On the possible role of excitatory amino acids in the striatum in mediating morphine-induced muscular rigidity.

The possible role of excitatory amino acids in the striatum in mediating tonic activity in the electromyogram (EMG) was studied. Glutamate diethylester (GDEE) (100-400 nmoles) induced a tonic activity in the EMG in a dose-dependent way when injected into the striatum. This effect was well antagonized by intrastriatal injection of quisqualic acid (5 and 25 nmoles), less by kainic acid (5 nmoles) and not significantly by N-methyl-D-aspartate (NMDA) (30 nmoles). Systemic administration of naloxone (2 mg/kg IP) did not inhibit the GDEE-induced activity in the EMG. The tonic activity in the EMG, induced by systemic administration of morphine (15 mg/kg IP) was not significantly influenced by injection of GDEE (200 nmoles) into the striatum, but was first decreased and then slightly enhanced by intrastriatal injection of quisqualic acid (25 and 50 nmoles), not affected by kainic acid (5 nmoles) and first slightly decreased and then strongly enhanced by NMDA (15 and 30 nmoles). Injection of kainic acid (5 nmoles), quisqualic acid (5 or 25 nmoles) or NMDA (30 nmoles) alone into the striatum did not produce any tonic activity in the EMG. Our results support the assumption that quisqualic acid, kainic acid and NMDA react with different types of receptors for excitatory amino acids in the striatum. Both quisqualicacid and NMDA showed a biphasic action, whereas kainic acid was ineffective. Furthermore, the activity in the EMG induced by morphine might be at least partly due to a functional antagonism of morphine against glutamate in striatal neurons.