Effect of NMDA antagonists on rapid and chronic tolerance to ethanol: Importance of intoxicated practice
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Effects of NMDA antagonists on the development and expression of tolerance to diazepam-induced motor impairment in mice
2016, Pharmacology Biochemistry and BehaviorCitation Excerpt :Ketamine is known to attenuate the development of rapidly learned and unlearned tolerance to chlordiazepoxide-induced motor impairment, measured by the tilt-plane test (Khanna et al., 1997). Furthermore, Wu et al. (1993)) and Khanna et al. (1991, 1992a, b, 1993b, 1994) showed the capacity of ketamine and MK-801 to inhibit the development of acute, rapid and chronic tolerance to motor incoordination produced by ethanol. Surprisingly enough, on their first attempt of evaluation of the above-mentioned connections, Khanna et al. (1992c)) observed no effect of ketamine on the development of rapid tolerance to chlordiazepoxide.
Chronic ethanol tolerance as a result of free-choice drinking in alcohol-preferring rats of the WHP line
2012, Pharmacological ReportsCitation Excerpt :These studies implicated a range of endogenous factors in the development of tolerance. Neurotransmitters and receptor system like GABAA [9], NMDA [20, 45], serotonin [14], dopamine [47], cannabinoid CB1 [7], and corticotropin releasing factor (CRF) [43] have been reported to be involved in the development of tolerance to ethanol. Higher GABAergic activity in medial septal or dorsal striatum has also been reported [17, 19].
Ontogeny of ethanol-induced motor impairment following acute ethanol: Assessment via the negative geotaxis reflex in adolescent and adult rats
2010, Pharmacology Biochemistry and BehaviorAniracetam and DNQX affect the acquisition of rapid tolerance to ethanol in mice
2009, Pharmacology Biochemistry and BehaviorN-methyl-D-aspartate glutamate receptors and alcoholism: Reward, dependence, treatment, and vulnerability
2003, Pharmacology and TherapeuticsCitation Excerpt :The contribution of NMDA receptors to tolerance- and withdrawal-related neuroplasticity has received growing attention. For example, features of the development of drug tolerance involve learning or experience-dependent neuroplasticity, as might be modeled by long-term potentiation (LTP) or long-term depression (LTD) (Kalant, 1993; Khanna et al., 1994; Trujillo & Akil, 1995). Consistent with this view, NMDA receptor antagonist coadministration appears to attenuate components of ethanol tolerance, particularly the environment-dependent component of tolerance (Szabo et al., 1994), while NMDA receptor facilitation may potentiate the development of this type of tolerance (Khanna et al., 1993; Wu et al., 1993; Rafi-Tari et al., 1996).