Morphology and connections of nucleus isthmi pars magnocellularis in chicks (Gallus gallus)
- 18 December 2003
- journal article
- research article
- Published by Wiley in Journal of Comparative Neurology
- Vol. 469 (2) , 275-297
- https://doi.org/10.1002/cne.11007
Abstract
The nucleus isthmi pars magnocellularis (Imc) and pars parvocellularis (Ipc) influence the receptive field structure of neurons in the optic tectum (TeO). To understand better the anatomical substrate of isthmotectal interactions, neuronal morphology and connections of Imc were examined in chicks (Gallus gallus). Cholera toxin B injection into TeO demonstrated a coarse topographical projection from TeO upon Imc. Retrogradely labeled neurons were scattered throughout Imc and in low density within the zone of anterogradely labeled terminals, suggesting a heterotopic projection from Imc upon TeO. This organization differed from the precise homotopic reciprocal connections of Ipc and the nucleus isthmi pars semilunaris (SLu) with TeO. By using slice preparations, extracellular biotinylated dextran amine injections demonstrated a dense projection from most neurons in Imc upon both Ipc and SLu. Intracellular filling of Imc neurons with biocytin revealed two cell types. The most common, Imc-Is, formed a widely ramifying axonal field in both Ipc and SLu, without obvious topography. A less frequently observed cell type, Imc-Te, formed a widely ramifying terminal field in layers 10–12 of TeO. No neurons were found to project upon both Ipc/SLu and TeO. Both types possessed local axon collaterals and flat dendritic fields oriented parallel to the long axis of Imc. Imc neurons contain glutamic acid decarboxylase, which is consistent with Imc participating in center-surround or other wide-field inhibitory isthmotectal interactions. The laminar and columnar pattern of isthmotectal terminals also suggests a means of interacting with multiple tectofugal pathways, including the stratified subpopulations of tectorotundal neurons participating in motion detection. J. Comp. Neurol. 469:275–297, 2004.Keywords
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