Developmental alterations of ethanol sensitivity in selectively bred high and low alcohol sensitive rats

Ontogeny of Acute Tolerance to Ethanol‐Induced Social Inhibition in Sprague–Dawley Rats

“…In the present study, young adolescent rats, in contrast to their older adolescent counterparts and adults, developed compensatory adaptations to the impairment of social behavior by ethanol within 30 minutes, a time interval over which their BrECs or BECs declined from about 120 to 80 mg%. This expression of acute tolerance among early adolescents extends previous ontogenetic findings obtained using high, hypnotic doses of ethanol (Draski et al, 2001;Silveri and Spear, 1998) to adaptations occurring in response to a moderate dose of ethanol (1 g/kg i.p.) and producing BECs of relevance to exposure levels emerging with binge use among human adolescents.…”

“…Acute tolerance has been observed for a number of ethanol effects, including motor impairment, sedation, and hypothermia in adult rodents (see Lê and Mayer, 1996, for references and review). Studies examining the ontogeny of acute tolerance have been restricted to the assessments of ethanol-induced sedation emerging at relatively high doses of ethanol and have reported ontogenetic declines in acute tolerance to the hypnotic effects of ethanol, with more pronounced acute tolerance expressed in adolescent than adult rodents (Draski et al, 2001;Grieve and Littleton, 1979;Spear, 1998,2002). Ontogenetic alterations in the development of acute tolerance to other ethanol effects have not been explored.…”

“…Given that previous studies reporting ontogenetic declines in the development of acute tolerance used relatively high doses of ethanol and assessed emergence of tolerance to ethanolinduced sedation over a period of several hours (Draski et al, 2001;Grieve and Littleton, 1979;Spear, 1998,2002), the main objective of the present study was to examine ontogenetic development of acute tolerance to a relatively low dose of ethanol (1 g/kg) when examined within 30 minutes after ethanol administration, using ethanol-induced social impairment as the target response measure. Because of recent findings (e.g., Philpot et al, 2003;Varlinskaya and Spear, 2004) that point to age differences in ethanol responsiveness even within the adolescent period, rats tested at a variety of ages (P28, P35, P42) in adolescence were compared with young adult (P70) animals.…”

Individual differences in initial sensitivity and acute tolerance predict patterns of chronic drug tolerance to nitrous-oxide-induced hypothermia in rats

“…Schuckit and colleagues (2001) estimate that approximately 40% of children of alcoholics are relatively insensitive to ethanol while only 10% of children of non-alcoholics have this characteristic. Animal research has investigated whether these initial intrasessional factors are associated with subsequent chronic tolerance development or drug consumption by using rodents from outbred and inbred strains, as well as knock-out mice and selectively bred lines for drug consumption, drug sensitivity, and acute tolerance [e.g., outbred strains (Tabakoff and Culp 1984;San-Marina et al 1989;Khanna et al 1990b;Khanna et al 1991); inbred strains (Crabbe et al 1982;Tabakoff and Culp 1984;Khanna et al 1990a;Crabbe et al 1994;Gehle and Erwin 2000); knock-out mice (Naassila et al 2002); lines selectively bred for consumption (Tampier and Mardones 1999;Tampier et al 2000;Bell et al 2001); lines selectively bred for sensitivity (Khanna et al 1985;Crabbe et al 1989;Limm andCrabbe 1992: Crabbe 1994;Browman et al 2000;Deitrich et al 2000;Draski et al 2001;Palmer et al 2002); lines selectively bred for acute tolerance (Deitrich et al 2000;Rustay et al 2001;Wu et al 2001)]. While the scientific literature is in general agreement that initial sensitivity and acute tolerance are relevant to the subsequent development of chronic tolerance and drug consumption, a coherent description of this relationship has not emerged.…”

Supplementing the liquid alcohol diet with chow enhances alcohol intake in C57 BL/6 mice

“…The blood alcohol levels were determined enzymatically as described (Draski et al, 2001). Briefly, a 40 μl venous blood sample was mixed with 2 ml of 3.0 % (v/v) perchloric acid.…”