Kainate receptors depress excitatory synaptic transmission at CA3 -> CA1 synapses in the hippocampus via a direct presynaptic action

Citation
M. Frerking et al., Kainate receptors depress excitatory synaptic transmission at CA3 -> CA1 synapses in the hippocampus via a direct presynaptic action, J NEUROSC, 21(9), 2001, pp. 2958-2966
Citations number
25
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE
ISSN journal
0270-6474 → ACNP
Volume
21
Issue
9
Year of publication
2001
Pages
2958 - 2966
Database
ISI
SICI code
0270-6474(20010501)21:9<2958:KRDEST>2.0.ZU;2-J
Abstract
Kainate receptor activation depresses synaptic release of neurotransmitter at a number of synapses in the CNS. The mechanism underlying this depressio n is controversial, and both ionotropic and metabotropic mechanisms have be en suggested. We report here that the AMPA/kainate receptor agonists domoat e (DA) and kainate (KA) cause a presynaptic depression of glutamatergic tra nsmission at CA3-->CA1 synapses in the hippocampus, which is not blocked by the AMPA receptor antagonist GYKI 53655 but is blocked by the AMPA/KA rece ptor antagonist CNQX. Neither a blockade of interneuronal discharge nor ant agonists of several neuromodulators affect the depression, suggesting that it is not the result of indirect excitation and subsequent release of a neu romodulator. Presynaptic depolarization, achieved via increasing extracellu lar K+, caused a depression of the presynaptic fiber volley and an increase in the frequency of miniature EPSCs. Neither effect was observed with DA, suggesting that DA does not depress transmission via a presynaptic depolari zation. However, the effects of DA were abolished by the G-protein inhibito rs N-ethylmaleimide and pertussis toxin. These results suggest that KA rece ptor activation depresses synaptic transmission at this synapse via a direc t, presynaptic, metabotropic action.