Ethanol Modulates Glutamatergic Transmission and NMDAR-Mediated Synaptic Plasticity in the Agranular Insular Cortex.

摘要: The agranular insular cortex (AIC) has recently been investigated by the alcohol field because of its connectivity to and modulatory control over limbic brainstem regions implicated in use disorder (AUD), it shown involvement animal models drinking. Despite evidence AIC AUD, there not yet an examination whether ethanol modulates glutamatergic γ-amino-butyric acid (GABA)ergic synaptic transmission plasticity AIC. Characterizing how states cortical processing neurons are modulated acute will likely reveal molecular targets which chronic alters function as drinking transitions from controlled problematic. Therefore, we collected brain slices ethanol-naive adult male mice, obtained whole-cell recording configuration layer 2/3 pyramidal neurons, bath-applied at pharmacologically relevant concentrations during electrophysiological assays GABAergic plasticity. We found that inhibited electrically evoked N-methyl-D-aspartate receptor (NMDAR)-mediated excitatory post-synaptic currents (EPSCs) a concentration-related fashion, had little effect on α-amino-3-hydrox-5-methylisoxazole-4-propionic acid-type (AMPAR)-mediated EPSCs. Ethanol no spontaneous (sEPSCs) or inhibitory GABAAR-mediated (sIPSCs). conditioning (low-frequency stimulation for 15 min 1 Hz) induced form long-term depression (LTD) AMPAR-mediated ability induce LTD was non-selective NMDAR antagonist (DL-2-amino-5-phosphonovaleric acid), also acute, intoxicating ethanol. Taken together these data suggest glutamate, but GABA system is uniquely sensitive ethanol, particular NMDAR-mediated processes may be disrupted