FAST SYNAPTIC POTENTIAL MEDIATED BY NMDA AND NON-NMDA RECEPTORS

Citation
Lr. Wolszon et al., FAST SYNAPTIC POTENTIAL MEDIATED BY NMDA AND NON-NMDA RECEPTORS, Journal of neurophysiology, 78(5), 1997, pp. 2693-2706
Citations number
62
Categorie Soggetti
Neurosciences,Physiology
Journal title
ISSN journal
00223077
Volume
78
Issue
5
Year of publication
1997
Pages
2693 - 2706
Database
ISI
SICI code
0022-3077(1997)78:5<2693:FSPMBN>2.0.ZU;2-R
Abstract
Excitatory synaptic transmission in the CNS often is mediated by two k inetically distinct glutamate receptor subtypes that frequently are co localized, the N-methyl-D-aspartate (MMDA) and non-NMDA receptors. The ir synaptic currents are typically very slow and very fast, respective ly. We examined the pharmacological and physiological properties of ch emical excitatory transmission at the mixed electrical and chemical sy napses between auditory afferents and the goldfish Mauthner cell, in v ivo. Previous physiological data have suggested the involvement of glu tamate receptors in this fast excitatory postsynaptic potential (EPSP) , the chemical component of which decays with a time constant of <2 ms . We demonstrate here that the pharmacological and voltage-dependent c haracteristics of the synaptic currents are consistent with glutamater gic transmission and that both NMDA and non-NMDA receptors are involve d. The two components surprisingly exhibit quite similar kinetics even at resting potential, with the NIL?DA response being only slightly sl ower. Due to its fast kinetics and characteristic voltage dependence, NMDA receptor-mediated transmission at these first-order synapses cont ributes significantly to paired pulse and frequency-dependent facilita tion of successive fast EPSPs during high-frequency repetitive firing, a presynaptic impulse pattern that induces activity-dependent homosyn aptic changes in both electrical and chemical transmission. Thus NMDA receptor kinetics in this intact preparation are suited to its functio nal requirements, namely speed of information transmission and the abi lity to trigger changes in synaptic efficacy.