Abstract
The latency of the tail-flick, following intrathecal infusion of the dopamine (DA) agonist, R-apomorphine was measured in rats with intact spinal cord or with spinal cord lesions. Apomorphine failed to influence the tail-flick response in intact rats, whereas it elevated the latency of the tail-flick in rats with either total spinal cord transection, or bilateral lesions of the dorsolateral funiculi (DLF), but not in rats with lesions in either the dorsal columns or the medioventral parts of the lateral funiculi. The findings suggest that pathways in the dorsolateral funiculi modulate DA-mediated sensory processes and possible mechanisms are discussed.
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