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The Journal of Neuroscience, April 19, 2006, 26(16):4178-4187; doi:10.1523/JNEUROSCI.0150-06.2006

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Behavioral/Systems/Cognitive
Rapid, Activity-Dependent Plasticity in Timing Precision in Neonatal Barrel Cortex

Michael I. Daw,¹ Neil V. Bannister,¹ and John T. R. Isaac^1,2

¹Medical Research Council Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, Bristol BS8 1TD, United Kingdom, and ²National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892

Correspondence should be addressed to Dr. John T. R. Isaac, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, Bethesda, MD 20892. Email: isaacj{at}ninds.nih.gov

Developing neuronal networks acquire the ability to precisely time events, a key feature required for information processing. In the barrel cortex, encoding of information requires a high-precision temporal code with a resolution of 5 ms; however, it is not known what process drives the maturation in timing precision. Here, we report that long-term potentiation (LTP) at thalamocortical synapses in the neonatal layer IV barrel cortex produces a dramatic improvement in the timing of neuronal output and synaptic input. LTP strongly reduces the latency and variability of synaptically evoked action potentials, improving the fidelity of timing to within that predicted to be required for adult sensory processing. Such changes in timing also occur during development in the neonate. LTP also reduces the summation of EPSPs shortening the window for coincidence detection for synaptic input. In contrast to these reliable effects, LTP produced only a modest and variable change in synaptic efficacy. Thus, our findings suggest that the primary role of this form of neonatal LTP is for the acquisition of timing precision and the refinement of coincidence detection, rather than an increase in synaptic strength. Therefore, neonatal thalamocortical LTP may be a critical prerequisite for the maturation of information processing in the barrel cortex.

Key words: development; glutamate; kainate receptor; AMPA receptor; long-term potentiation; spike timing

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Received Nov. 1, 2005; revised Feb. 28, 2006; accepted Feb. 28, 2006.

Correspondence should be addressed to Dr. John T. R. Isaac, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, Bethesda, MD 20892. Email: isaacj{at}ninds.nih.gov

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