NEUROTROPHIN RECEPTOR IMMUNOSTAINING IN THE RAT VENTRAL COCHLEAR NUCLEUS

By virtue of its known segregated distribution of cell types, their kn own neurotransmitters and neurophysiologic properties, the cochlear nu cleus is an excellent model and provides the opportunity to study the relation between neurotrophins and their receptors along with the func tional properties of the adult cochlear nucleus. To investigate the po tential role of neurotrophins in the mature cochlear nucleus, we deter mined the expression of the three major neurotrophin tyrosine kinase r eceptors (Trk) in the adult rat ventral cochlear nucleus, as revealed by antibodies against the full-Trk proteins. A qualitative and a carto graphic analysis showed a widespread distribution of the three Trk rec eptors throughout the nucleus. Immunostaining was mainly restricted to neurons as shown by the lack of double immunostaining with specific m arkers for glial cells. However, we observed variability in immunostai ning for given receptors. Three classes of cells were distinguished by their specificity for Trk receptors. The first one was a cell populat ion that stained for TrkA or TrkB. This population characterizes the m ajority of small and small round neurons and fusiform cells. The secon d group consists of TrkC-immunolabeled cells and comprises the majorit y of spherical, globular, granule and small multipolar cells. The thir d group consists of cells that seem to be immunopositive for all three Trk receptors. This group includes in part multipolar. giant and octo pus cells. A possible correlation between Trk expression and cell func tional properties is suggested: TrkA- and TrkB-immunoreactive cells co uld include inhibitory neurons while cells stained for TrkC could incl ude excitatory neurons. The abundant and widespread neuronal distribut ion of signal-transducing forms of TrkA, TrkB and TrkC predicts that t heir cognate ligands may exert significant effects on a large proporti on of neurons within the mature ventral cochlear nucleus. (C) 1997 Els evier Science B.V.