Deletion of neuronal gap junction protein connexin 36 impairs hippocampal LTP |
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Authors: | Wang Yongfu Belousov Andrei B |
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Affiliation: | Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 2146 W. 39th Avenue, Kansas City 66160, KS, USA |
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Abstract: | In the mammalian CNS, deletion of neuronal gap junction protein, connexin 36 (Cx36), causes deficiencies in learning and memory. Here we tested whether Cx36 deletion affects the hippocampal long-term potentiation (LTP), which is considered as a cellular model of learning and memory mechanisms. We report that in acute slices of the hippocampal CA1 area, LTP is reduced in Cx36 knockout mice as compared to wild-type mice. Western blot analysis of NMDA receptor subunits indicates a higher NR2A/NR2B ratio in Cx36 knockout mice, indicating that there is shift in the threshold for LTP induction in knockout animals. Data suggest a possibility that learning and memory deficiencies in Cx36 knockout mice are due to deficiencies in LTP mechanisms. |
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Keywords: | Gap junctions Connexin 36 LTP Hippocampus NMDA receptors |
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