Volume 38, Issue 3 pp. 212-220
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Regional and Developmental Heterogeneities of Central Muscarinic Receptor and Its Deviated Maturation in El Mouse

Koichi Mori M.D.

Corresponding Author

Koichi Mori M.D.

Department of Neuropsychiatry, Osaka City University Medical School, Osaka

Department of Neuropsychiatry, Osaka City University Medical School, 1–5-7, Asahi-cho, Akenoku, Osaka 545, Japan.Search for more papers by this author
Seiichiro Fujita M.D.

Seiichiro Fujita M.D.

Department of Neuropsychiatry, Osaka City University Medical School, Osaka

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Kenji Kawaguchi M.D.

Kenji Kawaguchi M.D.

Department of Neuropsychiatry, Osaka City University Medical School, Osaka

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Daisuke Furutsuka M.D.

Daisuke Furutsuka M.D.

Department of Neuropsychiatry, Osaka City University Medical School, Osaka

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Sakae Yamagami M.D.

Sakae Yamagami M.D.

Department of Neuropsychiatry, Osaka City University Medical School, Osaka

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Yukio Kawakita M.D.

Yukio Kawakita M.D.

Department of Neuropsychiatry, Osaka City University Medical School, Osaka

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Abstract

Abstract: El mice were given the pitching stimulation at 25 days of postnatal age, showing the initial appearance of convulsive seizures at about 75 days. The regional and developmental heterogeneities of the central muscarinic receptor and its deviation in El from dd-Y, as a normal control, were elucidated by the binding assays using [3H]-1-quinuclidinyl benzilate. In the hippocampus and the septal area, the receptor densities (Bmax) of El were down regulated. In the cerebral cortex they were up regulated. In the striatum they showed the crossing change from the down regulation at 25 days to the up regulation at 75 days. These deviations of El were not the response of the El convulsion and did not directly correlate with the pitching stimulation. As the convulsive seizures increased the pitching stimulation significantly decreased the Kd value of dd-Y(st), but it, conversely, increased that of El except in the septal area where there was no effect. These deviations of the receptor densities and affinities in El may reflect the dysfunction of the receptor regulation and may be related to the biochemical basis of epileptogenesis in the genetic model of epilepsy.

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