Literature DB >> 14648678

Calbindin-containing interneurons are a target for VIP-immunoreactive synapses in rat primary somatosensory cortex.

Jochen F Staiger1, Carmen Masanneck, Axel Schleicher, Werner Zuschratter.   

Abstract

Inhibitory interneurons in cerebral cortex are morphologically and physiologically extremely heterogeneous. This greatly interferes with an understanding of their functions. Progress has been made by classifying these neurons with the aid of molecular markers, e.g., neuropeptides or calcium-binding proteins, which are reliably expressed by certain subpopulations. We have used this approach to demonstrate an output of a subpopulation of cortical interneurons which express vasoactive intestinal polypeptide (VIP). By double immunostaining and correlated light and electron microscopy, we show that calbindin (CB)-containing interneurons located in layers II-VI of rat barrel cortex are targets of symmetric VIP-immunoreactive synapses. All CB-immunoreactive interneurons showed numerous contacts of VIP boutons on proximal and distal dendritic segments. A great majority of CB-immunoreactive interneurons (214/222) displayed such close appositions with VIP boutons on their soma as well. Quantification revealed that the number of VIP-immunoreactive boutons on CB-immunoreactive somata and dendrites of specified order is comparable for the different cortical layers. In conclusion, all calbindin-containing cortical interneurons seem to be under direct influence of other GABAergic interneurons expressing the peptide VIP. An indirect functional consequence of this may be disinhibition of pyramidal cells, which are considered the major target of calbindin interneurons. However, since the examined types of interneurons are intricately embedded in networks of yet different interneurons, the outcome of these multiple inhibitory interactions is likely to be less simplistic. It may be related to the timing of pyramidal cell discharge within and across layers of cortical columns. Copyright 2003 Wiley-Liss, Inc.

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Year:  2004        PMID: 14648678     DOI: 10.1002/cne.10953

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


  23 in total

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