaemia on the pituitary-gonadal axis in rats. Journal of Endocrinology (1989) 120, 261–268


Author(s):  
Shams M. Ghoneim ◽  
Frank M. Faraci ◽  
Gary L. Baumbach

The area postrema is a circumventricular organ in the brain stem and is one of the regions in the brain that lacks a fully functional blood-brain barrier. Recently, we found that disruption of the microcirculation during acute hypertension is greater in area postrema than in the adjacent brain stem. In contrast, hyperosmolar disruption of the microcirculation is greater in brain stem. The objective of this study was to compare ultrastructural characteristics of the microcirculation in area postrema and adjacent brain stem.We studied 5 Sprague-Dawley rats. Horseradish peroxidase was injected intravenously and allowed to circulate for 1, 5 or 15 minutes. Following perfusion of the upper body with 2.25% glutaraldehyde in 0.1 M sodium cacodylate, the brain stem was removed, embedded in agar, and chopped into 50-70 μm sections with a TC-Sorvall tissue chopper. Sections of brain stem were incubated for 1 hour in a solution of 3,3' diaminobenzidine tetrahydrochloride (0.05%) in 0.05M Tris buffer with 1% H2O2.


1993 ◽  
Vol 4 (3) ◽  
pp. 457-468 ◽  
Author(s):  
Dennis Y. Wen ◽  
Roberto C. Heros

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