The glutamate-induced chloride current in Aplysia neurones lacks pharmacological properties seen for excitatory responses to glutamate.

The pharmacological properties of the L-glutamate (Glu)-induced chloride current (ICl) in enzymatically isolated Aplysia neurones were examined using the 'concentration clamp' technique. The Glu-ICl did not cross-desensitize with the ICl evoked by gamma-aminobutyric acid or acetylcholine. Quisqualate, kainate (one out of eight) and N-methyl-D-aspartate (one out of nine) induced a small, non-desensitizing ICl in Glu-responding neurones. The quisqualate- and kainate-ICl did not cross-desensitize with the Glu-ICl. L-Aspartate did not induce a ICl in 11 neurones tested, which showed a Glu-ICl. Glutamate diethyl ester, Joro Spider toxin and ketamine did not suppress the Glu-ICl. Concanavalin A had no effect on the time course of desensitization. These results suggest that the Glu receptor-Cl channel complex in Aplysia neurones has pharmacological properties which differ from those of the excitatory Glu receptor-channel complexes in the crustacean muscle fibres and in the central neurones of vertebrates.