Deletion of neuronal gap junction protein connexin 36 impairs hippocampal LTP

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

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • CA1 Region, Hippocampal / metabolism
  • CA1 Region, Hippocampal / physiology*
  • Connexins / genetics
  • Connexins / physiology*
  • Long-Term Potentiation / genetics
  • Long-Term Potentiation / physiology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Receptors, N-Methyl-D-Aspartate / physiology

Substances

  • Connexins
  • Receptors, N-Methyl-D-Aspartate
  • connexin 36