Effect of chronic desipramine treatment on neurotransmitter-thyrotropin releasing hormone - thyrotropin interactions in the rat
Date
1987
Authors
Jaffer A.
Russell V.A.
Taljaard J.J.F.
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Abstract
Long-term administration of the antidepressant drug, desipramine (20 mg/kg/day, orally for 28 days), decreased the stimulatory effect of the α2-adrenoceptor agonist, clonidine (250 μg/kg, i.p.) on thyrotropin (TSH) secretion in the rat, but did not alter basal TSH secretion. β-Adrenoceptor-mediated inhibition of TSH secretion by isoproterenol (1 mg/kg, i.p.) was unaffected by chronic desipramine treatment, as were the stimulatory effect of TSH-releasing hormone (TRH, 5 μg/kg, i.v.) on TSH release and its inhibition by the α-adrenoceptor antagonist, phentolamine (2 mg/kg, i.p.). These findings suggest that chronic desipramine treatment induces subsensitivity of α2-adrenoceptors which modulate TSH secretion in the rat while not affecting β2-adrenoceptor-mediated inhibition of TSH release. These findings suggest that pituitary TRH receptors are unchanged but that changes occurred at the hypothalamic level in α2-adrenoceptor-mediated stimulation of TRH release. Although cerebral β-adrenoceptors have been shown convincingly to be down-regulated after chronic desipramine treatment, their function in the hypothalamic TRH system after 28 days of treatment with desipramine appears to be unimpaired.
Description
Keywords
clonidine, desipramine, isoprenaline, phentolamine, protirelin, thyrotropin, adverse drug reaction, animal experiment, central nervous system, nonhuman, oral drug administration, rat, Animal, Clonidine, Desipramine, Drug Interactions, Isoproterenol, Male, Phentolamine, Protirelin, Rats, Rats, Inbred Strains, Receptors, Adrenergic, Support, Non-U.S. Gov't, Thyrotropin
Citation
Neurochemical Research
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