NDLI: Activity-dependent changes in temporal components of neurotransmission at the juvenile mouse calyx of Held synapse

Content Provider	PubMed Central
Author	Fedchyshyn, Michael J. Wang, Lu-yang
Copyright Year	2007
Abstract	The temporal fidelity of synaptic transmission is constrained by the reproducibility of time delays such as axonal conduction delay and synaptic delay, but very little is known about the modulation of these distinct components. In particular, synaptic delay is not generally considered to be modifiable under physiological conditions. Using simultaneous paired patch-clamp recordings from pre- and postsynaptic elements of the calyx of Held synapse, in juvenile mouse auditory brainstem slices, we show here that synaptic activity (20–200 Hz) leads to activity-dependent increases in synaptic delay and its variance as well as desynchronization of evoked responses. Such changes were most robust at 200 Hz in 2 mm extracellular Ca2+ ([Ca2+]o), and could be attenuated by lowering [Ca2+]o to 1 mm, increasing temperature to 35°C, or application of the GABABR agonist baclofen, which inhibits presynaptic Ca2+ currents (I Ca). Conduction delay also exhibited slight activity-dependent prolongation, but this prolongation was only sensitive to temperature, and not to [Ca2+]o or baclofen. Direct voltage-clamp recordings of I Ca evoked by repeated action potential train template (200 Hz) revealed little jitter in the timing and kinetics of I Ca under various conditions, suggesting that increases in synaptic delay and its variance occur downstream of Ca2+ entry. Loading the Ca2+ chelator EGTA-AM into terminals reduced the progression rate, the extent of activity-dependent increases in various delay components, and their variance, implying that residual Ca2+ accumulation in the presynaptic nerve terminal induces these changes. Finally, by applying a test pulse at different intervals following a 200 Hz train (150 ms), we demonstrated that prolongation in the various delay components reverses in parallel with recovery in synaptic strength. These observations suggest that a depletion of the readily releasable pool of SVs during high-frequency activity may downregulate not only synaptic strength but also decrease the temporal fidelity of neurotransmission at this and other central synapses.
Related Links	http://dx.doi.org/10.1113/jphysiol.2007.129833
Ending Page	602
Page Count	22
Starting Page	581
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 2
Volume Number	581
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2007-06-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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