Abstract
As in other parts of the central nervous system (CNS) of the mouse, glutamatergic synapses onto dopamine (DA) neurons in the ventral tegmental area (VTA) mature postnatally. At birth many AMPA receptors (AMPARs) lack GluA2R subunit and most NMDARs contain the GluN2B subunit. Within 2 weeks these receptors are replaced with GluA2- and GluN2A- containing AMPARs and NMDARs, respectively. Recent data suggest that a single injection of cocaine (or another drug of addiction) triggers glutamate receptor redistribution with the reappearance of the subunits typically present in immature synapses, as if addictive drugs reopen the developmental critical period. Here we review the experimental evidence for this hypothesis and discuss the implications for circuit function.
Highlights
Fast excitatory synaptic transmission in the mammalian central nervous system (CNS) is mediated predominantly by ionotropic glutamate receptors of the AMPA- and NMDA-type
Taken together these findings suggest that experience-dependent insertion of CP-AMPA receptors (AMPARs) could alter synaptic plasticity and engage different forms of learning that are independent of NMDARs (Tayler et al, 2011)
Which are the mechanisms that enable the synaptic incorporation and retention of CP-AMPARs after a single cocaine injection in the ventral tegmental area (VTA) and after prolonged withdrawal in the nucleus accumbens (NAc)? What is the significance of the insertion of CP-AMPARs and the concomitant decrease in NMDAR function at these synapses? Previous findings in hippocampal interneurons expressing CP-AMPARs show that pairing of a hyperpolarizing current injection with synaptic release can enhance synaptic transmission (Lamsa et al, 2007)
Summary
Drug-evoked plasticity: do addictive drugs reopen a critical period of postnatal synaptic development?. Reviewed by: Carlo Sala, CNR Institute of Neuroscience, Italy Enrico Tongiorgi, University of Trieste, Italy. As in other parts of the central nervous system (CNS) of the mouse, glutamatergic synapses onto dopamine (DA) neurons in the ventral tegmental area (VTA) mature postnatally. At birth many AMPA receptors (AMPARs) lack GluA2R subunit and most NMDARs contain the GluN2B subunit. Within 2 weeks these receptors are replaced with GluA2- and GluN2A- containing AMPARs and NMDARs, respectively. Recent data suggest that a single injection of cocaine (or another drug of addiction) triggers glutamate receptor redistribution with the reappearance of the subunits typically present in immature synapses, as if addictive drugs reopen the developmental critical period. We review the experimental evidence for this hypothesis and discuss the implications for circuit function
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