The mechanism of L-DOPA for antinociception was investigated. Nociceptive 
behaviors in mice after an intrathecal (i.t.) administration of substance P were 
evaluated. L-DOPA (i.t.) dose-dependently attenuated the substance P-induced 
nociceptive behaviors. Co-administration of benserazide (i.t.), a DOPA 
decarboxylase inhibitor, abolished the antinociceptive effect of L-DOPA. The 
L-DOPA-induced antinociception was antagonized by sulpiride, a D2 blocker, but 
not by SCH 23390, a D1 blocker. These results suggest that L-DOPA relieves pain 
after conversion to dopamine, with the dopamine sedating pain transmission by 
way of the dopamine D2 receptor.