Abstract
Baclofen, a GABA derivative, has proven useful in the treatment of spasticity when given in low doses. Despite numerous studies its mechanism of action remains unclear. For example, baclofen has been found to inhibit dopaminergic cell activity but only at dosages over 50 times the antispasticity dose. Using extracellular single unit recording techniques, we have examined the effects of baclofen on the activity of rat nigral dopaminergic neurons and its interaction with haloperidol. Both acute and chronic haloperidol treatment significantly enhance the inhibitory effects of IV baclofen on these cells. Acute haloperidol pretreatment potentiates the inhibitory effects of single low doses of baclofen without significantly altering the dose response curve for baclofen, whereas chronic haloperidol treatment apparently potentiates both effects. Furthermore, low doses ofbaclofen reverse the depolarization inactivation of nigral DA cells caused by chronic haloperidol treatment. These results are discussed in relation to the action of baclofen on nigral inputs and its possible efficacy in the relief of some neuroleptic-induced side effects.
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