Abstract

In cats that were made paraplegic by total spinal cord transection, a number of changes occur that lead to spasticity. There is a gradual loss of prolonged spinal inhibition (presynaptic inhibition) that is accompanied by a decrease of Km and Vmax values for glutamic acid decarboxylase (GAD), both above and below the lesion. This enzyme is necessary for the conversion of glutamic acid to γ-aminobutyric acid (GABA), the transmitter mediating presynaptic inhibition. Although the Km and Vmax levels for GAD eventually return to the control values, presynaptic inhibition remains depressed. Diazepam enhances presynaptic inhibition in acute and, to a lesser extent, in chronic spinal cats. This increase in presynaptic inhibition is accompanied by a reduction in somatic muscular activity in both acute and chronic spinal animals.

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