Zigmond, Zachary

Methamphetamine (METH) is addictive and associated with a high rate of relapse. One relapse trigger is re-experiencing drug-associated contextual associations. Therefore it is possible that, by targeting METH-associated contextual memories, drug seeking behavior can be inhibited. Recent evidence has suggested that memory formation relies on actin polymerization, which allows dendritic spines to undergo structural and functional plasticity, key components of memory. To see if actin polymerization could be a target for the extinction of METH seeking memories we inhibited actin polymerization in animals that had been trained in either METH or food associated conditioned place preference. Pretest inhibition of actin cycling in the basolateral amygdala complex produced immediate and persistent extinction of METH seeking behavior. Additionally, inhibiting actin polymerization 24hrs before testing disrupted seeking behavior for METH but not food. These results indicate that METH-associated memories are selectively vulnerable to disruption through inhibition of actin dynamics.