Abstract

Studies in animal models, and to a lesser extent in humans, have revealed a wide range of long-lasting adaptations in neuronal excitability, synaptic function, neuron architecture, and expression of genes associated with neural plasticity after exposure to drugs or alcohol. Similar alterations have been observed in individuals with differential genetic vulnerabilities for substance abuse. As the techniques for identifying neural adaptations have multiplied and data have accumulated at a rapid pace, it has become clear that there is a formidable problem in determining which adaptations are critical for establishing and maintaining addiction, and which are not[1,2]. Two NIDA-supported symposia at the 2007 Society for Neurosciences (SFN) meeting address this problem. A symposium in the National Institute on Drug Abuse (NIDA) Frontiers in Addiction Research Miniconvention, “Neuronal Adaptations and Counteradaptations”, showcases three very different approaches in presentations by Robert Malenka, L. Judson Chandler, and Lorna Role. An SFN symposium, “Reconciling Molecular and Electrophysiological Evidence of Cocaine-Induced Neural Plasticity”, focuses on the apparent contradiction between molecular and neurophysiological changes in nucleus accumbens and recent studies that attempt to resolve this contradiction in presentations by Marina Wolf, Mark Thomas, Xiu-Ti Hu, and Laura Peoples. These symposia are represented by two papers in this issue[3,4].

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