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Developmental Decrease in Synaptic Facilitation at the Mouse Hippocampal Mossy Fibre Synapse
Author(s) -
MoriKawakami Fumiko,
Kobayashi Katsunori,
Takahashi Tomoyuki
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.045948
Subject(s) - facilitation , neural facilitation , neuroscience , cnqx , synapse , neurotransmission , dnqx , glutamate receptor , chemistry , hippocampal formation , biophysics , biology , excitatory postsynaptic potential , inhibitory postsynaptic potential , ampa receptor , receptor , biochemistry
Transmission at the hippocampal mossy fibre (MF)‐CA3 pyramidal cell synapse is characterized by prominent activity‐dependent facilitation, which is thought to provide a wide dynamic range in hippocampal informational flow. At this synapse in mice the magnitude of paired‐pulse facilitation and frequency‐dependent facilitation markedly decreased with postnatal development from 3 weeks (3W) to 9 weeks (9W). Throughout this period the mean amplitude and variance of unitary EPSCs stayed constant. By altering extracellular Ca 2+ /Mg 2+ concentrations the paired‐pulse ratio could be changed to a similar extent as observed during development. However, this was accompanied by an over 30‐fold change in EPSC amplitude, suggesting that the developmental change in facilitation ratio cannot simply be explained by a change in release probability. With paired‐pulse stimulation the Ca 2+ transients at MF terminals, monitored using mag‐fura‐5, showed a small facilitation, but its magnitude remained similar between 3W and 9W mice. Pharmacological tests using CNQX, adenosine, LY341495, H‐7 or KN‐62 suggested that neither presynaptic receptors (kainate, adenosine and metabotropic glutamate) nor protein kinases are responsible for the developmental change in facilitation. Nevertheless, loading the membrane‐permeable form of BAPTA attenuated the paired‐pulse facilitation in 3W mice to a much greater extent than in 9W mice, resulting in a marked reduction in age difference. These results suggest that the developmental decrease in the MF synaptic facilitation arises from a change associated with residual Ca 2+ , a decrease in residual Ca 2+ itself or a change in Ca 2+ ‐binding sites involved in the facilitation. A developmental decline in facilitation ratio reduces the dynamic range of MF transmission, possibly contributing to the stabilization of hippocampal circuitry.