Deficient Hippocampal Long-Term Potentiation in α-Calcium-Calmodulin Kinase II Mutant Mice

TLDR

The α‑CaMKII is highly enriched in postsynaptic densities of hippocampus and neocortex and may regulate long‑term potentiation (LTP). Mutant mice lacking α‑CaMKII were generated as part of a program to use genetically altered mice for studying memory mechanisms. These mice exhibited normal behavior, intact NMDA receptor function, but were deficient in inducing LTP, making them a useful model for linking LTP to learning.

Abstract

As a first step in a program to use genetically altered mice in the study of memory mechanisms, mutant mice were produced that do not express the α-calcium-calmodulin-dependent kinase II (α-CaMKII). The α-CaMKII is highly enriched in postsynaptic densities of hippocampus and neocortex and may be involved in the regulation of long-term potentiation (LTP). Such mutant mice exhibited mostly normal behaviors and presented no obvious neuroanatomical defects. Whole cell recordings reveal that postsynaptic mechanisms, including N -methyl-D-aspartate (NMDA) receptor function, are intact. Despite normal postsynaptic mechanisms, these mice are deficient in their ability to produce LTP and are therefore a suitable model for studying the relation between LTP and learning processes.