Future Directions Overview

My findings opened up several avenues for additional research. First, an
investigation of the role of silent synapses (see below) in cocaine-associated memory
strength will help to identify a mechanism through which NR2B-containing NMDARs
contribute to Fix-C and Esc-C memory. Second, site-specific inhibition of signaling
targets in the hippocampus and other brain regions associated with drug addiction will
help to further define the roles of different signaling pathway in Fix-C and Esc-C
memory acquisition, reconsolidation and reinstatement. Third, since NR2B antagonism
was effective against acquisition and reconsolidation of Fix-C and Esc-C memory but
ineffective against stress-induced reinstatement, future investigations into the
physiological changes that occur during withdrawal with respect to NR2B expression
could shed light on inherent differences between the processes of acquisition and
reconsolidation versus stress-induced reinstatement. Fourth, since my work has not
identified a signaling pathway that effectively attenuates stress-induced reinstatement of
Esc-C CPP, future studies should probe for the contribution of alternate signaling
pathways such as metabotropic glutamate receptor signaling. Fifth, my studies have
shown that varying the stimulus salience of cocaine reward through changes in the
pattern of drug administration results in differential drug-memory strength and the
recruitment of different signaling pathways. Future studies should investigate whether
varying the stimulus salience of an aversive memory such as fear conditioning will
similarly engage different signaling molecules.

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