Synaptic plasticity in the amygdala: comparisons with hippocampus.

Long-term potentiation (LTP) is a widely studied form of synaptic plasticity, and a considerable amount of evidence indicates that it could be involved in learning and memory. Intensive investigation of this phenomenon in the hippocampus has yielded tremendous insight into the workings of synapses in the mammalian central nervous system, but important questions remain to be answered. The most important of these are: (1) whether LTP is the basis of learning and memory, and (2) how similar are the induction, maintenance, and expression mechanisms in the rest of the brain to those in the hippocampus. Because the most important strategy for linking LTP to learning involves disrupting the mechanisms of LTP and examining the consequences on behavior, it is likely that the first question cannot be answered until the second has been addressed. Recent evidence indicates that although the general processes have much in common, significant differences exist among forebrain structures, including the hippocampus, basolateral amygdala, and ventral striatum. It is clear that the roles of receptors and calcium channels, kinases, and transcription factors vary within these structures, reflecting the different functions of these brain regions.

Deletion of the mental retardation gene Gdi1 impairs associative memory and alters social behavior in mice.

Non-specific mental retardation (NSMR) is a common human disorder characterized by mental handicap as the only clinical symptom. Among the recently identified MR genes is GDI1, which encodes alpha Gdi, one of the proteins controlling the activity of the small GTPases of the Rab family in vesicle fusion and intracellular trafficking. We report the cognitive and behavioral characterization of mice carrying a deletion of Gdi1. The Gdi1-deficient mice are fertile and anatomically normal. They appear normal also in many tasks to assess spatial and episodic memory and emotional behavior. Gdi1-deficient mice are impaired in tasks requiring formation of short-term temporal associations, suggesting a defect in short-term memory. In addition, they show lowered aggression and altered social behavior. In mice, as in humans, lack of Gdi1 spares most central nervous system functions and preferentially impairs only a few forebrain functions required to form temporal associations. The general similarity to human mental retardation is striking, and suggests that the Gdi1 mutants may provide insights into the human defect and into the molecular mechanisms important for development of cognitive functions.