Deafferentation-induced changes in protein kinase C expression in the rat cochlear nucleus

Isoforms of the signal transducing molecule, protein kinase C (PKC), may pl ay a role in neural plasticity following sensory deafferentation. To explor e the role of PKC in central auditory plasticity, we studied the effect of auditory deafferentation on the expression of PKC beta I, beta II, gamma, a nd delta in the rat dorsal (DCN) and ventral cochlear nucleus (VCN), using immunocytochemistry. Male rats were treated with kanamycin and furosemide t o induce hair cell loss. At various intervals post-treatment, brains were p erfusion-fixed and processed for immunocytochemistry. Following deafferenta tion, we observed a gradual increase in PKC beta I immunoreactivity (ir) in the deepest layers of the DCN, possibly representing synapses of primary a fferents or parallel fibers on unlabeled neurons. Correlated with this, we observed an increase in the number of neurons in the deep DCN that showed P KC delta ir. In controls, we observed PKC gamma ir in small ovoid cells con centrated in the middle layer of the DCN. From days 4 through 14 after deaf ferentation, we found an increase in the intensity of staining of these cel ls, with a return toward control levels by day 28. Finally, Purkinje-like c ells (PLC) in the VCN, which express only PKC delta in control rats, began to express PKC gamma after deafferentation, correlated with increased expre ssion of calbindin D28k in PLC. Thus PKC isoforms are differentially regula ted in the CN following deafferentation, supporting a role for PKC in audit ory plasticity. (C) 2000 Elsevier Science B.V. All rights reserved.