Physiological and Pharmacological Characteristics of uisqualic Acid-Induced K⁺-Current Response in the Ganglion Cells of Aplysia

Abstract

The extracellular application of either quisqualic acid (QA) or Phe-Met-Arg-Phe-NH₂ (FMRFamide) induces an outward current in identified neurons of Aplysia ganglion under voltage clamp. The time course of the QA-induced response is significantly slower than that induced by FMRFamide. The reversal potential for both responses was −92 mV and was shifted 17 mV in a positive direction for a twofold increase in the extracellular K⁺ concentration. The QA-induced response was markedly depressed in the presence of Ba²⁺, a blocker of inward rectifier K⁺-channel, whereas TEA, a Ca²⁺-activated K⁺-channel (BK_Ca) blocker, or 4-AP, a transient K⁺ (A)-channel blocker, had no effect on the response. The QA-induced K⁺-current was significantly suppressed by CNQX and GYKI52466, antagonists of non-NMDA receptors. However, the application of either kainate or AMPA, agonists for non-NMDA receptors, produced no type of response in the same neurons. The QA-induced K⁺-current response was not depressed at all by an intracellular injection of either guanosine 5′-O-(2-thiodiphosphate) (GDP-βS) or guanosine 5′-O-(3-thiotriphosphate) (GTP-γS), but the FMRFamide-induced response was markedly blocked by both GDP-βS and GTP-γS in the same cell. Furthermore, the QA- and FMRFamide-induced K⁺-current responses were both decreased markedly when the temperature was lowered to 15°C, from 23°C. These results suggested that the QA-induced K⁺-current response is produced by an activation of a novel type of QA-receptor and that this response is not produced by an activation of the G protein.