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Correlation Study of Cognitive Disorder Induced by Ethanol and M1 Receptor in Hippocampus in Mice / 中国医科大学学报
Journal of China Medical University ; (12): 602-605, 2015.
Artigo em Chinês | WPRIM | ID: wpr-463199
ABSTRACT
Objective To investigate the effect of ethanol on level of the main hippocampal subtype of muscarinic receptor(M1)in mice,and evalu?ate whether the content change on this receptor could be linked with alterations in cognition,so as to further reveal the mechanism of brain damage in?duced by ethanol. Methods Sixty female mice were randomly divided into four groups. The model mice were induced by intragastric administration of ethanol at dose of 8%,16%,and 32%respectively of 0.2 mL/10 g for 8 weeks according to the protocol,and control group were treated with intra?gastric administration of distilled water. The capability of learning and memory were examined by Morris water maze,and ELISA method was used to measure the M1 receptor content in hippocampus in each group of mice. Results Compared with first day,the mean escape latency period on the fifth day was significantly shortened in each group. There was no significant difference between ethanol and control group for the mean escape latency period on the fifth day. Compared with the control group,the active time in the target quadrant was significantly shortened in 16%and 32%ethanol group. M1 receptor content in hippocampus formation was significantly decreased in all the ethanol group mice. The ethanol concentration was nega?tive correlated with the M1 receptor content. Conclusion Chronic alcoholism can induce the memory impairment in mice,which might be associat?ed with the low level of M1 receptor subtype in hippocampus of mice.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of China Medical University Ano de publicação: 2015 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of China Medical University Ano de publicação: 2015 Tipo de documento: Artigo