1 Neuropharmacological actions of all possible‐state isomers of α‐(carboxycyclopropyl)glycine (CCG), conformationally restricted analogues of glutamate, were examined for electrophysiological effects in the isolated spinal cord of the newborn rat. 2 Eight CCG stereoisomers demonstrated a large variety of depolarizing activities. Among them, the (2R, 3S, 4S) isomers of CCG (D‐CCG‐II) showed the most potent depolarizing activity, followed by the (2S, 3R, 4S) isomer (L‐CCG‐IV). 3 The depolarization evoked by L‐CCG‐IV, D‐CCG‐II and other D‐CCG isomers was effectively depressed by N‐methyl‐D‐aspartate (NMDA) antagonists. D‐CCG‐II was about 5 times more potent than NMDA in causing a depolarization. 4 The (2S, 3S, 4S) isomer of CCG (L‐CCG‐I) was more potent than L‐glutamate in causing a depolarization of spinal motoneurones. The depolarization was slightly depressed by NMDA antagonists, but residual amplitudes of responses to L‐CCG‐I in the presence of NMDA antagonists were almost insensitive to 6,7‐dinitro‐quinoxaline‐2,3‐dione (DNQX) or 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX), suggesting that L‐CCG‐I might be a novel potent agonist. 5 After application of the (2S, 3S, 4R) isomer of CCG (L‐CCG‐III), responses to L‐glutamate, D‐and L‐aspartate were markedly enhanced. The enhancement lasted for a period of several hours without a further application of L‐CCG‐III. 6 L‐CCG‐III also caused a depolarization, but it seemed unlikely that the potentiation of the glutamate response was directly related to the depolarization evoked by L‐CCG‐III. 7 The potentiation might be due to inhibition of uptake processes, but L‐CCG‐III was superior to L‐(−)‐threo‐3‐hydroxyaspartate, a potent uptake inhibitor of L‐glutamate and L‐aspartate, in enhancing the response to L‐glutamate in terms of amplitude and duration of responses. 8 CCG isomers should provide useful pharmacological tools for analysis of glutamate neurotransmitter systems.
British Journal of Pharmacology – Wiley
Published: Dec 1, 1989
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