Effect of methamphetamine on rat spinal cord. Dopamine receptor-mediated depression of monosynaptic reflex.
The experiments were performed on spinal rats transected at Cl. Intravenous administration of methamphetamine-HCl (MA-HCl, 2 mg/kg) and apomorphine-HCl (5 mg/kg) reduced the amplitude of the monosynaptic reflex (MSR), while the polysynaptic reflex was increased by methamphetamine. Depression of the monosynaptic reflex by both drugs was antagonized by haloperidol, but not by phentolamine. Depression of the monosynaptic reflex by methamphetamine was not antagonized by pretreatment with reserpine; however, the result was explained by the assumption that methamphetamine releases newly-synthesized dopamine or that methamphetamine may act directly on dopamine receptors. Depression of the monosynaptic reflex induced by methamphetamine was independent of peripheral changes in blood pressure. Oxygen tension in the spinal cord was slightly reduced by methamphetamine in rats treated with phentolamine and a change of pO2 in the spinal cord was ruled out as a possible mechanism of action. These results suggest that dopaminergic neurons in the spinal cord of the rat depress the transmission of monosynaptic spinal reflexes.
D000818:Animals; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008694:Methamphetamine / Q000494:pharmacology*; D010100:Oxygen / Q000032:analysis; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000502:physiology*; D012023:Reflex, Monosynaptic / Q000187:drug effects*; D013116:Spinal Cord / Q000187:drug effects* / Q000502:physiology
D011954:Receptors, Dopamine; D008694:Methamphetamine; D010100:Oxygen