Afferent facilitation induced by iontophoretic application of acidic amino acids in the ampullary electroreceptors of Plotosus.
In an attempt to identify the afferent transmitter in acousticolateralis receptors, effects of some acidic amino acids were examined in ampullary electroreceptors of the marine catfish Plotosus anguillaris, which have only afferent innervation. The ampulla (sensory epithelium) was first hyperpolarized in situ to suppress receptor-cell activity and release of transmitter, and hence resting afferent discharges completely. In the absence of transmitter, amino acids were applied to the ampulla by iontophoresis through three-barreled electrodes. Afferent impulses were recorded from the nerve trunk by a suction electrode, and single-unit responses were analyzed by their instantaneous frequency (F) records. L-Glutamate (Glu) induces single-unit responses postsynaptically at discrete spots over the ampulla. The F records showed graded and slow time courses, and F peaks increased sigmoidally against Glu doses with Hill coefficients of 2-3. Response maxima reached 120-210 Hz in doses of one log unit over the threshold. Glu response showed little desensitization. At the Glu-sensitive spots, kainate (KA) and quisqualate (QA) induced more persistent excitation and L-homocysteate (HCA) weaker excitation than did Glu, with similar latency. L-Aspartate (Asp) induced small slow responses with long latency in only one third of the tested Glu spots. D-Glutamate (D-Glu), D-aspartate (D-Asp), L-cysteate (CA), L-cysteine sulfinate (CSA), and N-methyl-DL-aspartate generally induced no response. Some aspartate analogues, L- and D-Asp, CA, and CSA induced persistent potentiation of Glu responses. Apparent affinity increase and change in response shape during potentiation indicated suppression of Glu uptake. However, apparent slope change in the log dose-response curves suggested that additional mechanisms were involved. In contrast, QA, KA, Glu, and HCA induced the excitation only. Comparable topical application of the transmitter was simulated by stimulating a few receptor cells at Glu spots to induce focal responses. Some aspects of the focal and Glu responses were compared. Pharmacological and neurochemical evidence so far available on this material is discussed with respect to the Glu hypothesis. Glu, even though a potent agonist in terms of afferent excitation, seems to act on extrasynaptic receptor sites in the nonmyelinated nerve terminals.
Nagai
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Obara
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D000344:Afferent Pathways / Q000187:drug effects*; D000596:Amino Acids / Q000494:pharmacology*; D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D005071:Evoked Potentials / Q000187:drug effects; D005399:Fishes; D005971:Glutamates / Q000494:pharmacology; D007478:Iontophoresis; D018377:Neurotransmitter Agents / Q000502:physiology; D011930:Reaction Time; D011984:Sensory Receptor Cells / Q000187:drug effects*; D013569:Synapses / Q000187:drug effects
D000596:Amino Acids; D005971:Glutamates; D018377:Neurotransmitter Agents; D001224:Aspartic Acid