| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
NEUROSCIENCE |
1 Department of Cell Physiology and Pharmacology, University of Leicester, Leicester LE1 9HN, UK
2 Department of Computing Science and Mathematics, University of Stirling, Stirling FK9 4LA, UK
3 MRC Toxicology Unit, University of Leicester, Leicester LE1 9HN, UK
It is well established that synaptic transmission declines at temperatures below physiological, but many in vitro studies are conducted at lower temperatures. Recent evidence suggests that temperature-dependent changes in presynaptic mechanisms remain in overall equilibrium and have little effect on transmitter release at low transmission frequencies. Our objective was to examine the postsynaptic effects of temperature. Whole-cell patch-clamp recordings from principal neurons in the medial nucleus of the trapezoid body showed that a rise from 25°C to 35°C increased miniature EPSC (mEPSC) amplitude from –33 ± 2.3 to –46 ± 5.7 pA (n = 6) and accelerated mEPSC kinetics. Evoked EPSC amplitude increased from –3.14 ± 0.59 to –4.15 ± 0.73 nA with the fast decay time constant accelerating from 0.75 ± 0.09 ms at 25°C to 0.56 ± 0.08 ms at 35°C. Direct application of glutamate produced currents which similarly increased in amplitude from –0.76 ± 0.10 nA at 25°C to –1.11 ± 0.19 nA 35°C. Kinetic modelling of fast AMPA receptors showed that a temperature-dependent scaling of all reaction rate constants by a single multiplicative factor (Q10 = 2.4) drives AMPA channels with multiple subconductances into the higher-conducting states at higher temperature. Furthermore, Monte Carlo simulation and deconvolution analysis of transmission at the calyx of Held showed that this acceleration of the receptor kinetics explained the temperature dependence of both the mEPSC and evoked EPSC. We propose that acceleration in postsynaptic AMPA receptor kinetics, rather than altered presynaptic release, is the primary mechanism by which temperature changes alter synaptic responses at low frequencies.
(Received 31 October 2006;
accepted after revision 27 November 2006;
first published online 30 November 2006)
Corresponding author I.D. Forsythe, MRC Toxicology unit, University of Leicester, Leicester LE1 9HN, UK. Email: IDF{at}le.ac.uk
This article has been cited by other articles:
|
|
 |
|
  J. Johnston, S. J. Griffin, C. Baker, A. Skrzypiec, T. Chernova, and I. D. Forsythe Initial segment Kv2.2 channels mediate a slow delayed rectifier and maintain high frequency action potential firing in medial nucleus of the trapezoid body neurons J. Physiol., July 15, 2008; 586(14): 3493 - 3509. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. H. Hennig, M. Postlethwaite, I. D. Forsythe, and B. P. Graham Interactions between multiple sources of short-term plasticity during evoked and spontaneous activity at the rat calyx of Held J. Physiol., July 1, 2008; 586(13): 3129 - 3146. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Koike-Tani, T. Kanda, N. Saitoh, T. Yamashita, and T. Takahashi Involvement of AMPA receptor desensitization in short-term synaptic depression at the calyx of Held in developing rats J. Physiol., May 1, 2008; 586(9): 2263 - 2275. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Renden and H. von Gersdorff Synaptic Vesicle Endocytosis at a CNS Nerve Terminal: Faster Kinetics at Physiological Temperatures and Increased Endocytotic Capacity During Maturation J Neurophysiol, December 1, 2007; 98(6): 3349 - 3359. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. L. P. Habets and J. G. G. Borst Dynamics of the readily releasable pool during post-tetanic potentiation in the rat calyx of Held synapse J. Physiol., June 1, 2007; 581(2): 467 - 478. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. Plested, M. C. Ashby, and A. Scimemi Getting hot under the calyx J. Physiol., April 1, 2007; 580(1): 13 - 14. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
