The actions of a range of excitatory amino acids at (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid-depolarizing receptors on neonatal rat motoneurones.

Depolarizations induced by a range of amino acids including some sulphur-containing excitatory transmitter candidates were evoked from motoneurones in the neonatal rat spinal cord under conditions that precluded activation of known ionotropic glutamate receptors. The responses could be partially and differentially depressed by continuous application of several metabotropic glutamate receptor (mGluR) antagonists or by receptor desensitization with the mGluR agonist, (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD]. In most cases [the exceptions being (1S,3R)-ACPD and to a lesser extent, quisqualate], the major component of these depolarizations was resistant to antagonism by phenylglycine-derived mGluR antagonists or desensitization of (1S,3R)-ACPD-sensitive receptors. Of the excitatory responses observed with the tested agonists, those evoked by L-glutamate itself were generally the least affected by blockade of known glutamate receptors.