Increased excitability of spinal pain reflexes and altered frequency-dependent modulation in the dopamine D3-receptor knockout mouse

► Dopamine D3 receptor dysfunction increases pain reflexes in vivo and reduces their FM modulation in the spinal cord in vitro. ► D1 and D2 receptor agonists and the Ca2+-channel ligand, pregabalin, can restore the FM modulation. ► Our data suggest a role for the D3 receptor in the modulation of pain-associated spinal cord pathways. ► The D3 receptor knockout mouse may serve as a new model for the study of increased nociception.