The role of the fourth cerebroventricle in nicotine-stimulated prolactin release in the rat

Involvement of catecholamines

S. G. Matta, Burt Sharp

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

The central mechanism(s) whereby peripherally administered nicotine (N) stimulates prolactin secretion has not been clarified. The current studies showed that an i.c.v. injection of N into the fourth ventricle (IV) produced a significant dose-dependent elevation of plasma prolactin [buffer < N 0.125 μg = N 0.25 μg (P < .05) < N 0.5 μg = N 2.5 μg (P < .01)]. Injecting the nicotinic cholinergic (NAch) antagonist, mecamylamine, into the IV (20 or 40 μg) or i.v. (0.5 mg/kg b.wt.) before the administration of N by the alternate route indicated that nicotine was activating NAch receptors accessible from the IV. Because brain stem catecholaminergic cell groups, adjacent to the IV, project to hypothalamic regions involved in modulating prolactin release, the involvement of IV catecholaminergic neurons in N- stimulated prolactin release was investigated. Ablation of central catecholaminergic neurons by 6-hydroxydopamine abolished the prolactin response to N injected i.c.v. (1 or 2.5 μg; P < .05) or i.v. (0.03 or 0.05 mg/kg b.wt.; P < .05). To assess the role of norepinephrine and epinephrine, LY 10853, an inhibitor of dopamine-β-hydroxylase, was given i.p. 4 h before i.v. nicotine; the prolactin response was attenuated (P < .01). Selective inhibitors of epinephrine synthesis, SKF 64139 or 2,3-dichloro-α- methylbenzylamine, administered on the same schedule, reduced (P < .01) the prolactin response to N without altering responsiveness to the dopamine receptor antagonist, domperidone. Because the enzyme inhibitors may also affect alpha-2 adrenoreceptors, a selective alpha-2 antagonist, idazoxan (1 or 5 μg), was injected into the hypothalamic region of the third ventricle before N (1 μg) in the IV; the peak prolactin response was significantly reduced (P < .05). Further evaluation of adrenoreceptor subtypes was done with 1 μg of prazosin (alpha-1) or propranolol (beta) before N in the i.v.; each antagonist reduced the prolactin response (P < .05). Thus, peripherally administered N appears to act in the region of the fourth ventricle where it stimulates catecholaminergic neurons. These neurons induce prolactin secretion via hypothalamic alpha and beta adrenergic receptors.

Original languageEnglish (US)
Pages (from-to)1285-1291
Number of pages7
JournalJournal of Pharmacology and Experimental Therapeutics
Volume260
Issue number3
StatePublished - 1992
Externally publishedYes

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Nicotine
Prolactin
Fourth Ventricle
Catecholamines
Neurons
Epinephrine
Idazoxan
Domperidone
Mecamylamine
Receptors, Adrenergic, alpha
Third Ventricle
Dopamine Antagonists
Prazosin
Oxidopamine
Receptors, Adrenergic, beta
Cholinergic Antagonists
Enzyme Inhibitors
Mixed Function Oxygenases
Propranolol
Brain Stem

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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title = "The role of the fourth cerebroventricle in nicotine-stimulated prolactin release in the rat: Involvement of catecholamines",
abstract = "The central mechanism(s) whereby peripherally administered nicotine (N) stimulates prolactin secretion has not been clarified. The current studies showed that an i.c.v. injection of N into the fourth ventricle (IV) produced a significant dose-dependent elevation of plasma prolactin [buffer < N 0.125 μg = N 0.25 μg (P < .05) < N 0.5 μg = N 2.5 μg (P < .01)]. Injecting the nicotinic cholinergic (NAch) antagonist, mecamylamine, into the IV (20 or 40 μg) or i.v. (0.5 mg/kg b.wt.) before the administration of N by the alternate route indicated that nicotine was activating NAch receptors accessible from the IV. Because brain stem catecholaminergic cell groups, adjacent to the IV, project to hypothalamic regions involved in modulating prolactin release, the involvement of IV catecholaminergic neurons in N- stimulated prolactin release was investigated. Ablation of central catecholaminergic neurons by 6-hydroxydopamine abolished the prolactin response to N injected i.c.v. (1 or 2.5 μg; P < .05) or i.v. (0.03 or 0.05 mg/kg b.wt.; P < .05). To assess the role of norepinephrine and epinephrine, LY 10853, an inhibitor of dopamine-β-hydroxylase, was given i.p. 4 h before i.v. nicotine; the prolactin response was attenuated (P < .01). Selective inhibitors of epinephrine synthesis, SKF 64139 or 2,3-dichloro-α- methylbenzylamine, administered on the same schedule, reduced (P < .01) the prolactin response to N without altering responsiveness to the dopamine receptor antagonist, domperidone. Because the enzyme inhibitors may also affect alpha-2 adrenoreceptors, a selective alpha-2 antagonist, idazoxan (1 or 5 μg), was injected into the hypothalamic region of the third ventricle before N (1 μg) in the IV; the peak prolactin response was significantly reduced (P < .05). Further evaluation of adrenoreceptor subtypes was done with 1 μg of prazosin (alpha-1) or propranolol (beta) before N in the i.v.; each antagonist reduced the prolactin response (P < .05). Thus, peripherally administered N appears to act in the region of the fourth ventricle where it stimulates catecholaminergic neurons. These neurons induce prolactin secretion via hypothalamic alpha and beta adrenergic receptors.",
author = "Matta, {S. G.} and Burt Sharp",
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T1 - The role of the fourth cerebroventricle in nicotine-stimulated prolactin release in the rat

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AU - Matta, S. G.

AU - Sharp, Burt

PY - 1992

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N2 - The central mechanism(s) whereby peripherally administered nicotine (N) stimulates prolactin secretion has not been clarified. The current studies showed that an i.c.v. injection of N into the fourth ventricle (IV) produced a significant dose-dependent elevation of plasma prolactin [buffer < N 0.125 μg = N 0.25 μg (P < .05) < N 0.5 μg = N 2.5 μg (P < .01)]. Injecting the nicotinic cholinergic (NAch) antagonist, mecamylamine, into the IV (20 or 40 μg) or i.v. (0.5 mg/kg b.wt.) before the administration of N by the alternate route indicated that nicotine was activating NAch receptors accessible from the IV. Because brain stem catecholaminergic cell groups, adjacent to the IV, project to hypothalamic regions involved in modulating prolactin release, the involvement of IV catecholaminergic neurons in N- stimulated prolactin release was investigated. Ablation of central catecholaminergic neurons by 6-hydroxydopamine abolished the prolactin response to N injected i.c.v. (1 or 2.5 μg; P < .05) or i.v. (0.03 or 0.05 mg/kg b.wt.; P < .05). To assess the role of norepinephrine and epinephrine, LY 10853, an inhibitor of dopamine-β-hydroxylase, was given i.p. 4 h before i.v. nicotine; the prolactin response was attenuated (P < .01). Selective inhibitors of epinephrine synthesis, SKF 64139 or 2,3-dichloro-α- methylbenzylamine, administered on the same schedule, reduced (P < .01) the prolactin response to N without altering responsiveness to the dopamine receptor antagonist, domperidone. Because the enzyme inhibitors may also affect alpha-2 adrenoreceptors, a selective alpha-2 antagonist, idazoxan (1 or 5 μg), was injected into the hypothalamic region of the third ventricle before N (1 μg) in the IV; the peak prolactin response was significantly reduced (P < .05). Further evaluation of adrenoreceptor subtypes was done with 1 μg of prazosin (alpha-1) or propranolol (beta) before N in the i.v.; each antagonist reduced the prolactin response (P < .05). Thus, peripherally administered N appears to act in the region of the fourth ventricle where it stimulates catecholaminergic neurons. These neurons induce prolactin secretion via hypothalamic alpha and beta adrenergic receptors.

AB - The central mechanism(s) whereby peripherally administered nicotine (N) stimulates prolactin secretion has not been clarified. The current studies showed that an i.c.v. injection of N into the fourth ventricle (IV) produced a significant dose-dependent elevation of plasma prolactin [buffer < N 0.125 μg = N 0.25 μg (P < .05) < N 0.5 μg = N 2.5 μg (P < .01)]. Injecting the nicotinic cholinergic (NAch) antagonist, mecamylamine, into the IV (20 or 40 μg) or i.v. (0.5 mg/kg b.wt.) before the administration of N by the alternate route indicated that nicotine was activating NAch receptors accessible from the IV. Because brain stem catecholaminergic cell groups, adjacent to the IV, project to hypothalamic regions involved in modulating prolactin release, the involvement of IV catecholaminergic neurons in N- stimulated prolactin release was investigated. Ablation of central catecholaminergic neurons by 6-hydroxydopamine abolished the prolactin response to N injected i.c.v. (1 or 2.5 μg; P < .05) or i.v. (0.03 or 0.05 mg/kg b.wt.; P < .05). To assess the role of norepinephrine and epinephrine, LY 10853, an inhibitor of dopamine-β-hydroxylase, was given i.p. 4 h before i.v. nicotine; the prolactin response was attenuated (P < .01). Selective inhibitors of epinephrine synthesis, SKF 64139 or 2,3-dichloro-α- methylbenzylamine, administered on the same schedule, reduced (P < .01) the prolactin response to N without altering responsiveness to the dopamine receptor antagonist, domperidone. Because the enzyme inhibitors may also affect alpha-2 adrenoreceptors, a selective alpha-2 antagonist, idazoxan (1 or 5 μg), was injected into the hypothalamic region of the third ventricle before N (1 μg) in the IV; the peak prolactin response was significantly reduced (P < .05). Further evaluation of adrenoreceptor subtypes was done with 1 μg of prazosin (alpha-1) or propranolol (beta) before N in the i.v.; each antagonist reduced the prolactin response (P < .05). Thus, peripherally administered N appears to act in the region of the fourth ventricle where it stimulates catecholaminergic neurons. These neurons induce prolactin secretion via hypothalamic alpha and beta adrenergic receptors.

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