Serotonin and the regulation of the pituitary-adrenal system after deafferentation of the hypothalamus

Попова, Н. К.; Maslova, L. N.; Науменко, Э. В.

doi:10.1016/0006-8993(72)90251-x

Cited by 58 publications

(23 citation statements)

References 14 publications

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“…In general, these data are in agreement with those of D ix it and Buckley [1969] and D ix it [1971] who demonstrated that altering the brain content of serotonin did not appreciably affect basal plasma corticosterone levels or the adrenocortical response to shaking or cold stress. However, this does not preclude the possibility that other stresses may involve sero toninergic mechanisms on the HHA system, since Popova et al [1972] showed that electric shock, but not cold stress, is mediated via serotoninergic fibers.…”

Section: Discussionmentioning

confidence: 99%

Adrenocortical Responses of Rats to Acute Hypoxic and Hypercapnic Stresses after Treatment with Aminergic Agents

Marotta¹,

Sithichoke²,

Garcy³

et al. 1976

Neuroendocrinology

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Monoaminergic influences on the regulation of the hypothalamo-hypophyseal-adrenocortical (HHA) system during acute stresses (hypoxia and hypercapnia) were investigated in male rats. Plasma corticosterone levels were used to assess HHA activity, and the alterations in monoaminergic activity were induced by pretreating the animals with various pharmacologic agents (reserpine, αMT, FLA-63, pCPA, L-Dopa, pargyline, Lilly 110140, phentolamine and propranolol). Dexamethasone-treated rats were utilized to assess the site at which these monoaminergic substances acted. The latter experiments showed that these agents did not have a marked effect directly on the adrenal cortex and thus the site(s) of action was at the level of the anterior pituitary and/or above. Altering the serotoninergic system did not appreciably influence the HHA response to hypoxia and hypercapnia, whereas increasing the activity of the adrenergic system partially prevented the rise usually observed in plasma corticosterone levels during these stresses. These data suggest that different aminergic pathways may be utilized for different stresses.

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Section: Discussionmentioning

confidence: 99%

Adrenocortical Responses of Rats to Acute Hypoxic and Hypercapnic Stresses after Treatment with Aminergic Agents

Marotta¹,

Sithichoke²,

Garcy³

et al. 1976

Neuroendocrinology

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“…It has been reported that vasopressin has a CRF-like activity (Portanova and Sayers, 1973;Fehm et al, 1975;Gillies et al, 1978). Zimmerman et al (1977) suggested that AVP neurons which project from PVN to ME have an important role in releasing ACTH from the pituitary.…”

mentioning

confidence: 98%

“…Serum corticosterone levels have been reported to increase in rats after administration of 5-HT (Krieger & Krieger, 1970;Mayer et al, 1978); 5-hydroxytryptophan, a serotonin precursor (Popova et al, 1972;Imura et al, 1973); quipazine (Fuller et al, 1978) and 1-(m-trifluoromethylphenyl)-piperazine (Fuller and Clemens, 1979), the direct serotonin agonists; pchloramphetamine and fenfluramine, serotonin releasing drugs (Fuller and Snoddy, 1980); fluoxethin, a serotonin uptake in hibitor (Fuller and Snoddy, 1979). Jones et al (1976) demonstrated that 5-HT stimulated CRF release from rat hypothalami in in vitro experiments, but few studies (Karteszi et al, 1981) have examined the effects of these compounds on CRF activity in the hypothalamus employing in vivo methods.…”

mentioning

confidence: 99%

The effect of serotonin agonist 1-(trifluoromethylphenly)-piperazine on corticotropin releasing factor and arginine vasopressin in rat hypothalamic nuclei.

et al. 1982

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Effects of 1-(m-trifluoromethylphenyl)-piperazine, a serotonin agonist, were examined on rat plasma levels of adrenocorticotropin (ACTH) and arginine vasopressin (AVP), and on hypothalamic contents of corticotropin releasing factor (CRF) and AVP, to investigate the role of brain serotonin in ACTH regulation.Both plasma ACTH and AVP levels increased markedly 30 min after injection of the compound and were still elevated at 80 min. CRF and AVP contents in the median eminence decreased 30 min after injection but returned to the basal levels by 80 min. The AVP content in the supraoptic nucleus was elevated 80 min after injection.The CRF and AVP content did not significantly change in the paraventricular, suprachiasmatic and arcuate nuclei. Serotonin or 1-(m-trifluoromethylphenyl)-piperazine did not stimulate the release of ACTH in pituitary cell cultures. These results suggest that both CRF and AVP were secreted into the portal vessels by 1-(mtrifluoromethylphenyl)-piperazine to release ACTH from the anterior pituitary and that both the ACTH and AVP release were stimulated via the brain serotonergic mechanism.

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“…Some authors re gard noradrenalin [G a n o n g , 1972] and serotonin [Vermes and T elegd y. 1972;V ermes et al, 1972] as inhibitory, but others suggest that noradrenalin [Ulrich and Yawiler, 1973;Lippa el al., 1972;Bhargava et al, 1972] and serotonin [Naumenko, 1968;Popova et al, 1972] may be stimulatory trans mitters in the regulation of ACTH release. Acetylcholine may mediate stressinduced ACTH release in the anterior hypothalamus [Hedge and Smelik, 1968;Kaplanski and Smelik, 1973].…”

mentioning

confidence: 99%

Effect of Gamma-Aminobutyric Acid (GABA) and GABA Antagonist Drugs on ACTH Release

Makara

Stark²

1974

Neuroendocrinology

182

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Corticotrophin (ACTH) release has been studied in rats given intraventricular gamma-aminobutyric acid (GABA) infusions or injections of picrotoxin and bicuculline. As an index of ACTH release the corticosterone level of blood or plasma was determined. GABA (1 M/liter), infused at a rate of 1 µl/min into the 3rd ventricle, inhibited the rise in plasma corticosterone normally produced by surgical trauma. 60 min after surgical trauma the rats given GABA infusions had lower blood corticosterone levels than the control rats given infusions of 1 M/liter of proline, 1 M/liter of glycine, or 0.15 M/liter of sodium chloride. Picrotoxin, an antagonist of GABA, is a potent stimulus of ACTH release. In sub-convulsive intraperitoneal doses it produced a significant rise in plasma corticosterone in conscious rats with complete hypothalamic deafferentation. Under pentobarbital anesthesia 12.5 µg of picrotoxin injected into the 3rd ventricle produced a small but significant rise in plasma corticosterone in rats with hypothalamic deafferentation. After intraventricular injections of bicuculline methiodide a significant rise in plasma corticosterone occurred in rats with hypothalamic deafferentation; the ACTH releasing effect of 2.5 µg of bicuculline methiodide was strongly inhibited by a simultaneous infusion of 0.15 M/liter of GABA. On the basis of this pharmacological evidence, we suggest that GABA may be an inhibitory neurotransmitter of hypothalamic interneurons and/or afferent pathways involved in the regulation of ACTH release.

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Serotonin and the regulation of the pituitary-adrenal system after deafferentation of the hypothalamus

Cited by 58 publications

References 14 publications

Adrenocortical Responses of Rats to Acute Hypoxic and Hypercapnic Stresses after Treatment with Aminergic Agents

Adrenocortical Responses of Rats to Acute Hypoxic and Hypercapnic Stresses after Treatment with Aminergic Agents

The effect of serotonin agonist 1-(trifluoromethylphenly)-piperazine on corticotropin releasing factor and arginine vasopressin in rat hypothalamic nuclei.

Effect of Gamma-Aminobutyric Acid (GABA) and GABA Antagonist Drugs on ACTH Release

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