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Alcohol consumption increases basal extracellular glutamate in the nucleus accumbens core of S prague– D awley rats without increasing spontaneous glutamate release
Author(s) -
Pati Dipanwita,
Kelly Kyle,
Stennett Bethany,
Frazier Charles J.,
Knackstedt Lori A.
Publication year - 2016
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13284
Subject(s) - glutamate receptor , microdialysis , nucleus accumbens , chemistry , metabotropic glutamate receptor , medicine , excitatory postsynaptic potential , tetrodotoxin , endocrinology , extracellular , pharmacology , biology , biochemistry , receptor
Abstract Glutamate neurotransmission in the nucleus accumbens core ( NA c) mediates ethanol consumption. Previous studies using non‐contingent and voluntary alcohol administration in inbred rodents have reported increased basal extracellular glutamate levels in the NA c. Here, we assessed basal glutamate levels in the NA c following intermittent alcohol consumption in male S prague‐ D awley rats that had access to ethanol for 7 weeks on alternating days. We found increased basal NA c glutamate at 24 h withdrawal from ethanol and thus sought to identify the source of this glutamate. To do so, we employed a combination of microdialysis, slice electrophysiology and western blotting. Reverse dialysis of the voltage‐gated sodium channel blocker tetrodotoxin did not affect glutamate levels in either group. Electrophysiological recordings in slices made after 24 h withdrawal revealed a decrease in spontaneous excitatory postsynaptic current ( sEPSC ) frequency relative to controls, with no change in sEPSC amplitude. No change in metabotropic glutamate receptor 2/3 ( mG lu2/3) function was detected as bath application of the mG lu2/3 agonist LY 379268 decreased spontaneous and miniature EPSC frequency in slices from both control and ethanol‐consuming rats. The increase in basal glutamate was not associated with changes in the surface expression of GLT ‐1, however, a decrease in slope of the no‐net‐flux dialysis function was observed following ethanol consumption, indicating a potential decrease in glutamate reuptake. Taken together, these findings indicate that the increase in basal extracellular glutamate occurring after chronic ethanol consumption is not mediated by an increase in action potential‐dependent glutamate release or a failure of mG lu2/3 autoreceptors to regulate such release.