Contextual memory deficits observed in mice overexpressing small conductance Ca2+-activated K+ type 2 (KCa2.2, SK2) channels are caused by an encoding deficit.
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.
Stackman
Robert W
RW
Program in Psychobiology, Department of Psychology, Florida Atlantic University, Boca Raton, Florida 33431-0991, USA. rstackma@fau.edu
Bond
Chris T
CT
Adelman
John P
JP
D000818:Animals; D005239:Fear / Q000502:physiology; D005786:Gene Expression Regulation; D005838:Genotype; D006624:Hippocampus / Q000503:physiopathology; D008569:Memory Disorders / Q000235:genetics*; D051379:Mice; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000235:genetics*; D013569:Synapses / Q000502:physiology
C496898:Kcnn2 protein, mouse; D051640:Small-Conductance Calcium-Activated Potassium Channels