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Dysfunction of Cholinergic and Dopaminergic Neuronal Systems in β‐Amyloid Protein‐Infused Rats
Author(s) -
Itoh Akio,
Nitta Atsumi,
Nadai Masayuki,
Nishimura Kyoko,
Hirose Mitsuhiko,
Hasegawa Takaaki,
Nabeshima Toshitaka
Publication year - 1996
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 - 10.1046/j.1471-4159.1996.66031113.x
Subject(s) - cholinergic , dopamine , microdialysis , dopaminergic , acetylcholine , cholinergic neuron , choline acetyltransferase , medicine , endocrinology , neurotransmitter , amyloid (mycology) , alzheimer's disease , amyloid precursor protein , neuroscience , chemistry , biology , central nervous system , pathology , disease
Accumulations of β‐amyloid protein are characteristic and diagnostic features of the brain of Alzheimer's disease patients; however, the physiological role of this protein in CNS is unknown. We have previously reported that continuous infusion of β‐amyloid protein into rat cerebral ventricle impairs learning ability and decreases choline acetyltransferase activity, a marker enzyme of cholinergic neuron. In this study, the effects of β‐amyloid protein infusion on the release of neurotransmitters in cholinergic and dopaminergic neuronal systems were investigated by using an in vivo brain microdialysis method. Nicotine‐stimulated release of acetylcholine and dopamine in these animals was significantly lower than that in vehicle‐infused rats. Further, dopamine release induced by high‐K stimulation was decreased in β‐amyloid protein‐infused rats compared with vehicle‐infused rats. These results suggest that the release of the two transmitters, acetylcholine and dopamine, was decreased by β‐amyloid protein and that learning deficits observed in the β‐amyloid protein‐infused rats are partly due to the impairment of neurotransmitter release. Furthermore, continuous infusion of β‐amyloid protein may be a useful method to produce the animal model of Alzheimer's disease.