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Central Noradrenergic Lesion Impairs the Adrenocorticotrophin Response to Release of Endogenous Catecholamines
Author(s) -
AlDamluji Saad,
White Anne
Publication year - 1992
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1992.tb00174.x
Subject(s) - endocrinology , medicine , catecholamine , endogeny , hydroxydopamine , adrenergic , neurotoxin , postsynaptic potential , denervation , oxidopamine , agonist , adrenergic neurons , lesion , norepinephrine , chemistry , free nerve ending , receptor , dopamine , dopaminergic , psychiatry , substantia nigra
Activation of hypothalamic α 1 ‐adrenoceptors stimulates the secretion of corticotrophin‐releasing factors which in turn stimulate pituitary adrenocorticotrophin (ACTH). This mechanism is important in the physiological control of ACTH secretion. This study assesses the feasibility of using the ACTH response to release of endogenous catecholamines as a means of detecting a hypothalamic noradrenergic lesion in vivo . Intracerebroventricular infusion of the catecholamine neurotoxin, 6‐hydroxydopamine, was used to destroy noradrenergic nerve endings in rats, with the purpose of producing a model that could be used to study alterations in ACTH responses that may result from a lesion involving central noradrenergic neurons. 6‐Hydroxydopamine (250 μg icv) significantly reduced hypothalamic noradrenaline content, indicating damage to noradrenergic nerve endings, without affecting postsynaptic receptor function, as judged by preservation of the effect of a selective α 1 ‐adrenergic agonist. Pharmacological release of endogenous catecholamines, effected by combined administration of a catecholamine precursor and an α 2 ‐adrenergic antagonist, stimulated the secretion of ACTH in control, but not in 6‐hydroxydopamine‐treated rats. Degeneration of hypothalamic noradrenergic nerve endings is not followed by denervation hypersensitivity, and is therefore accompanied by impairment of the ACTH response to release of endogenous catecholamines.