Hippocampus synaptic plasticity has been related to learning and adaptive processes developed during chronic administration of drug abuse. Leading authors suggest the existence of a common neurobiological mechanism mediating drug addiction and memory.
Previous results from our laboratory demonstrated that re-exposure to the environmental context associated to the Diazepam (DZ) withdrawal experience was able to induce withdrawal symptoms in absence of drug exposure. This behavior was linked to an increase in the synaptic plasticity, registered in the hippocampal dentate gyrus, during the encoding and retrieval of the memory associated to withdrawal. (Monti, C. Synapse 2010).
It is known that the brain specific atypical protein kinase C isoform Mzeta (PKMæ) and its persistence are both necessary and sufficient for LTP maintenance (Kelly et al., 2007;Ling et al., 2002;Ling et al., 2006;Serrano et al., 2005). Furthermore, inhibition of PKMæ, by bath application of ZIP, an inhibitory peptide, is able to reverse established late LTP and also memory storage (Pastalkova et al., 2006).
