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Nankai M, Fage D, Carter C: Striatal NMDA receptor subtypes: the pharmacology of N-methyl-D-aspartate-evoked dopamine, gamma-aminobutyric acid, acetylcholine and spermidine release. Eur J Pharmacol. 1995 Nov 3;286(1):61-70.
We have examined the inhibitory potencies of MK 801, memantine, dextromethorphan, Mg2+ and of strychnine-insensitive glycine site antagonists on the N-methyl-D-aspartate (NMDA)-evoked (300 microM) release of [14C] acetylcholine and [3H] spermidine or [14C] gamma-aminobutyric acid [14C] GABA and [3H] dopamine from rat striatal slices. MK 801, dextromethorphan and all glycine antagonists examined (7-chlorokynurenate, L-689,560 ((+/-)-trans-2-carboxy-5,7-dichlorotetrahydroquinoline-4-phenylure a), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 6,7-dichloroquinoxaline-2,3-dione (DNQX), and (+)-HA966 ((3-amino-1-hydroxypyrrolidin-2-one) more potently inhibited NMDA-evoked dopamine and GABA release than acetylcholine and spermidine release by a factor of 3-21. MgCl2, which does not inhibit NMDA-evoked spermidine release, and memantine which only weakly antagonised NMDA-evoked spermidine release, inhibited NMDA-evoked dopamine, acetylcholine and GABA release with similar potencies. No pharmacological differences were observed between NMDA-evoked dopamine and GABA release. These findings extend those suggesting that NMDA-evoked acetylcholine and spermidine release are mediated by different NMDA receptor subtypes in the striatum and suggest a third native subtype with a distinct pharmacology that regulates striatal dopamine and GABA release. |
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