Aims: Stimulation of primary motor cortex (M1) produces antinociception in both rats and humans. We studied in rats with experimental neuropathy whether stimulation of M1 decreases nociceptive responses of spinal dorsal horn neurons and whether striatal or spinal dopamine D₂ receptors play a significant role in relaying the descending antinociceptive effect. Methods: Single unit recordings of wide- dynamic range (WDR) and nociceptive-specific (NS) neurons in the spinal dorsal horn were performed under pentobarbital anesthesia 2-3 weeks following spinal nerve ligation. Neurons were classified as WDR neurons, giving a response to innocuous brush and noxious heat, or NS neurons, giving a response only to noxious heat. Responses of WDR and NS neurons were determined with and without concomitant electric stimulation of M1. A role of striatal and spinal dopamine D₂ receptors in the antinociceptive effect was assessed by administering 1 g of raclopride, a selective dopamine D₂ receptor antagonist into the striatum or the spinal cord. Results: In the saline control condition, M1 stimulation decreased heat-evoked responses of WDR and NS neurons. Blocking of striatal or spinal dopamine D₂ receptors by raclopride attenuated the M1 stimulation-induced inhibition of heat-evoked responses of spinal WDR neurons. In contrast, the inhibitory effect of M1 stimulation on heat-evoked responses of spinal NS neurons was enhanced by blocking striatal dopamine D₂ receptors. Following blocking of spinal dopamine D₂ receptors, the M1 stimulation- induced inhibition in spinal NS neurons was reversed to facilitation. Conclusions: Electric stimulation of M1 suppresses noxious heat-evoked responses of spinal dorsal horn WDR and NS neurons in neuropathic animals. Both striatal and spinal dopamine D₂ receptors are involved in mediating the descending antinociceptive effect from M1 to the spinal dorsal horn, although their role partly varies with the subtype of the spinal nociceptive neuron.