Glutamate is the Transmitter for N2v Retraction Phase Interneurons of the Lymnaea Feeding System

M. J. Brierley , M. S. Yeoman , and P. R. Benjamin Sussex Centre for Neuroscience, School of Biological Sciences, University of Sussex, Brighton, East Sussex BN1 9QG, United Kingdom Brierley, Matthew J., Mark S. Yeoman, and Paul R. Benjamin. Glutamate is the transmitter for the N2v retraction phase...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of neurophysiology 1997-12, Vol.78 (6), p.3408-3414
Hauptverfasser: Brierley, M. J, Yeoman, M. S, Benjamin, P. R
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:M. J. Brierley , M. S. Yeoman , and P. R. Benjamin Sussex Centre for Neuroscience, School of Biological Sciences, University of Sussex, Brighton, East Sussex BN1 9QG, United Kingdom Brierley, Matthew J., Mark S. Yeoman, and Paul R. Benjamin. Glutamate is the transmitter for the N2v retraction phase interneurons of the Lymnaea feeding system. J. Neurophysiol. 78: 3408-3414, 1997. Electrophysiological and pharmacological methods were used to examine the role of glutamate in mediating the excitatory and inhibitory responses produced by the N2v rasp phase neurons on postsynaptic cells of the Lymnaea feeding network. The N2v  B3 motor neuron excitatory synaptic response could be mimicked by focal or bath application of L -glutamate at concentrations of 10 3 M. Quisqualate and -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) were potent agonists for the B3 excitatory glutamate receptor (10 3 M), whereas kainate only produced very weak responses at the same concentration. This suggested that non- N -methyl- D -aspartate (NMDA), AMPA/quisqualate receptors were present on the B3 cell. The specific non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 5 M) blocked 85% of the excitatory effects on the B3 cell produced by focal application of glutamate (10 3 M), confirming the presence of non-NMDA receptors. CNQX also blocked the major part of the excitatory postsynaptic potentials on the B3 cell produced by spontaneous or current-evoked bursts of spikes in the N2v cell. As with focal application of glutamate, a small delayed component remained that was CNQX insensitive. This provided direct evidence that glutamate acting via receptors of the non-NMDA, AMPA/quisqualate type were responsible for mediating the main N2v  B3 cell excitatory response. NMDA at 10 2 M also excited the B3 cell, but the effects were much more variable in size and absent in one-third of the 25 B3 cells tested. NMDA effects on B3 cells were not enhanced by bath application of glycine at 10 4 M or reduction of Mg 2+ concentration in the saline to zero, suggesting the absence of typical NMDA receptors. The variability of the B3 cell responses to NMDA suggested these receptors were unlikely to be the main receptor type involved with N2v  B3 excitation. Quisqualate and AMPA at 10 3 M also mimicked N2v inhibitory effects on the B7 and B8 feeding motor neurons and the modulatory slow oscillator (SO) interneuron, providing further evidence for the role of AMPA/quisqualat
ISSN:0022-3077
1522-1598
DOI:10.1152/jn.1997.78.6.3408