DEFICITS IN MEMORY AND HIPPOCAMPAL LONG-TERM POTENTIATION IN MICE WITH REDUCED CALBINDIN D-28K EXPRESSION

The influx of calcium into the postsynaptic neuron is likely to be an important event in memory formation. Among the mechanisms that nerve c ells may use to alter the Lime course or size of a spike of intracellu lar calcium are cytosolic calcium binding or ''buffering'' proteins. T o consider the role in memory formation of one of these proteins, calb indin D-28K, which is abundant in many neurons, including the CA1 pyra midal tells of the hippocampus, transgenic mice deficient in calbindin D-28K have been created. These mice show selective impairments in spa tial learning paradigms and fail to maintain long-term potentiation. T hese results suggest a role for calbindin D28K protein in temporally e xtending a neuronal calcium signal, allowing the activation of calcium -dependent intracellular signaling pathways underlying memory function .