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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Neuropharmacological studies in rodents on the action of RX 781094, a new selective alpha 2-adrenoceptor antagonist.

Several neuropharmacological effects of RX 781094, a new selective alpha 2-adrenoceptor antagonist, have been investigated in rodents. In rats, RX 781094 (0.1-1.0 mg kg-1, i.v.) produced a rapid dose-related reversal of cortical EEG synchronisation and behavioural sedation, induced by clonidine or the more selective alpha 2-adrenoceptor agonist, guanoxabenz. The alpha 2-adrenoceptor antagonists yohimbine and mianserin were also effective in blocking guanoxabenz-induced EEG synchronisation but had a lower potency than did RX 781094. In specificity experiments, RX 781094 (1.0 mg kg-1, i.v.) failed to antagonise the EEG synchronisation and pronounced behavioural sedation induced by the CNS depressant sodium pentobarbitone (15 mg kg-1, i.v.). In mice, pretreatment (i.v. or p.o.) with RX 781094 inhibited in a dose-dependent way both guanoxabenz-induced behavioural hypoactivity and clonidine-induced hypothermia. By itself, RX 781094 had no effect on the temperature of normal mice. In sleep-waking studies in rats, RX 781094 (0.1 and 1.0 mg kg-1, i.v.) had no measurable stimulant or depressant effect on the CNS, in contrast to (+)-amphetamine (1.0 mg kg-1, i.v.) which elicited marked CNS stimulation. These results support the conclusion that RX 781094 is a potent antagonist at central alpha 2-adrenoceptors.[1]


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