the GABA-A agonists muscimol and THIP reduced ethanol intake, but also water (Moore et al. 2007). Nicotinic acetylcholine receptor function may also be involved as shown in a recent study using mecamylamine, hexamethonium, dihydro-beta-erythroidine (DHβE), methyllycaconitine (MLA), nicotine and cytisine in a modified DID assay (Hendrickson et al. 2009). The non-specific antagonist mecamylamine reduced ethanol intake and lowered BECs, while the peripheral antagonist hexamethonium did not. Neither the specific competitive nicotinic antagonist DHβE nor the α7 selective antagonist MLA reduced alcohol intake. Nicotine, and cytisine, the β4* receptor full antagonist and β2 partial agonist, also reduced ethanol drinking. Some of these treatments had modest effects on sucrose drinking as well. These authors also performed a rough analysis of drinking patterns, averaging intake into 15 min bins. Nicotine pretreatment predominantly reduced ethanol drinking during the first hour, while mecamylamine affected drinking during the second hour. cFos/tyrosine hydroxylase double labeling experiments suggested that mecamylamine pretreatment before ethanol DID drinking reduced the number of double-labeled cells in the ventral tegmental area while nicotine pretreatment did not (Hendrickson et al. 2009). In addition, one study has shown that the CRF1 antagonist CP-154,526 reduced ethanol intake and BEC during 4 h DID sessions that resulted
