Contextual memory deficits observed in mice overexpressing small conductance Ca2+-activated K+ type 2 (KCa2.2, SK2) channels are caused by an encoding deficit

Learn Mem. 2008 Mar 27;15(4):208-13. doi: 10.1101/lm.906808. Print 2008 Apr.

Abstract

Hippocampal-dependent synaptic plasticity and memory are modulated by apamin-sensitive small conductance Ca2+-activated K+ (SK) channels. Transgenic mice overexpressing SK2 channels (SK2+/T mice) exhibit marked deficits in hippocampal memory and synaptic plasticity, as previously reported. Here, we examined whether SK2 overexpression affects the encoding or retention of contextual memory. Compared with wild-type littermates, SK2+/T mice exhibited significantly less context-dependent freezing 10 min and 24 h after conditioning. Interestingly, this contextual memory impairment was eliminated if SK2+/T mice were permitted longer pre-exposure to the conditioning chamber. These data support converging evidence that SK2 channels restrict the encoding of hippocampal memory.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Fear / physiology
  • Gene Expression Regulation
  • Genotype
  • Hippocampus / physiopathology
  • Memory Disorders / genetics*
  • Mice
  • Small-Conductance Calcium-Activated Potassium Channels / genetics*
  • Synapses / physiology

Substances

  • Kcnn2 protein, mouse
  • Small-Conductance Calcium-Activated Potassium Channels