PMID- 2860212
OWN - NLM
STAT- MEDLINE
DCOM- 19850725
LR  - 20171213
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 53
IP  - 4
DP  - 1985 Apr
TI  - Afferent facilitation induced by iontophoretic application of acidic amino acids 
      in the ampullary electroreceptors of Plotosus.
PG  - 853-67
AB  - 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.
FAU - Nagai, T
AU  - Nagai T
FAU - Obara, S
AU  - Obara S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Amino Acids)
RN  - 0 (Glutamates)
RN  - 0 (Neurotransmitter Agents)
RN  - 30KYC7MIAI (Aspartic Acid)
SB  - IM
MH  - Afferent Pathways/*drug effects
MH  - Amino Acids/*pharmacology
MH  - Animals
MH  - Aspartic Acid/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Drug Synergism
MH  - Evoked Potentials/drug effects
MH  - Fishes
MH  - Glutamates/pharmacology
MH  - Iontophoresis
MH  - Neurotransmitter Agents/physiology
MH  - Reaction Time
MH  - Sensory Receptor Cells/*drug effects
MH  - Synapses/drug effects
EDAT- 1985/04/01 00:00
MHDA- 1985/04/01 00:01
CRDT- 1985/04/01 00:00
PHST- 1985/04/01 00:00 [pubmed]
PHST- 1985/04/01 00:01 [medline]
PHST- 1985/04/01 00:00 [entrez]
AID - 10.1152/jn.1985.53.4.853 [doi]
PST - ppublish
SO  - J Neurophysiol. 1985 Apr;53(4):853-67. doi: 10.1152/jn.1985.53.4.853.