Memories associated with substance use disorders, or substance-associated cues increase
the likelihood of craving and relapse during abstinence. There is a growing consensus that manipulation
of synaptic plasticity may reduce the strength of substance abuse-related memories. On the biological
front, there are new insights that suggest memories associated with substance use disorder may
follow unique neurobiological pathways that render them more accessible to pharmacological intervention.
In parallel to this, research in neurochemistry has identified several potential candidate molecules
that could influence the formation and maintenance of long-term memory. Drugs that target
these molecules (blebbistatin, isradipine and zeta inhibitory peptide) have shown promise at the preclinical
stage. In this review, we shall provide an overview of the evolving understanding on the biochemical
mechanisms involved in memory formation and expound on the premise that substance use
disorder is a learning disorder.
Keywords: Addiction, memory, relapse, cue, blebbistatin, isradipine, PKM zeta.
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