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Calcium/Calmodulin Kinase II Mutant Mice: Deficient Long-term Potentiation and Impaired Spatial Learning
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1992
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Glutamategated Ion ChannelSynaptic TransmissionNeurotransmissionCellular PhysiologyImpaired Spatial LearningNeurochemistryHealth SciencesMolecular PhysiologyCortical RemodelingIon ChannelsDeficient Long-term PotentiationNervous SystemPharmacologyCell BiologySynaptic PlasticityNeurophysiologyPhysiologyLong-term PotentiationNeuroscienceMolecular NeurobiologyCentral Nervous SystemMedicine
Long-term potentiation (LTP) is a type of synaptic plasticity that has been widely studied as a candidate mechanism for some types of learning and memory (Bliss and Gardner Medwin 1973; Bliss and Lomo 1973; Schwartzkroin and Webster 1975; McNaughton et al. 1978). In some hippocampal synapses where LTP has been studied, the voltage-sensitive and glutamategated ion channel, the N-methyl-d-aspartate receptor (NMDAR) plays a critical role in the induction of LTP by regulating a calcium (Ca++) current (Collingridge and Singer 1990). The Ca++ influx facilitated by an opening of NMDARs leads to an increase in the synaptic connection via a series of biochemical events that include activation of Ca++ and/or calmodulin-dependent kinases.