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Neurosci Lett. 2011 Sep 8;502(1):30-2. doi: 10.1016/j.neulet.2011.07.018. Epub 2011 Jul 20.

Deletion of neuronal gap junction protein connexin 36 impairs hippocampal LTP.

Author information

1
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 2146 W. 39th Avenue, Kansas City, KS 66160, USA.

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.

PMID:
21798314
PMCID:
PMC3159746
DOI:
10.1016/j.neulet.2011.07.018
[Indexed for MEDLINE]
Free PMC Article

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