The effects of benzodiazepines on spinal homosynaptic depression

Clonazepam (0.5 mg/kg, i.v.) changed the characteristic pattern of the exponential decline of the monosynaptic responses, the early tetanic rundown, evoked by trains of 10 stimuli (2, 5 or 10 Hz) applied to either the biceps-semitendinosus or triceps surae nerve, and recorded from the ventral root in spinal cats. In the case of the biceps-semitendinosus, clonazepam did not affect the first monosynaptic response or the last five monosynaptic responses forming the plateau, while the second monosynaptic response was markedly depressed, especially at the higher frequencies tested. The triceps surae reacted differently to the administration of clonazepam, in that the first response was increased and the amount of depression of the second response was lessened, with no change of the plateau. All the effects of clonazepam were reversed by the benzodiazepine antagonist, ethyl 8-fluoro-5,6-dihydro-5-methyl-6-oxo-4H-imidazo[1,5-a] [1,4]benzodiazepine-3-carboxylate (Ro15-1788; 5 mg/kg, i.v.), which alone had no effect of its own on any parameters, suggesting that the effects of clonazepam were mediated by central benzodiazepine receptors. Diazepam (1.0 mg/kg, i.v.), caused the same changes in the homosynaptic depression of the biceps-semitendinosus pathway as did clonazepam, but increased the plateau instead of the second response in that of the triceps surae pathway.