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STRESS-INDUCED RELEASE OF BRAIN NOREPINEPHRINE AND ITS INHIBITION BY DRUGS

Journal of Pharmacology and Experimental TherapeuticsPublished 1 January 1964
E.W. Maynert, Omer Levi
Citations209
SJR quartileQ1
SJR score1.11
SNIP0.83

TL;DR

The shock-induced decrease in norepinephrine failed to occur in animals treated with a monoamine oxidase inhibitor (Catron, tranylcypromine or harmaline), and a catechol O-methyl transferase inhibitors (pyrogallol) did not affect the stress-induced disappearance of the amine.

Abstract

Kittens given 60 mg/kg of morphine sulfate revealed a 37% decline in brain-stem norepinephrine and a 64% decline in adrenal epinephrine in 5 hours. These effects were entirely prevented by barbiturate anesthesia. Two forms of physical stress—exposure to cold and electric shocks applied to the feet—caused decreases in brain norepinephrine in rats. Various parameters of the electric shock procedure were studied in detail. Rats could be made to lose 17% of their brain-stem norepinephrine in 5 minutes and 37% in 45 minutes. Neither brainstem 5-hydroxytryptamine nor whole brain acetylcholine was changed under conditions causing a 40% decrease in NE. One hour of rest was sufficient for norepinephrine to be replenished after a 40% decline. Sedative doses of chlorpromazine or phenobarbital inhibited the release of brain-stem norepinephrine in shocked rats. However, strongly depressant doses of morphine did not have this action. Atropine, phenoxybenzamine, mecamylamine and pyrrobutamine were also inactive. However, tripelennamine had a partial effect. The shock-induced decrease in norepinephrine failed to occur in animals treated with a monoamine oxidase inhibitor (Catron, tranylcypromine or harmaline). A catechol O-methyl transferase inhibitor (pyrogallol) did not affect the stress-induced disappearance of the amine.

Keywords

NeuroscienceBiochemistry, Genetics and Molecular Biology