Literature DB >> 9634140

Dual morphology and topography of the corticothalamic terminals originating from the primary, supplementary motor, and dorsal premotor cortical areas in macaque monkeys.

E M Rouiller1, J Tanné, V Moret, I Kermadi, D Boussaoud, E Welker.   

Abstract

In the motor, somatosensory, and auditory systems of rodents and cats, the corticothalamic connection is composed of a main projection formed by small endings and a minor projection terminating with giant endings. To establish whether the corticothalamic projection originating from motor cortical areas in primates exhibits the same duality, the anterograde tracer biotinylated dextran amine was injected in eight macaque monkeys in the primary motor (M1; n = 3), the supplementary motor (SMA; n = 3) and the dorsal premotor (PMd; n = 2) cortical areas to label corticothalamic axons. The corticothalamic projection originating from these three motor cortical areas was characterized by the presence of axon terminals constituting the same two types of endings, observed both as boutons en passant and terminaux. The population of small endings exhibited a mean cross-sectional maximum diameter of 0.95 microm (S.D. = 0.23), a range of diameters not overlapping that of giant endings (mean diameter = 3.46 microm, S.D. = 0.74 microm). Topographically, the giant endings originating from M1 were located in the same thalamic nucleus (ventroposterolateral nucleus, oral part) in which the small endings were found. In contrast, the giant endings originating from SMA and PMd were located in a thalamic nucleus (mediodorsal nucleus) distinct from the main termination zone formed by small endings. Along the rostrocaudal axis, the giant endings were distributed in a restricted zone, irrespective of the origin of the projection (M1, SMA, PMd). The dual morphology of corticothalamic endings, previously found in rodents and cats, is present in the motor system of subhuman primates for both primary and nonprimary motor cortical areas.

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Year:  1998        PMID: 9634140     DOI: 10.1002/(sici)1096-9861(19980629)396:2<169::aid-cne3>3.0.co;2-z

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


  21 in total

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