Postnatal maturation of mossy fibre excitatory transmission in mouse CA3 pyramidal cells: a potential role for kainate receptors.

Cécile Marchal, Christophe Mulle
The Journal of Physiology. 2004-11-01; 561(1): 27-37
DOI: 10.1113/jphysiol.2004.069922

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1. J Physiol. 2004 Nov 15;561(Pt 1):27-37. Epub 2004 Sep 9.

Postnatal maturation of mossy fibre excitatory transmission in mouse CA3
pyramidal cells: a potential role for kainate receptors.

Marchal C(1), Mulle C.

Author information:
(1)Laboratoire Physiologie Cellulaire de la Synapse, CNRS UMR 5091, Institut
François Magendie, Université Bordeaux 2, 33077 Bordeaux Cedex, France.

Kainate receptors (KARs) are abundantly expressed in the central nervous system
at a period of intense synaptogenesis and might participate in the maturation of
neural networks. We have described the postnatal development of mossy fibre
excitatory synaptic transmission in CA3 pyramidal cells and we have explored the
potential role of KARs in synaptic maturation. In CA3 pyramidal cells, mossy
fibre stimulation evokes EPSCs as early as postnatal day 3 (P3). At this early
stage, mossy fibre (MF)-EPSCs are fully blocked by GYKI 53655, an AMPA receptor
(AMPAR) antagonist. A postsynaptic KAR component can only be detected from P6.
Thus, AMPAR-EPSCs precede KAR-EPSCs during postnatal maturation at this synapse.
All MF-EPSCs display a KAR component after P10. A key issue of the present work
is that between P6 and P9, the presence of a postsynaptic KAR component tightly
coincides with AMPAR-mediated EPSCs of large amplitude, and with the onset of low
frequency facilitation (from 0.1 Hz to 1 Hz), a presynaptic form of short-term
synaptic plasticity. In addition, mice lacking functional KARs throughout
postnatal development display MF-EPSCs of significantly smaller amplitude at
stages of maturation where synaptic KARs are normally present, due to both pre-
and postsynaptic impairment of synaptic transmission. These data suggest a role
for KARs in the maturation of mossy fibre synapses.

DOI: 10.1113/jphysiol.2004.069922
PMCID: PMC1665334
PMID: 15358807 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus