The plasticity of alcohol addiction suggests novel approaches to pharmacological intervention

摘要: Publisher Summary This chapter focuses on the molecular and cellular alterations in glutamatergic system that appears to underlie alcohol-associated plasticity. The vast majority of neurons across all brain regions possess inputs, with half synapses using glutamate as a neurotransmitter. Glutamate affects neuronal function by activating either postsynaptic ionotropic or metabotropic receptors (mGluRs). Many behavioral manifestations alcohol dependency involve NMDA receptor system. Evidence from both humans animal models suggests N-methyl- D -aspartate (NMDA) are major mediators dependency, tolerance, craving, relapse. Cellular synaptic plasticity have demonstrated changes sub-cellular localization accompanied re-organization dendritic spines. It is suggested ethanol may regulate activity-dependent trafficking at density spines, which explain ethanol-induced adaptive processes dependency. A study has physical link between mGluR5 anchoring proteins perisynaptic sites. experimental approaches focus reversing neuroadaptations common other drugs abuse would likely increase efficacy novel pharmacotherapies poly-drug abusers.