Abstract

Mice injected with DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine], a selective noradrenergic neurotoxin, had marked depletions of central noradrenaline and an attenuated post-decapitation reflex. DSP-4-treated mice exhibited an increased sensitivity to the alpha 2-adrenoceptor agonist clonidine as measured by inhibition of the pinna reflex, but normal sensitivity as measured by hypothermia. This differential sensitivity may reflect the presence of supersensitive postsynaptic alpha 2-adrenoceptors in some, but not all, CNS regions after DSP-4 treatment.

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