Synaptic plasticity in drug reward circuitry.

Drug addiction is a major public health issue worldwide. The persistence of drug craving coupled with the known recruitment of learning and memory centers in the brain has led investigators to hypothesize that the alterations in glutamatergic synaptic efficacy brought on by synaptic plasticity may play key roles in the addiction process. Here we review the present literature, examining the properties of synaptic plasticity within drug reward circuitry, and the effects that drugs of abuse have on these forms of plasticity.

LTP in the mouse nucleus accumbens is developmentally regulated.

Glutamatergic transmission in the nucleus accumbens (NAc) has been shown to be important for behavioral adaptations in response to drugs of abuse. NMDA-receptor dependent long-term potentiation (LTP) of glutamatergic synaptic transmission has been hypothesized to underlie many lasting alterations in behavior. Thus, we examined LTP in NAc core and find that it is developmentally regulated.

Morphological and biochemical strategies for monitoring trafficking of epitope-tagged G protein-coupled receptors in agonist-naive and agonist-occupied states.

Epitope tagged alpha 2-AR subtypes have been used to address a variety of cell biological questions, and the strategies used are readily applicable to all GPCR as well as other cell surface proteins. We have provided detailed protocols for successful utilization of the epitope-tagged receptor in the studies of protein localization and trafficking in epithelial cells, and the mechanisms by which this is achieved. We have also described reversible biotinytion strategies to examine agonist-dependent (and independent) receptor turnover at the cell surface.