Ascorbate-induced release of LHRH: Noradrenergic and opioid modulation

Brian T. Miller; Theodore J. Cicero

doi:10.1016/0361-9230(87)90171-7

Ascorbate-induced release of LHRH: Noradrenergic and opioid modulation

Brian T. Miller, Theodore J. Cicero

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

Ascorbic acid caused a calcium-dependent release of luteinizing hormone-releasing hormone (LHRH) from the rat mediobasal hypothalamus in vitro. The ascorbate-induced release of LHRH was effectively blocked by the adrenergic α-receptor blocker phentolamine, but not by the β-receptor blocker propranolol. The effect of ascorbate was also suppressed by the mu receptor selective opiate agonist sufentanil. These results suggest that the effects of ascorbic acid on the in vitro release of LHRH are mediated by endogenous norepinephrine. Moreover, our results are consistent with the hypothesis that the release of LHRH in the rat is regulated by the hypothalamic noradrenergic system, which is in turn modulated in some, as yet undetermined, fashion by opioid peptides.

Original language	English (US)
Pages (from-to)	95-99
Number of pages	5
Journal	Brain Research Bulletin
Volume	19
Issue number	1
DOIs	https://doi.org/10.1016/0361-9230(87)90171-7
State	Published - Jul 1987

Keywords

Ascorbic acid
Endogenous opioid peptides
Hypothalamus
LHRH
Noradrenergic receptors
Noradrenergic system
Opioid receptors

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/0361-9230(87)90171-7

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title = "Ascorbate-induced release of LHRH: Noradrenergic and opioid modulation",

abstract = "Ascorbic acid caused a calcium-dependent release of luteinizing hormone-releasing hormone (LHRH) from the rat mediobasal hypothalamus in vitro. The ascorbate-induced release of LHRH was effectively blocked by the adrenergic α-receptor blocker phentolamine, but not by the β-receptor blocker propranolol. The effect of ascorbate was also suppressed by the mu receptor selective opiate agonist sufentanil. These results suggest that the effects of ascorbic acid on the in vitro release of LHRH are mediated by endogenous norepinephrine. Moreover, our results are consistent with the hypothesis that the release of LHRH in the rat is regulated by the hypothalamic noradrenergic system, which is in turn modulated in some, as yet undetermined, fashion by opioid peptides.",

keywords = "Ascorbic acid, Endogenous opioid peptides, Hypothalamus, LHRH, Noradrenergic receptors, Noradrenergic system, Opioid receptors",

author = "Miller, {Brian T.} and Cicero, {Theodore J.}",

note = "Funding Information: {\textquoteleft}Supported in part by grants AA-03539 and AA-07144 from the National Institute on Alcohol Abuse and Alcoholism and DA-03833 from the National Institute on Drug Abuse. 2Current address: Brian T. Miller, Ph.D., University of Texas Medical Branch, Department of Anatomy and Neurosciences, Galveston, TX 77550. “Recipient of Research Scientist Award (DA-00095) from the National Institute on Drug Abuse. Requests for reprints should be addressed to Theodore J. Cicero.",

year = "1987",

month = jul,

doi = "10.1016/0361-9230(87)90171-7",

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PY - 1987/7

Y1 - 1987/7

N2 - Ascorbic acid caused a calcium-dependent release of luteinizing hormone-releasing hormone (LHRH) from the rat mediobasal hypothalamus in vitro. The ascorbate-induced release of LHRH was effectively blocked by the adrenergic α-receptor blocker phentolamine, but not by the β-receptor blocker propranolol. The effect of ascorbate was also suppressed by the mu receptor selective opiate agonist sufentanil. These results suggest that the effects of ascorbic acid on the in vitro release of LHRH are mediated by endogenous norepinephrine. Moreover, our results are consistent with the hypothesis that the release of LHRH in the rat is regulated by the hypothalamic noradrenergic system, which is in turn modulated in some, as yet undetermined, fashion by opioid peptides.

AB - Ascorbic acid caused a calcium-dependent release of luteinizing hormone-releasing hormone (LHRH) from the rat mediobasal hypothalamus in vitro. The ascorbate-induced release of LHRH was effectively blocked by the adrenergic α-receptor blocker phentolamine, but not by the β-receptor blocker propranolol. The effect of ascorbate was also suppressed by the mu receptor selective opiate agonist sufentanil. These results suggest that the effects of ascorbic acid on the in vitro release of LHRH are mediated by endogenous norepinephrine. Moreover, our results are consistent with the hypothesis that the release of LHRH in the rat is regulated by the hypothalamic noradrenergic system, which is in turn modulated in some, as yet undetermined, fashion by opioid peptides.

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KW - Noradrenergic receptors

KW - Noradrenergic system

KW - Opioid receptors

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Ascorbate-induced release of LHRH: Noradrenergic and opioid modulation

Abstract

Keywords

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