Experience-dependent intrinsic plasticity in interneurons of barrel cortex layer IV.
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.
Sun
Qian-Quan
QQ
Department of Zoology and Physiology, University of Wyoming, Laramie, WY 82071, USA. neuron@uwyo.edu
D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000502:physiology; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001703:Biophysics; D001710:Biotin / Q000031:analogs & derivatives / Q000378:metabolism; D002540:Cerebral Cortex / Q000166:cytology* / Q000502:physiology; D003198:Computer Simulation; D004558:Electric Stimulation; D003576:Electron Transport Complex IV / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D018507:Gene Expression Regulation, Developmental / Q000235:genetics; D005968:Glutamate Decarboxylase / Q000235:genetics; D049452:Green Fluorescent Proteins / Q000235:genetics; D066298:In Vitro Techniques; D007395:Interneurons / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D008959:Models, Neurological; D009473:Neuronal Plasticity / Q000502:physiology*; D010320:Parvalbumins / Q000378:metabolism; D018408:Patch-Clamp Techniques / Q000379:methods; D010852:Picrotoxin / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011336:Probability; D011810:Quinoxalines / Q000494:pharmacology; D012683:Sensory Deprivation / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects; D050599:Vesicular Glutamate Transport Protein 2 / Q000378:metabolism; D014738:Vibrissae / Q000294:innervation
D015761:4-Aminopyridine; D001710:Biotin; D003576:Electron Transport Complex IV; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D005968:Glutamate Decarboxylase; D049452:Green Fluorescent Proteins; D010320:Parvalbumins; D010852:Picrotoxin; D026902:Potassium Channel Blockers; D011810:Quinoxalines; D050599:Vesicular Glutamate Transport Protein 2; C070614:neurobiotin; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; C402565:glutamate decarboxylase 1