The cells of origin of the primate spinothalamic tract

Abstract

Spinothalamic tract cells in the lumbar, sacral and caudal segments of the primate spinal cord were labelled by the retrograde transport of horseradish peroxidase (HRP) injected into the thalamus. The laminar distribution of stained spinothalamic cells in the lumbosacral enlargement differed according to whether the HRP was injected into the lateral or the medial thalamus. Lateral injections labelled cells in most laminae, but the largest numbers of cells were in laminae I and V. The highest concentrations of cells labelled from the medial thalamus were in laminae VI-VIII. Ninety percent or more of the stained spinothalamic cells in the lumbosacral enlargement were contralateral to the injection site. In the conus medullaris stained spinothalamic cells were most numerous in laminae I, V and VI following lateral thalamic injections of HRP. Many of the cells of the conus were in Stilling's nucleus. Twenty-three percent of the cells in the conus were ipsilateral to the injection site in the lateral thalamus. Only a few cells in the conus were labelled by medial thalamic injections. The total number of spinothalamic cells from L5 caudally was estimated to be at least 1,200-2,500. An injection of HRP into the midbrain resulted in laminar distribution of labelled cells much like that produced by a lateral thalamic injection. The types of spinothalamic tract cells and the sizes of their somata were determined for different laminae. The cell types resemble those already described from Golgi and other studies of the spinal cord gray matter. The spinothalamic tract cells in lamina I included Waldeyer cells and numerous small fusiform, pyriform or triangular cells. Those in lamina II included limitrophe and central cells. Spinothalamic cells in lamina III were central cells. Most of the labelled cells in laminae IV-X were polygonal, although there were also flattened cells in these layers. The smallest spinothalamic cells were in laminae I-III, while the largest were in laminae V and VII-IX. Spinothalamic cells in the conus medullaris included cells like those in the lumbosacral enlargement, but also a special cell type in Stilling's nucleus. Some cells in the conus had dendrites that crossed the midline. Spinothalamic axons could sometimes be traced to the ventral white commissure within one or a few sections. In longitudinal sections, most labelled axons were in the ventral part of the lateral funiculus on the side of the injection, although a few were in the ventral funiculus or on the contralateral side. The axons were widely dispersed, and a few were located adjacent to the pia-glial membrane.

Parallel Processing of Nociceptive A-δ Inputs in SII and Midcingulate Cortex in Humans

“…This latter hypothesis implies a bilateral thalamic projection of spinothalamic fibers, which, although scarce, has been substantiated (Willis et al, 1979;Apkarian and Hodge, 1989). The important delay observed between the early and late pMCC responses suggests that the latter should depend on a much slower conducting system, but the hypothesis of a dependence on C-fiber activation is incompatible with its latency (Mouraux et al, 2004).…”

Morphology and synaptic connections of ultrafine primary axons in lamina I of the spinal dorsal horn: candidates for the terminal axonal arbors of primary neurons with unmyelinated (C) axons

“…It has now been established through the use of anatomical and physiological techniques that Rexed's (1952) lamina I is one of the major locations of long distance projection neurons in the spinal and medullary dorsal horns (e.g., Price and Dubner, 1977;Gobel et al, 1981;Hockfield and Gobel, 1978;Willis et al, 1979 for reviews). Most lamina I neurons receive nociceptive inputs from primary neurons with small caliber axons which conduct in the C and A6 ranges (Christensen and Perl, 1970;Kumazawa and Perl, 1978;Light et al, 1979;Bennett et , 1981).…”

De novo expression of neurokinin‐1 receptors by spinoparabrachial lamina I pyramidal neurons following a peripheral nerve lesion

“…Therefore, changes in the properties of these neurons may occur in neuropathic pain states and may be important for the triggering and/or maintenance of the pain-related condition. These lamina I neurons project mainly to the lateral parabrachial nucleus (LPb; Bernard et al, 1995;Cechetto et al, 1985;Craig, 1995;Feil and Herbert, 1995;Wiberg and Blomqvist, 1984) and to the thalamus (Carstens and Trevino, 1978;Craig and Burton, 1981;Giesler et al, 1979Giesler et al, , 1981Willis et al, 1979). Lamina I neurons were originally classified into four types in the rat, independently of being projection or local circuit neurons Coimbra, 1983, 1986).…”