Add time:09/05/2019         Source:sciencedirect.com

The hypothesis that chlordimeform increased the amplitude of components N1P1 and P1N3 in rat pattern-reversal visual evoked potentials through actions on α2-adrenergic receptors was tested with two sets of experiments. First, rats received single injections of either vehicle, an α2-adrenergic antagonist yohimbine (0.1, 0.5, or 2.0 mg/kg), or an α2-adrenergic agonist clonidine (0.05, 0.1, or 0.5 mg/kg). Yohimbine alone had no effect on pattern-reversal evoked potential amplitude. Clonidine treatment produced a dosage related increase in amplitude of both components similar to that produced by chlordimeform (W. K. Boyes and R. S. Dyer, 1984, Brain Res. Bull., 10, 817–823). Second, rats were given double injections of either vehicle or yohimbine (0.05, 0.5, 2.0, or 5.0 mg/kg) followed by either vehicle, clonidine (0.1 or 0.2 mg/kg) or chlordimeform (10, 20, or 40 mg/kg). Yohimbine pretreatment attenuated the effects of subsequent treatment with either clonidine or chlordimeform. These results support the hypothesis that chlordimeform alters rat pattern-reversal evoked potentials through actions as a central nervous system α2-adrenergic agonist.

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