Fetally-induced noradrenergic hyperinnervation of cerebral cortex results in persistent down-regulation of beta-receptors.

Abstract:

:Methylazoxymethanol acetate (MAM)-induced cortical hypoplasia resulted in a 2-fold increase in the concentration of norepinephrine and its metabolite, 3-methoxyl-4-hydroxyphenylglycol sulfate, and a 26% decrease in the Bmax for the beta-receptor ligand, [3H]dihydroalprenolol (DHA) in the rat cortex. Chronic treatment with desmethylimipramine did not further decrease DHA-labeled sites although prior lesion of the noradrenergic terminals with 6-hydroxydopamine markedly increased the number in the MAM-lesioned cortex.

journal_name

Brain Res

journal_title

Brain research

authors

Beaulieu M,Coyle JT

doi

10.1016/0165-3806(82)90195-x

subject

Has Abstract

pub_date

1982-08-01 00:00:00

pages

491-4

issue

4

eissn

0006-8993

issn

1872-6240

journal_volume

256

pub_type

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