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Effects of Nucleus Basalis Lesions on the Muscarinic and Nicotinic Modulation of [ 3 H] Acetylcholine Release in the Rat Cerebral Cortex
Author(s) -
Meyer Edwin M.,
W. Arendash Gary,
Judkins Jennifer H.,
Ying Lily,
Wade Cathy,
Ken William R.
Publication year - 1987
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1987.tb02433.x
Subject(s) - nucleus basalis , muscarinic acetylcholine receptor , acetylcholine , nicotinic agonist , chemistry , cerebral cortex , endocrinology , oxotremorine , cholinergic , choline acetyltransferase , medicine , ibotenic acid , muscarinic acetylcholine receptor m4 , neuroscience , cholinergic neuron , receptor , biology , central nervous system , biochemistry
Presynaptic muscarinic and nicotinic receptors in the cerebral cortex reportedly inhibit and increase acetyl‐choline (ACh) release, respectively. In this study, we investigated whether these receptors reside on cholinergic nerve terminals projecting to the cerebral cortex from the nucleus basalis magnocellularis (nbm). Adult male rats received unilateral infusions of ibotenic acid (5 μg/1 μl) in the nbm. Two weeks later, cerebral cortical cholinergic markers (choline acetyltransferase activity, high‐affinity choline uptake, and coupled ACh synthesis) were significantly reduced in synaptosomes prepared from the lesioned hemispheres compared to contralateral controls. The depolarization‐induced release of [ 3 H]ACh from these synaptosomes was also reduced in the lesioned hemispheres, reflecting the reduced synthesis of transmitter. However, the nbm lesions had no effect on the inhibition of release induced by 100 μ M oxotremorine. Synaptosomal [ 3 H]ACh release was not altered by nicotine or the nicotinic agonists anabaseine and 2‐(3‐pyridyl)‐l, 4, 5, 6‐tetrahydropyrimdine. Nicotine (10–100 μ M ) did increase [ 3 H]ACh release in control and lesioned hemispheres in cortical minces, but to a similar extent. These results suggest that neither muscarinic nor nicotinic receptors modulating ACh release reside on nbm‐cholinergic terminals.