Monoaminergic mechanism of electroacupuncture analgesia.

We studied the effects of systemic injections of monoamine depletors, enhancers or receptor blockers on electroacupuncture analgesia (EAA) in mice. The following results emerged. (i) EAA is reduced by depletors of monoamines (tetrabenazine, TBZ depletes all monoamines; para-chlorophenylalanine, PCPA depletes serotonin; alpha-methyl-para-tyrosine, AMPT depletes catecholamines). However, depletion of noradrenaline and increase of serotonin by disulfiram enhances EAA. (ii) Replacement of depleted monoamines after TBZ treatment by their precursors (5-HTP or L-DOPA) restores EAA. (iii) EAA is enhanced by potentiating serotonin and dopamine by probenecid. EAA is also enhanced by the administration of monoamine precursors (L-DOPA for dopamine, 5-HTP for serotonin). The dopamine receptor stimulator, apomorphine, reduces EAA. (iv) EAA is also reduced by receptor blockade of catecholamines (by haloperidol), or blockade of noradrenaline (by yohimbine) or serotonin (by cinanserin). However, blockade of dopamine by pimozide has no significant effect on EAA. There are two main conclusions: (i) EAA results are similar to those previously reported for SPA for all drugs except apomorphine and pimozide; and (ii) EAA shows consistent results only with manipulations of serotonin: the data indicating that EAA (at 200 Hz) is mediated by serotonin. Since previous studies show that raphe or DLF (dorsolateral fasciculus) lesions abolish EAA, we postulate that descending axons from raphe release serotonin to inhibit trigeminal or spinal cord nociception during EAA.