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Presynaptic plasticity at two giant auditory synapses in normal and deaf mice
Author(s) -
Oleskevich S.,
Youssoufian M.,
Walmsley B.
Publication year - 2004
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.2004.066662
Subject(s) - neuroscience , synapse , synaptic augmentation , synaptic plasticity , neurotransmission , neural facilitation , excitatory postsynaptic potential , excitatory synapse , synaptic scaling , calyx , biology , synaptic vesicle , metaplasticity , inhibitory postsynaptic potential , anatomy , vesicle , receptor , biochemistry , genetics , membrane
Large calyceal synapses are often regarded as simple relay points, built for high‐fidelity and high‐frequency synaptic transmission and a minimal requirement for synaptic plasticity, but this view is oversimplified. Calyceal synapses can exhibit surprising activity‐dependent developmental plasticity. Here we compare basal synaptic transmission and activity‐dependent plasticity at two stereotypical calyceal synapses in the auditory pathway, the endbulb and the calyx of Held. Basal synaptic transmission was more powerful at the calyx than the endbulb synapse: the amplitude of evoked AMPA receptor‐mediated excitatory postsynaptic currents (eEPSCs) was significantly greater at the calyx, as were the release probability, and the number of release sites. The quantal amplitude was smaller at the calyx, consistent with the smaller amplitude of spontaneous miniature EPSCs at this synapse. High‐frequency trains of stimuli revealed that the calyx had a larger readily releasable pool of vesicles (RRP), less tetanic depression and less asynchronous transmitter release. Activity‐dependent synaptic plasticity was assessed in congenitally deaf mutant mice ( dn/dn ). Previously we showed that a lack of synaptic activity in deaf mice increases synaptic strength at the endbulb of Held via presynaptic mechanisms. In contrast, we have now found that deafness does not affect synaptic transmission at the calyx synapse, as eEPSC and mEPSC amplitude, release probability, number of release sites, size of RRP, tetanic depression and asynchronous release were unchanged compared to normal mice. Synaptic transmission at the calyx synapse is more powerful and has less capacity for developmental plasticity compared to the endbulb synapse.