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J Neurophysiol (November 30, 2005). doi:10.1152/jn.00910.2005
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Submitted on August 31, 2005
Accepted on November 26, 2005

Contribution of Individual Spikes in Burst-Induced Long-Term Synaptic Modification

Robert C Froemke1, Ishan A Tsay2, Mohamad Raad1, John D Long1, and Yang Dan3*

1 Division of Neurobiology, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, USA
2 Graduate Group in Biophysics, University of California, Berkeley, Berkeley, CA, USA
3 Division of Neurobiology, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, USA; Graduate Group in Biophysics, University of California, Berkeley, Berkeley, CA, USA

* To whom correspondence should be addressed. E-mail: ydan{at}berkeley.edu.

Long-term synaptic modification depends on the relative timing of individual pre- and postsynaptic spikes, but the rules governing the effects of multi-spike bursts remain to be fully understood. In particular, some studies suggest that the spike timing dependence of synaptic modification breaks down with high-frequency bursts. In this study, we have characterized the effects of pre- and postsynaptic bursts on long-term modification of layer 2/3 synapses in visual cortical slices from young rats. We found that, while pairing-induced synaptic modification depends on the burst frequency, this dependence can be explained in terms of the timing of individual pre- and postsynaptic spikes. Later spikes in each burst are less effective in synaptic modification, but spike efficacy is regulated differently in pre- and postsynaptic bursts. Presynaptically, spike efficacy is progressively weakened, in parallel with short-term synaptic depression. Postsynaptically, spike efficacy is suppressed to a lesser extent, and it depends on postsynaptic potassium channel activation. Such timing-dependent interaction among multiple spikes can account for synaptic modifications induced by a variety of spike trains, including the frequency-dependent transition from depression to potentiation induced by a postsynaptic burst preceding a presynaptic burst.




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