Neural plasticity related to drug addiction can be modeled by behavioral sensitization in animals through the chronic administration of drugs. Long term-de-potentiation (LTD) in the nucleus accumbens (NAc) is proposed to be involved in neural plasticity resulting from addictive drugs. The exact mechanism of LTD remains unknown; however, previous experiments have linked LTD with cocaine re-exposure and the endocytosis of GluR2-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR) in the NAc. In this experiment, we looked at the relapse related behavior resulting from this neural plasticity. Mice, after ten days of self-administration of cocaine and seven days of extinction, were given infusions of an inactive or active TAT peptide designed to block the endocytosis of the AMPARs. We hypothesized that this would block LTD in the NAc and therefore decrease cocaine seeking behavior seen after relapse. Reinstatement then took place with the injection of cocaine to induce relapse. The results of this experiment showed a difference in response to the active and the inactive peptide. The mice with the active peptide TAT infusions showed successful response inhibition, a decrease in reinstatement of cocaine seeking behavior.
This research was supported by the Undergraduate Research Scholarship (URS).
Back, Johanna J.
The blockade of endocytosis of GluR2-containing AMPARs in the nucleus accumbens and its effect on reinstatement for cocaine-seeking behavior.
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