| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Biological Sciences, University at Buffalo, State University of New York, Buffalo, New York
Submitted 27 November 2007; accepted in final form 20 March 2008
Several mechanisms can underlie short-term synaptic depression, including vesicle depletion, receptor desensitization, and changes in presynaptic release probability. To determine which mechanisms affect depression under physiological conditions, we studied the synapse formed by auditory nerve fibers onto bushy cells in the anteroventral cochlear nucleus (the "endbulb of Held") using voltage-clamp recordings of brain slices from P15–P21 mice near physiological temperatures. Depression of both 
-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) excitatory postsynaptic currents (EPSCs) showed two phases of recovery. The fast component of depression for the AMPA EPSC was eliminated by cyclothiazide and aniracetam, suggesting it results from desensitization. The fast component of depression for the NMDA EPSC was reduced by the low-affinity antagonist L-AP5, suggesting it results from saturation. The remaining depression in AMPA and NMDA components is identical and therefore presynaptic in origin. It is likely to result from presynaptic vesicle depletion. Recovery from depression after trains of activity was slowed by the application of EGTA-AM, suggesting that the endbulb has a residual-calcium-dependent form of recovery. We developed a model that incorporates depletion, desensitization, and calcium-dependent recovery. This model replicated experimental findings over a range of experimental conditions. The model further indicated that desensitization plays only a minor role during prolonged activity, in large part because presynaptic release is so depleted. Thus depletion appears to be the dominant mechanism of depression at the endbulb during normal activity. Furthermore, calcium-dependent recovery at the endbulb is critical to prevent complete rundown during high activity and to preserve the reliability of information transmission.
This article has been cited by other articles:
|
|
 |
|
  J. A. M. Lorteije, S. I. Rusu, C. Kushmerick, and J. G. G. Borst Reliability and Precision of the Mouse Calyx of Held Synapse J. Neurosci., November 4, 2009; 29(44): 13770 - 13784. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Pliss, H. Yang, and M. A. Xu-Friedman Context-Dependent Effects of NMDA Receptors on Precise Timing Information at the Endbulb of Held in the Cochlear Nucleus J Neurophysiol, November 1, 2009; 102(5): 2627 - 2637. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Yang and M. A. Xu-Friedman Impact of Synaptic Depression on Spike Timing at the Endbulb of Held J Neurophysiol, September 1, 2009; 102(3): 1699 - 1710. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Strenzke, S. Chanda, C. Kopp-Scheinpflug, D. Khimich, K. Reim, A. V. Bulankina, A. Neef, F. Wolf, N. Brose, M. A. Xu-Friedman, et al. Complexin-I Is Required for High-Fidelity Transmission at the Endbulb of Held Auditory Synapse J. Neurosci., June 24, 2009; 29(25): 7991 - 8004. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Wang and P. B. Manis Short-Term Synaptic Depression and Recovery at the Mature Mammalian Endbulb of Held Synapse in Mice J Neurophysiol, September 1, 2008; 100(3): 1255 - 1264. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
