Literature DB >> 20554844

Subtype-specific dendritic Ca(2+) dynamics of inhibitory interneurons in the rat visual cortex.

Kwang-Hyun Cho1, Jin Hwa Jang, Hyun-Jong Jang, Myung-Jun Kim, Shin Hee Yoon, Takaichi Fukuda, Frank Tennigkeit, Wolf Singer, Duck-Joo Rhie.   

Abstract

The Ca(2+) increase in dendrites that is evoked by the backpropagation of somatic action potentials (APs) is involved in the activity-dependent modulation of dendritic and synaptic functions that are location dependent. In the present study, we investigated dendritic Ca(2+) dynamics evoked by backpropagating APs (bAPs) in four subtypes of inhibitory interneurons classified by their spiking patterns: fast spiking (FS), late spiking (LS), burst spiking (BS), and regular-spiking nonpyramidal (RSNP) cells. Cluster analysis, single-cell RT-PCR, and immunohistochemistry confirmed the least-overlapping nature of the grouped cell populations. Somatic APs evoked dendritic Ca(2+) transients in all subtypes of inhibitory interneurons with different spatial profiles along the tree: constantly linear in FS and LS cells, increasing to a plateau in BS cells and bell-shaped in RSNP cells. The increases in bAP-evoked dendritic Ca(2+) transients brought about by the blocking of A-type K(+) channels were similar in whole dendritic trees of each subtype of inhibitory interneurons. However, in RSNP cells, the increases in the distal dendrites were larger than those in the proximal dendrites. On cholinergic activation, nicotinic inhibition of bAP-evoked dendritic Ca(2+) transients was observed only in BS cells expressing cholecystokinin and vasoactive intestinal peptide mRNAs, with no muscarinic modulation in all subtypes of inhibitory interneurons. Cell subtype-specific differential spatial profiles and their modulation in bAP-evoked dendritic Ca(2+) transients might be important for the domain-specific modulation of segregated inputs in inhibitory interneurons and differential control between the excitatory and inhibitory networks in the visual cortex.

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Year:  2010        PMID: 20554844     DOI: 10.1152/jn.00146.2010

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


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