Brief exposure to enriched environment rapidly shapes the glutamate
synapse in the rat brain: a metaplastic fingerprint
Abstract
Environmental enrichment (EE) has been shown to produce beneficial
effects in addiction disorders; however, due to its configurational
complexity, the underlying mechanisms are not yet fully elucidated.
Recent evidence suggests that EE, acting as a metaplastic agent, may
affect glutamatergic mechanisms underlying appetitive memory and, in
turn, modulate reward-seeking behaviors: here, we have investigated such
possibility following a brief EE exposure. Adult male Sprague-Dawley
rats were exposed to EE for 22h and the expression of critical elements
of the glutamate synapse was measured 2h after the end of EE in the
medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and
hippocampus (Hipp) brain areas, which are critical for reward and
memory. We focused our investigation on the expression of NMDA and AMPA
receptor subunits, their scaffolding proteins SAP102 and SAP97,
vesicular and membrane glutamate transporters vGluT1 and GLT-1, and
critical structural components such as proteins involved in morphology
and function of glutamatergic synapses, PSD95 and Arc/Arg3.1. Our
findings demonstrate that a brief EE exposure induces metaplastic
changes in glutamatergic mPFC, NAc, and Hipp. Such changes are
area-specific and involve postsynaptic NMDA/AMPA receptor subunit
composition, as well as changes in the expression of their main
scaffolding proteins, thus influencing the retention of such receptors
at synaptic sites. Our data indicate that brief EE exposure is
sufficient to dynamically modulate the glutamatergic synapses in
mPFC-NAc-Hipp circuits, which may modulate rewarding and memory
processes.