PubMed · 9078749
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H Suwaki, T Utsumi. 1997. [Pathological intoxication].. https://pubmed.ncbi.nlm.nih.gov/9078749/
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Genetically engineered animals (e.g., transgenics, gene knockouts, gene knockins) are being utilized with increasing frequency to investigate the mechanisms of action of alcohol and anesthetics. By creating and analyzing animals that harbor precise, preplanned changes in candidate genes, researchers are rapidly making progress toward uncovering how these drugs exert their effects on the central nervous system to bring about their behavioral effects. Since these sedative / hypnotic agents are likely to exert their effects by altering neurotransmission, the majority of investigations to date have focused on neurotransmitter receptors and modulators of neurotransmission such as kinases.
The role of the dorsal striatum in mediating the sedation produced by a moderate (0.75 g/kg) and an intoxicating (1.25 g/kg) EtOH dose was investigated in the open field by determining the capacity of direct intrastriatal injections of RY 008, a partial inverse agonist of the benzodiazepine (BDZ) receptor, to antagonize EtOH's effects. SR 95531, the competitive high-affinity GABAA antagonist was used as a reference compound. Intrastriatal RY 008 (50, 500 ng) and SR 95531 (50 ng) antagonized the sedation produced by the 0.75 g/kg EtOH dose. However, RY 008 did not alter the sedation produced by the 1.25 g/kg dose. RY 008 alone was without effect. RY 008 also failed to negatively modulate GABAergic function at alpha1beta2gamma2 or alpha6beta2gamma2 receptor subtypes expressed in Xenopus oocytes. Intrastriatal modulation of the moderate EtOH dose was site specific: no antagonism by RY 008 after intraaccumbens infusions was observed. The results suggest that central GABAA-BDZ receptors in the dorsal striatum play an important role in mediating the sedation produced by a moderate EtOH dose in the open field.