Current-clamp experiments on an identified neurone have demonstrated the presence of L-glutamate receptors in the insect central nervous system. The cell body of the fast coxal depressor motor neurone (Df) in the metathoracic ganglion of the cockroach Periplaneta americana exhibits a hyperpolarizing response to L-glutamate, accompanied by an increase in membrane conductance. The response is dependent on both intracellular and extracellular chloride concentration, but is not affected by changes in potassium concentration. The hyperpolarization reverses at −82mV (the equilibrium potential for chloride), is mimicked by the action of L-aspartate, blocked by the antagonists picrotoxin and γ-D-glutamylglycine (γ-DGG) at high concentrations (1.0×10−4mol l−1), and is enhanced by L-amino phosphonobutyrate (L-APB). The response is insensitive to glutamate diethyl ester (GDEE), cis-2,3-piperazine dicarboxylic acid (cis-2,3- PDA) and D-amino phosphonobutyrate (D-APB). The 1-glutamate-activated increase in chloride conductance does not cross-desensitize with the γ-aminobutyric acid (GAB A) response on the same cell. It is less sensitive than the GAB Aresponse to block by picrotoxin. In addition, γ-DGG specifically blocks the L-glutamate receptor.
A depolarizing response is elicited by kainate and quisqualate; it is associated with an increase in conductance, and exhibits a much slower time course than the response to 1-glutamate, indicating a different underlying mechanism. L-Cysteate produces a small depolarizing response of similar time course to that produced by 1-glutamate. L-Homocysteate and N-methyl-D-aspartate (NMDA) are ineffective on the cell body membrane when applied at concentrations up to 1.0×10−3mol l−1. This first detailed description of the properties of L-glutamate receptors on an identified insect neurone reveals that they are not readily accommodated in the existing classification of receptor subtypes, based on vertebrate pharmacology.
