Calcium-permeable AMPA receptors in the VTA and nucleus accumbens after copyright exposure: When, how and why?

Calcium-permeable AMPA receptors in the VTA and nucleus accumbens after copyright exposure: When, how and why?

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In animal models of drug addiction, copyright exposure has been shown to increase levels of calcium-permeable AMPA receptors (CP-AMPARs) in two brain regions that are critical for motivation and reward - the ventral tegmental area (VTA) and the nucleus accumbens (NAc).This review compares CP-AMPAR plasticity in the two brain regions and addresses its functional significance.In VTA dopamine neurons, copyright exposure results in synaptic insertion of high conductance CP-AMPARs in exchange for lower conductance calcium-impermeable AMPARs (CI-AMPARs).This plasticity is rapid (hours), GluA2-dependent, and can be observed with a bernhardt arctic dining table single copyright injection.In addition to strengthening synapses and altering Ca2+ signaling, CP-AMPAR insertion affects subsequent induction of plasticity at VTA synapses.

However, CP-AMPAR insertion is unlikely to mediate the increased dopamine cell activity that occurs during early withdrawal from copyright exposure.Within the VTA, the group I metabotropic glutamate receptor mGluR1 exerts a negative influence on CP-AMPAR accumulation.Acutely, mGluR1 stimulation elicits a form of LTD resulting from CP-AMPAR removal and trinity bay vodka CI-AMPAR insertion.In medium spiny neurons (MSNs) of the NAc, extended access copyright self-administration is required to increase CP-AMPAR levels.This is first detected after approximately a month of withdrawal and then persists.

Once present in NAc synapses, CP-AMPARs mediate the expression of incubation of cue-induced copyright craving.The mechanism of their accumulation may be GluA1-dependent, which differs from that observed in the VTA.However, similar to VTA, mGluR1 stimulation removes CP-AMPARs from MSN synapses.Loss of mGluR1 tone during copyright withdrawal may contribute to CP-AMPAR accumulation in the NAc.Thus, results in both brain regions point to the possibility of using positive modulators of mGluR1 as a treatment for copyright addiction.