Brad Fitzpatrick
A group of slow-witted, mutant mice and a protein called RIM1α may provide insight into learning and memory mechanisms. University of Texas Southwestern researchers showed that knockout mice missing RIM1α, a presynaptic protein previously studied in vitro, performed worse at learning and memory tasks than did two other sets of genetically altered mice, each a mutant for proteins involved in neurotransmitter release.1
The oft-studied molecular players in learning and memory, including calcium influx, the NMDA receptor, and protein kinases, are postsynaptic, whereas RIM1 is presynaptic. The deficits observed in RIM1-knockout mice, says lead author Craig Powell, are likely a perturbation of short- and long-term presynaptic plasticity.
A causal link, however, between RIM1 and plasticity has not been fully established in vivo. "We still have to find out what is the mechanism. What is the unique property that RIM brings to the brain that explains changes in behavior?" says ...
