Neuroscience 2007, the 37th annual meeting of the Society for Neuroscience  2007.11.3-7

Program#/Poster#: 146.7/L17

Title: Prior activation of GABAergic neurons to excitatory neurons by thalamic axons within a single barrel in the mouse thalamocortical system: Relevance to the spike timing dependent plasticity

Location: San Diego Convention Center: Halls B-H
Presentation Start/End Time: Sunday, Nov 04, 2007, 10:00 AM -11:00 AM

Authors: *F. KIMURA1, C. ITAMI2, K. IKEZOE3, H. TAMURA3, I. FUJITA4, K. OBATA5, Y. YANAGAWA6, M. OHSHIMA7;
1Div. of Neurophysiolgy, D14, Osaka Univ. Med. Sch., Suita, Japan; 2Dept. Physiol., Saitama Med. Univ., Moro, Japan; 3Grad. Sch. Eng. Sci., Osaka Univ., Toyonaka, Japan; 4Grad. Sch. Eng. Sci., Osaka Univ., Toyonaka, CREST, Japan; 5Riken Brain Sci. Inst., Wako, Japan; 6Dept. Genet. and Behav. Neurosci., Gunma Univ. Grad. Sch. Med., Maebashi, Japan; 7Dept. Physiol., Kansai Univ. Hlth. Sci., Kumatori, Japan

Thalamic inputs to layer IV cortical cells are often followed by a rapid and strong suppression due to feedforward inhibition that constrains the cortical information flow. Such feedforward inhibition is thought to play an important role in regulating spike timing, thus enabling plasticity to occur in cerebral cortex. For such feedforward inhibition to work effectively, thalamic inputs to GABAergic neurons must be substantially earlier to arrive, compared with those to excitatory neurons. We performed latency analysis on multiple (dual or triple) EPSPs simultaneously recorded from a single barrel elicited by thalamic stimulation in the thalamocortical slices from the somatosensory barrel area in GAD67-GFP (delta neo) mice, in which GABAergic neurons are specifically labeled with GFP fluorescence. The latency for GABAergic cells ranged from 1.3 to 3.2 ms, and that for excitatory cells from 1.8 to 3.8 ms, thus there was substantial overlap in population data across the barrels. However, in simultaneous recordings in the same barrel, the latencies for GABA cells were always shorter than those for excitatory cells ( n=21 ). Such latency difference was also found for white matter stimulation. Stimulation at thalamus and white matter allowed us to estimate the conduction velocity for axons; axons making synapses onto GABA cells had faster conduction velocity than those on excitatory cells. We then destroyed myelination by infusing lysolethicin with an osmotic minipump, but the latency difference survived, indicating that the difference of conduction velocity was not due to the extent of myelination. Moreover, we noticed that axons innervating GABA cells had lower threshold than those innervating excitatory cells. Taken together, we conclude that thalamic axons onto GABA cells have thicker diameter than those on excitatory cells, which leads to activation of inhibitory cells prior to excitatory cells. Relevance to spike timing dependent plasticity in the barrel cortex will be discussed.

Support: Grant-in-Aid for Scientific Research on Priority Areas to FK: 18021022