α Calcium/Calmodulin Kinase II Mutant Mice: Deficient Long-term Potentiation and Impaired Spatial Learning
- *Howard Hughes Medical Institute at Center for Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; †Howard Hughes Medical Institute at Salk Institute, La Jolla, California 92037; ‡Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309
This extract was created in the absence of an abstract.
Excerpt
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.
To date, the evidence supporting the linkage between LTP and learning and memory primarily comes from the analysis of rats in which the NMDAR is blocked by an antagonist, aminophosphonovaleric acid (APV) (Morris et al. 1986; Staubli Thibault et...
