Effects of chlorpromazine, imipramine and baclofen on the spinal polysynaptic reflex in acute, chronic and 6-hydroxydopamine-treated spinal rats.

Effects of the drugs affecting monoaminergic neurotransmission were examined on the spinal polysynaptic reflex (PSR) in anesthetized spinal rats. Chlorpromazine HCI (0.5-2.0 mg/kg, i.v.) and baclofen (0.63-2.5 mg/kg) depressed and imipramine HCI (1.25-5.0 mg/kg) increased the amplitude of PSR in acute spinal animals, recorded as evoked electromyogram in the gastrocnemius muscle by electrical stimulation of the common peroneal nerve. However, chlorpromazine and imipramine showed effects neither on PSR in chronic spinal rats, nor in acute spinal rats with the intracisternal administration of 6-hydroxydopamine, which caused depletion of the spinal noradrenaline, dopamine and serotonin, and selective depletion of the spinal noradrenaline, respectively. Baclofen depressed the amplitude of PSR in both preparations with almost the same potency as that in acute spinal ones. Imipramine HCI (2.5 mg/kg, i.v.), chlorpromazine HCI (1.0 mg/kg) and baclofen (1.25 mg/kg) depressed the mono- and polysynaptic heights of the ventral root potentials in acute spinal rats. However, their depression of polysynaptic height was not so strong. These observations strongly suggest that, at the receptor sites on spinal interneurons where the descending monoaminergic neurons terminate, spinal monoamines, especially noradrenaline, are involved in PSR modification by chlorpromazine and imipramine, but not in PSR depression by baclofen.