Corticotropin Release: Inhibition by Intrahypothalamic Implantation of Atropine

Hedge, George A.; Smelik, P. G.

doi:10.1126/science.159.3817.891

Cited by 117 publications

(35 citation statements)

References 7 publications

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“…For example, carbachol, a cholinergic agonist with both nicotinic and muscarinic properties, implanted in the hypothalamus of a variety of animal species or given intraventricularly, causes release of corticosteroids from the adrenal, presumably via increased ACTH release. Conversely, hypothalamic implantation of atropine prevents stress-induced ACTH release [Hedge and Smelik, 1968;Hedge and DeWeid, 1971 ;Kaplanski and Smelik, 19731. Also, the intravenous administration of nicotinic or muscarinic cholinergic agonists to rats and dogs results in adrenocortical activation, and the increased release of 17-OH-corticosteroids [ Suzuki et al, 19751, and this effect is blocked by hypophysectomy or radiation induced lesions of the anterior median eminence.…”

Section: Adrenocorticotropic Hormone (Acth) and Cortisolmentioning

confidence: 99%

Cholinomimetic and anticholinergic drugs used to investigate an acetylcholine hypothesis of affective disorders and stress

Janowsky

Risch

1984

Drug Development Research

126

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The cholinomimetic agents, physostigmine, neostigmine, and arecoline, and the anticholinergic agents, atropine, scopolamine, and methscopolamine, have been used to explore an acetylcholine hypothesis of affect disorders and stress. Cholinomimetic drugs cause many of the same effects as do naturally occurring stressors. These include increases in negative affect, the induction of affective disorders, increases in stress neuroendocrines including ACThH, cortisol, beta‐endorphin, growth hormone, prolactin, epinephrine, and noprepinephrine, increases in blood pressure and pulse rate, and increases in analgesia. These parallel effects, combined with the effect of stress on central acetylcholine activity, suggest a stress‐acetylcholine linkage.

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Section: Adrenocorticotropic Hormone (Acth) and Cortisolmentioning

confidence: 99%

Cholinomimetic and anticholinergic drugs used to investigate an acetylcholine hypothesis of affective disorders and stress

Janowsky

Risch

1984

Drug Development Research

126

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“…However, the importance of muscarinic receptors is indicated by the observations that atropine prevents (Hedge & Smelik, 1968) and pilocarpine stimulates (Suzuki, Abe & Hirose, 1975) corticotrophin release in vivo.…”

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confidence: 99%

Hypothalamic receptors influencing the secretion of corticotrophin releasing hormone in the rat

Buckingham

Hodges

1979

The Journal of Physiology

121

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SUMMARY1. The production of corticotrophin releasing hormone (CRH) by the rat hypothalamus in vitro was studied in the presence and absence of various neurotransmitter substances and drugs which mimic or antagonize their actions.2. Acetylcholine, nicotine and bethanechol increased, in a dose-related manner, hypothalamic CRH release and content but the maximal responses to bethanechol or nicotine were less than those to acetylcholine.3. The actions of acetylcholine were antagonized by atropine, pempidine and hexamethonium but were completely inhibited only when atropine and pempidine were given together. The effects of nicotine were abolished by pempidine but not by atropine while those of bethanechol were abolished by atropine but not by pempidine.4. Acetylcholine-induced hypothalamic CRH activity was also antagonized by cyproheptadine but not by methysergide.5. 5-Hydroxytryptamine caused dose-related increases in hypothalamic CRH release and content. Its effects were antagonized by cyproheptadine and methysergide but not by atropine, pempidine or hexamethonium.6. Acetylcholine-induced increases in hypothalamic CRH production were reduced by GABA, noradrenaline, adrenaline, methoxamine and phenylephrine but not by isoprenaline. The actions of GABA were antagonized by bicuculline and those of noradrenaline by phentolamine but not by atenolol.7. The results suggest the presence of nicotinic and muscarinic cholinoceptors, 5-hydroxytryptamine receptors, a-adrenoceptors and GABA-receptors within the hypothalamus all of which may be important in the control of CRH secretion.

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“…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]. However, other transmitters may also be involved in neural inhibition by hypothalamic pathways.…”

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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Corticotropin Release: Inhibition by Intrahypothalamic Implantation of Atropine

Cited by 117 publications

References 7 publications

Cholinomimetic and anticholinergic drugs used to investigate an acetylcholine hypothesis of affective disorders and stress

Cholinomimetic and anticholinergic drugs used to investigate an acetylcholine hypothesis of affective disorders and stress

Hypothalamic receptors influencing the secretion of corticotrophin releasing hormone in the rat

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

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