Effects of diphenylaminoethanol and lidocaine on central inhibition

Abstract

In normal cats, 1, 1-diphenyl-2-aminoethanol (DPAE) caused ataxia, intentional tremors, and convulsions whereas lidocaine caused ataxia and convulsions but no tremors. In decerebrate cats, DPAE markedly inhibited cerebellar disfacilitation of spinal monosynaptic reflexes, slightly depressed reticular inhibition and had no effect on direct inhibition. The unconditioned monosynaptic reflex was facilitated by low doses and depressed by high doses of DPAE. DPAE did not affect reticular facilitation indicating that DPAE did not block cerebellar disfacilitation by depressing the facilitatory input to lower motoneurones. Lidocaine markedly reduced cerebellar disfacilitation and also reduced reticular and presynaptic inhibition as well as pressor and facilitatory responses.

It is concluded that the tremors and ataxia of DPAE are manifestations of the preferential blockade of cerebellar disfacilitation, and that this action of DPAE may take place at the inhibitory synapses of cerebellar Purkinje cells on neuronal systems responsible for the tonic excitatory input to lower motoneurones.