Intermittent ethanol exposure during adolescence impairs cannabinoid type 1 receptor-dependent long-term depression and recognition memory in adult mice

摘要

Experimental timeline, voluntary oral EtOH consumption, BEC, and correlation between total EtOH intake and BEC. a EtOH-exposed mice had free EtOH access [20% (v/v)] during 4 weeks in the adolescence (pnd 32–56). Each week, the mice were exposed to 2 or 4 h of free EtOH access, as required. After 2 weeks of withdrawal (i.e. during adulthood), 42 animals (13 per experimental group) were treated with JZL184 or vehicle for five consecutive days (pnd 67–71), and subjected to the NOR test the last 3 days of JZL184 treatment (pnd 69–71). The remaining animals were sacrificed for electrophysiology, anatomy, biochemistry, and molecular techniques in adulthood (pnd 74–78). b Daily EtOH intake during DID [grams of EtOH per kilogram per 2 or 4 h (g/kg/2 or 4 h)]. c Total EtOH intake (g/kg/h) during adolescence (pnd 32–56) and d BEC (mg/dL) of C57BL/6J mice at the last day of EtOH treatment (pnd 56). e Correlation between total EtOH intake throughout adolescence period and BEC measured at the end of the EtOH access. f Left: Stimulating electrode (S) placed in the middle 1/3 of the DML to stimulate MPP. R recording electrode, GC granule cells, MCF mossy cell fibers, LPP lateral perforant path. Right: Time course of {"type":"entrez-nucleotide","attrs":{"text":"LY354740","term_id":"1257481336","term_text":"LY354740"}}LY354740 [1 µM]-induced inhibition of evoked fEPSP after MPP stimulation (filled circles) normalized to baseline. All data are expressed as mean ± SEM. Unpaired t- test; ***p < 0.001