2 Subunit-Containing GABA Receptor Subtypes Are Upregulated and Contribute to Alcohol-Induced Functional Plasticity in the Rat Hippocampus.

Alcohol (EtOH) intoxication causes changes in the rodent brain -aminobutyric acid receptor (GABAR) subunit composition and function, playing a crucial role in EtOH withdrawal symptoms and dependence. Building evidence indicates that withdrawal from acute EtOH and chronic intermittent EtOH (CIE) results in decreased EtOH-enhanced GABAR subunit-containing extrasynaptic and EtOH-insensitive 12 subtype synaptic GABARs but increased synaptic 42 subtype, and increased EtOH sensitivity of GABAR miniature postsynaptic currents (mIPSCs) correlated with EtOH dependence. Here we demonstrate that after acute EtOH intoxication and CIE, upregulation of hippocampal 42 subtypes, as well as increased cell-surface levels of GABAR 2 and 1 subunits, along with increased 211 GABAR pentamers in hippocampal slices using cell-surface cross-linking, followed by Western blot and coimmunoprecipitation.