Deletion of neuronal gap junction protein connexin 36 impairs hippocampal LTP

► Genetic deletion of neuronal Cx36 causes learning and memory deficiencies. ► Here we tested whether genetic deletion of Cx36 affects hippocampal LTP. ► We find that LTP is reduced in Cx36 knockout mice. ► Analysis shows a higher NR2A/NR2B receptor subunit ratio in Cx36 knockout mice. ► Reduced LTP may be the cause of learning and memory deficits in Cx36 knockout mice. 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.