4.4 Article

Experience-Dependent Intrinsic Plasticity in Interneurons of Barrel Cortex Layer IV

Journal

JOURNAL OF NEUROPHYSIOLOGY
Volume 102, Issue 5, Pages 2955-2973

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00562.2009

Keywords

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Funding

  1. National Institute of Neurological Disorders and Stroke [5R01-NS-057415]

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Sun Q-Q. Experience-dependent intrinsic plasticity in interneurons of barrel cortex layer IV. J Neurophysiol 102: 2955-2973, 2009. First published September 9, 2009; doi:10.1152/jn.00562.2009. It is unclear whether intrinsic excitabilities of specific interneurons are modulated by sensory experiences. Here, I examined the intrinsic excitabilities of interneurons in sensory-spared and sensory-deprived cortices of GAD67-GFP mice. The results showed that whisker trimming, begun at postnatal day 7 for 3 wk, induced significant changes in intrinsic and firing properties of fast-spiking (FS) but not regular spiking nonpyramidal (RSNP) cells. Firing threshold, spike frequency, spike adaptation index, and input resistance of FS cells were significantly altered by sensory deprivation such that FS cells became less excitable. An up-regulation of IA currents in FS cells appeared to be responsible. Along with changes in the intrinsic properties of FS cells, whisker trimming also induced a robust reduction in the number of vesicular glutamate transporter 2 positive varicosities and parvalbumin expression and the strength of thalamocortical (TC) excitatory postsynaptic currents in FS cells in the sensory-deprived barrels. The probability of spike induction by TC stimulus was reduced by 30% and the spike jitter was increased in sensory-deprived FS cells. These results suggest that the FS networks are selectively inhibited by sensory deprivation. The concurrent changes of intrinsic properties and expression of parvalbumin in FS but not RSNP cells with TC synapses support a contribution from the TC pathway and glutamate to sensory-induced activity-dependent intrinsic plasticity of inhibitory networks in barrel cortex.

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