TrkA, trkB, and trkC messenger RNA expression by bulbospinal cells of the rat

Previous research has shown that corticospinal as well as rubrospinal neuro ns express the high-affinity trkB and trkC receptors but not the high-affin ity trkA receptor. To determine if bulbospinal neurons in other brainstem a reas show the same pattern of trk receptor expression, bulbospinal cells we re labelled via the injection of the retrograde tracer FluoroGold into the spinal cord. Brainstem sections were then processed for in situ hybridizati on using oligonucleotide probes to the trkA, trkB, and trkC receptors. The results indicated that, although trkA expression occurred in brainstem area s that contain bulbospinal neurons (e.g., the vestibular nuclei, and the po ntine reticular formation), very few FluoroGold-labelled cells expressed th e trkA receptor. In contrast, at least 90% of bulbospinal cells in each bra instem area examined expressed the trkB receptor. Quantitative analysis ind icated differences in the level of trkB labelling between bulbospinal cells in different brainstem areas, with the highest levels seen in the locus co eruleus and magnocellular portion of the red nucleus, and the lowest levels seen in the medial and superior vestibular nuclei and the raphe obscurus. With the exception of the accessary trigeminal nucleus, over 84% of bulbosp inal cells in each brainstem area also expressed the trkC receptor. TrkC re ceptor expression was greatest in the locus coeruleus and subcoeruleus and lowest in the accessory trigeminal nucleus. the raphe magnus, and the vesti bular nuclei. Results indicate that, as with other descending pathways, virtually all bul bospinal pathways should be amenable to treatment with brain-derived neurot rophic factor, neurotrophin-4/5 or neurotrophin-3, but not nerve growth fac tor, following spinal cord damage. (C) 1999 IBRO. Published by Elsevier Sci ence Ltd.