title: Physiological and pharmacological characteristics of quisqualic 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 Ba(2+), a blocker of inward rectifier K(+)-channel, whereas TEA, a Ca(2+)-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-betaS) or guanosine 5'-O-(3-thiotriphosphate) (GTP-gammaS), but the FMRFamide-induced response was markedly blocked by both GDP-betaS and GTP-gammaS in the same cell. Furthermore, the QA- and FMRFamide-induced K(+)-current responses were both decreased markedly when the temperature was lowered to 15 degrees C, from 23 degrees 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.
authors.affiliation: Department of Physiology and Advanced Medical Science Research Center, School of Medicine, Iwate Medical University, Morioka, 020-8505, Japan. skimura@iwate-med.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Kimura
authors.forename: S
authors.initials: S
authors.lastname: Kawasaki
authors.forename: K
authors.initials: K
authors.lastname: Takashima
authors.forename: K
authors.initials: K
authors.lastname: Sasaki
mesh_terms: D000200:Action Potentials; D000818:Animals; D001048:Aplysia / Q000502:physiology*; D004594:Electrophysiology; D019835:FMRFamide / Q000494:pharmacology; D019204:GTP-Binding Proteins / Q000096:biosynthesis / Q000494:pharmacology; D005724:Ganglia / Q000502:physiology; D007700:Kinetics; D015221:Potassium Channels / Q000502:physiology*; D016318:Quisqualic Acid / Q000494:pharmacology*; D017470:Receptors, Glutamate / Q000502:physiology; D013696:Temperature
chemical_list: D015221:Potassium Channels; D017470:Receptors, Glutamate; D019835:FMRFamide; D016318:Quisqualic Acid; D019204:GTP-Binding Proteins