Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 1113-1117 |
| Number of pages | 5 |
| Journal | Journal of Neurochemistry |
| Volume | 66 |
| Issue number | 3 |
| Publication status | Published - 01-03-1996 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Biochemistry
- Cellular and Molecular Neuroscience
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Dysfunction of cholinergic and dopaminergic neuronal systems in β-amyloid protein-infused rats. / Itoh, Akio; Nitta, Atsumi; Nadai, Masayuki; Nishimura, Kyoko; Hirose, Mitsuhiko; Hasegawa, Takaaki; Nabeshima, Toshitaka.
In: Journal of Neurochemistry, Vol. 66, No. 3, 01.03.1996, p. 1113-1117.Research output: Contribution to journal › Article
TY - JOUR
T1 - Dysfunction of cholinergic and dopaminergic neuronal systems in β-amyloid protein-infused rats
AU - Itoh, Akio
AU - Nitta, Atsumi
AU - Nadai, Masayuki
AU - Nishimura, Kyoko
AU - Hirose, Mitsuhiko
AU - Hasegawa, Takaaki
AU - Nabeshima, Toshitaka
PY - 1996/3/1
Y1 - 1996/3/1
N2 - 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.
AB - 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.
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M3 - Article
VL - 66
SP - 1113
EP - 1117
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry
SN - 0022-3042
IS - 3
ER -