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Chunk #7 — 1 Acute Ethanol Actions — 1.1 Ligand-Gated Ion Channels and Postsynaptic Ethanol Effects — 1.1.1 Cys-loop Ligand-Gated Ion Channels

Source
Synaptic effects induced by alcohol.
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yes

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EtOH potentiation of glycine-activated chloride channels appears to be dependent on receptor subunit composition. Potentiation is consistently greater at receptors containing the α1 subunit (Davies et al. 2003; Mascia et al. 1996; Mihic et al. 1997), at least when expressed in xenopus laevis oocytes (Valenzuela et al. 1998b, although see McCool et al. 2003; Yevenes et al. 2008). Receptors containing the α2 subunit also exhibit EtOH potentiation (McCool et al. 2003), but may be less sensitive than those containing the α1 subunit (Mascia et al. 1996). Inclusion of the β subunit along with α2 eliminates potentiation (McCool et al. 2003). Potentiation has also been observed in neurons from the brain and spinal cord, particularly in regions where the α1 subunit is expressed (Aguayo et al. 1996; Ye et al. 2001). Potentiation of the function of GABAA and glycine receptors is thought to increase inhibition of neurons. The relative influence of effects on synaptic versus extrasynaptic channels in producing this inhibition remains to be determined.