Abstract
With recent technical advancements in mouse embryology and in DNA recombination, it is now possible to engineer specific mutations in any gene within the mouse genome. With this powerful new genetic strategy the functional significance of a single gene can be studied at the molecular, cellular and behavioral levels, allowing a multifaceted investigation of complex neurobiological problems such as the cellular and molecular basis of learning and memory. In this review we will describe the use of targeted gene disruption to study roles of nonreceptor tyrosine kinases in the biochemical processes underlying long-term potentiation (LTP), a candidate cellular mechanism of learning and memory.
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