TRKA IMMUNOREACTIVE NEURONS IN THE RAT SPINAL-CORD

We report the presence in rat spinal cord of a novel neuronal system e xpressing tyrosine kinase receptor (trkA), the high affinity receptor for nerve growth factor (NGF). TrkA immunoreactive cell bodies were ob served in the intermediate grey matter of the spinal cord and were cla ssified into three main groups: central canal cells located dorsolater al to the aqueduct, partition cells located between lamina X, and the lateral border of the intermediate grey, and a morphologically heterog eneous group which included large cells located near the lateral borde r. In situ hybridization confirmed that cells in all these areas expre ss trkA mRNA. Combined immunofluorescence and retrograde Fluoro-Gold l abelling was used to further characterise the projections and neurotra nsmitter profile of the trkA cells. Although often located in the vici nity of preganglionic cell groups, trkA immunoreactive cells are not t hemselves preganglionic. Rather, the central canal and partition cells belong to a neurochemically complex cholinergic propriospinal system. Many partition cells coexpress trkA, choline acetyltransferase (ChAT) , the low affinity neurotrophin receptor, p75, and nicotinamide adenin e dinucleotide phosphate-diaphorase (NADPH-d). In contrast, trkA immun oreactive central canal cells express ChAT, but do not express p75 and only a subpopulation express NADPH-d. The large trkA immunoreactive c ells located on the lateral border do not express ChAT. TrkA immunorea ctive fibres were also present and were located in the dorsal horn, in the dorsal columns, and in a bundle ventral to the aqueduct. However, double labelling revealed that the trkA immunoreactive fibres are not intrinsic but are primary afferent in origin and coexpress p75. The l ocation of this novel trkA neuronal system is consistent with it havin g a role in the segmental integration of autonomic outflow. NGF could affect this system by modulating neuronal phenotype and/or synaptic ef ficacy. (C) 1997 Wiley-Liss, Inc.