Key result
Intracerebroventricular injection of kainic acid and quisqualic acid induced spike discharges and increased monoamine metabolite levels, effects which were modulated by the non-NMDA antagonist pCB-PzDA.
The non-NMDA antagonist pCB-PzDA not only antagonizes excitatory amino acids but also directly activates dopaminergic neurons in the rat striatum.
pCB-PzDA modulates excitatory amino acid effects in rats; leaves open whether non-NMDA antagonism activates striatal dopamine in humans.
The CNS action of kainic acid (KA), quisqualic acid (QA) and 1-(4-chlorobenzoyl)-piperazine-2, 3-dicarboxylic acid (pCB-PzDA) was investigated in male Sprague Dawley rats, and their effects on monoamine metabolite levels in rat striatum were studied using brain dialysis.Intracerebroventricularly injected KA and QA (100nmol) induced spike discharges, and pCB-PzDA (100nmol) suppressed electrocorticograms (ECoG) for 1 hour. pCB-PzDA aggravated KA induced spike discharges and inhibited QA-induced spike discharges.Dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels increased transitorily by injection of 10nmol and continuously by injection of 100nmol of KA. KA increased the 5-hydroxyindoleachtic acid (5-HIAA) level 2 hours after the administration dosedependently. Though 10nmol of QA increased the HVA level slightly, 100nmol of QA increased the DOPAC, HVA and 5-HIAA levels. Though 100nmol of pCB-PzDA increased the DOPAC and HVA levels, it inhibited the increases in DOPAC, HVA and 5-HIAA levels induced by KA. On the other hand, pCB-PzDA inhibited the increases in DOPAC, HVA and 5-HIAA levels induced by QA for 1 hour, after which the DOPAC and HVA levels increased additively.These findings suggest that pCB-PzDA acts not only as a non-NMDA antagonist but also on dopaminergic neurons directly.
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Masatsune YAMAMOTO (1992) studied this question. Kainic acid, quisqualic acid, and pCB-PzDA vs. Control (vehicle) was evaluated on Electrocorticogram spike discharges and monoamine metabolite levels (DOPAC, HVA, 5-HIAA). Intracerebroventricular injection of kainic acid and quisqualic acid induced spike discharges and increased monoamine metabolite levels, effects which were modulated by the non-NMDA antagonist pCB-PzDA.
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