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I. Miyai

Bio: I. Miyai is an academic researcher from Osaka University. The author has contributed to research in topics: Cholinergic neuron & Magnetic resonance imaging. The author has an hindex of 2, co-authored 2 publications receiving 33 citations.

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Journal ArticleDOI
I. Miyai1, S. Ueno1, Shiro Yorifuji1, Harutoshi Fujimura1, Seiichiro Tarui1 
TL;DR: Results imply regulation of nAChR transcripts by cell to cell interactions and may provide supporting evidence for the occurrence of supersensitivity in deafferentated cholinergic neurons.
Abstract: We investigated the effect of a unilateral lesion of the nucleus basalis magnocellularis (nbm) on the expression of nicotinic acetylcholine receptors (nAChRs) in the rat cerebral cortex. Cortical nAChR concentration as determined by [3H]nicotine binding was unaffected by the nbm lesion. Expression levels of nAChR subunit mRNAs were measured using cDNA clones coding for the receptor subunits, alpha-3, alpha-4, and beta-2. At 1 week postlesion, expression levels of alpha-4, and beta-2 were increased by an average of 82% and 19%, respectively. On the other hand, expression levels of these mRNAs on the lesioned side 4 weeks after lesioning did not differ from those on the control side. Expression of alpha-3 was not altered by the nbm lesion. These results imply regulation of nAChR transcripts by cell to cell interactions. Coincrease of alpha-4 and beta-2 transcripts may provide supporting evidence for the occurrence of supersensitivity in deafferentated cholinergic neurons.

25 citations

Journal ArticleDOI
TL;DR: Dyskinesia in the primate following injection of an excitatory amino acid antagonist into the medial segment of the globus pallidus in Parkinson's disease is studied.
Abstract: 8 Gessa R, Tagliamonte A, Gessa GL. Blockade by apomorphine of haloperidol-induced dyskinesia in schizophrenic patients. Lancet 1972;ii:981-2. 9 Clarke CE, Boyce S, Robertson RG, Sambrook MA, Stahl SM, Crossman AR. Behavioural effects of (+ )-4-propyl-9-hydroxynaphthoxazine (PHNO) in pnmates rendered parkinsonian with 1 -methyl-4-phenyl1 ,2,3,6-tetrahydropyridine (MPTP). Arch Pharmacol 1988;338:35-8. 10 Grandas Perez FG, Jenner PG, Nomoto M, et al. (+ )-4-propyl-9-hydroxynaphthoxazine in Parkinson's disease. Lancet 1986;i:906. 11 Graham WC, Crossman AR. Autoradiographic localisation of dopamine D, binding sites in areas receiving striatal input. Eur J Pharmacol 1987;142:479-81. 12 Robertson RG, Farmery SM, Sambrook MA, Crossman AR. Dyskinesia in the primate following injection ofan excitatory amino acid antagonist into the medial segment of the globus pallidus. Brain Res 1989;476:317-22. 13 Parent A, Lavoie B, Smith Y, Bedard P. The dopaminergic nigropallidal projection in primates: distinct cellular origin and relative sparing in MPTP-treated monkeys. In: Streifler, ed. Adv Neurol, Vol XX. New York: Raven, 1989.

8 citations


Cited by
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Journal ArticleDOI
TL;DR: Abnormalities of the nicotinic receptor in the diseases examined appear to be closely associated with primary histopathological changes: dopaminergic cell loss in Parkinson's disease and Lewy body dementia, amyloid plaques and tangles in subicular and entorhinal areas in Alzheimer's disease.

388 citations

Journal ArticleDOI
TL;DR: Changes in nicotinic acetylcholine receptors in Alzheimer's disease are distinct from those in normal aging and are likely to contribute to clinical features and possibly neuropathology.

233 citations

Journal ArticleDOI
TL;DR: Correlation of choline acetyltransferase activity with synaptophysin immunoreactivity indicated there is a deficit of cholinergic presynaptic terminals in postmortem human brain following head injury.
Abstract: Loss of cholinergic neurotransmission is implicated in memory impairment and cognitive dysfunction after head injury. The aim of the present study was to investigate presynaptic markers, particularly in relation to cholinergic neurotransmission in human postmortem brain from patients who died following a head injury and age-matched controls. Choline acetyltransferase activity and high-affinity nicotinic receptor binding sites were assayed in the inferior temporal gyrus, cingulate gyrus, and superior parietal cortex of 16 head-injured patients and 8 controls. Synaptophysin immunoreactivity was determined in the left cingulate gyrus from the same patient groups. In the head-injured group, choline acetyltransferase activity was consistently reduced in each cortical region compared to control subjects. The presence of a subdural haematoma and a prolonged survival period after head injury tended to be associated with lower choline acetyltransferase activity. In contrast to the marked reduction in choline acetyltransferase activity, nicotine receptor binding was unchanged in head-injured compared to control patients. Synaptophysin immunoreactivity in the cingulate gyrus was reduced by approximately 30% (p < 0.05) in the head-injured group compared to controls. Correlation of choline acetyltransferase activity with synaptophysin immunoreactivity indicated there is a deficit of cholinergic presynaptic terminals in postmortem human brain following head injury.

120 citations

Journal Article
TL;DR: Analysis of the MR findings and correlation of the clinical findings has permitted a tentative subdivision of adult-onset adrenoleukodystrophy population into four subtypes that appear to differ in respect to prognosis and possibly pathogenesis.
Abstract: PURPOSE To describe the MR findings of brain and spinal cord in adult-onset adrenoleukodystrophy. METHODS One hundred sixty-four adult patients ranging from 19 to 74 years of age (119 men and 45 women) with clinically and biochemically proved adrenoleukodystrophy underwent MR of the brain. In 30 patients the spinal cord also was evaluated with MR. RESULTS The brain MR findings were abnormal in 54 of 119 males and in 9 of 45 female heterozygotes and consisted of varying degrees of demyelination of the cerebral white matter in 40 patients, corpus callosum in 25 patients, corticospinal tracts in 46 patients, visual tracts in 31 patients, and auditory tracts in 18 patients. The thoracic spinal cord showed diffuse atrophy in 18 of 20 men and in 8 of 10 women. CONCLUSION It is important to recognize the MR findings of adult-onset adrenoleukodystrophy, because not uncommonly the clinical and MR findings of adrenoleukodystrophy are misdiagnosed as multiple sclerosis, olivopontocerebellar or spinocerebellar atrophy, amyotrophic lateral sclerosis, or dementia. Analysis of the MR findings and correlation of the clinical findings has permitted a tentative subdivision of adult-onset adrenoleukodystrophy population into four subtypes that appear to differ in respect to prognosis and possibly pathogenesis. MR evaluation of the brain in adrenoleukodystrophy also is helpful in patient selection for experimental therapy, which is most effective if offered in the early stage of the disease.

120 citations

Journal ArticleDOI
Boyd Rt1
TL;DR: The molecular cloning of genes encoding neuronal nicotinic acetylcholine receptors (nAChRs) has made possible a better understanding of the pharmacology and toxicology of cholinergic compounds and may allow for precise control of neurotransmission mediated by acetylCholine in diverse populations of neurons.
Abstract: The molecular cloning of genes encoding neuronal nicotinic acetylcholine receptors (nAChRs) has made possible a better understanding of the pharmacology and toxicology of cholinergic compounds. Neuronal nAChRs are related in structure to the nAChRs present at the neuromuscular junction. They are composed of multiple subunits designated either alpha and beta. Eight alpha and three beta subunit genes have been cloned. The alpha subunits contain the ligand binding sites, whereas beta subunits are structural subunits that contribute to the function of the receptor. A large number of nAChRs can be formed from different combinations of alpha and beta subunits. Different combinations of alpha and beta subunits can produce receptors in vitro with distinct ion conducting properties. Each subunit gene is expressed in a distinct pattern in the nervous system. The expression of at least some of the nAChR subunit genes is regulated during development and by cell-cell interactions. Each neuronal nAChR subtype has a distinct pharmacology. Both alpha and beta subunits contribute to the pharmacological properties of each subtype. The expression of multiple nAChR subtypes may allow for precise control of neurotransmission mediated by acetylcholine in diverse populations of neurons.

87 citations