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Deafferentation-induced changes in protein kinase C expression in the rat cochlear nucleus
M M Garcia1, R Edward, G B Brennan
1Department of Otolaryngology, Tulane University School of Medicine, New Orleans, LA 70112-2699, USA. mgarcia@mailhost.tcs.tulane.edu
Abstract:
Isoforms of the signal transducing molecule, protein kinase C (PKC), may play a role in neural plasticity following sensory deafferentation. To explore the role of PKC in central auditory plasticity, we studied the effect of auditory deafferentation on the expression of PKC betaI, betaII, gamma, and delta in the rat dorsal (DCN) and ventral cochlear nucleus (VCN), using immunocytochemistry. Male rats were treated with kanamycin and furosemide to induce hair cell loss. At various intervals post-treatment, brains were perfusion-fixed and processed for immunocytochemistry. Following deafferentation, we observed a gradual increase in PKC betaI immunoreactivity (ir) in the deepest layers of the DCN, possibly representing synapses of primary afferents or parallel fibers on unlabeled neurons. Correlated with this, we observed an increase in the number of neurons in the deep DCN that showed PKC delta ir. In controls, we observed PKC gamma ir in small ovoid cells concentrated in the middle layer of the DCN. From days 4 through 14 after deafferentation, we found an increase in the intensity of staining of these cells, with a return toward control levels by day 28. Finally, Purkinje-like cells (PLC) in the VCN, which express only PKC delta in control rats, began to express PKC gamma after deafferentation, correlated with increased expression of calbindin D28k in PLC. Thus PKC isoforms are differentially regulated in the CN following deafferentation, supporting a role for PKC in auditory plasticity.
Insights
Protein kinase C (PKC) isoforms are differentially regulated in the cochlear nucleus following auditory deafferentation. This suggests PKC plays a role in central auditory plasticity and neural adaptation.
Area of Science:
- Neuroscience
- Auditory system research
- Molecular biology
Background:
- Signal transducing molecules like protein kinase C (PKC) are implicated in neural plasticity.
- Sensory deafferentation can trigger adaptive changes in neural circuits.
Purpose of the Study:
- To investigate the role of specific PKC isoforms (betaI, betaII, gamma, delta) in central auditory plasticity.
- To examine the expression patterns of PKC isoforms in the rat cochlear nucleus (CN) after auditory deafferentation.
Main Methods:
- Auditory deafferentation was induced in male rats using kanamycin and furosemide to cause hair cell loss.
- Immunocytochemistry was employed to analyze the expression and localization of PKC isoforms in the dorsal (DCN) and ventral cochlear nucleus (VCN) at various time points post-treatment.
Main Results:
- PKC betaI immunoreactivity increased in the deep DCN layers following deafferentation.
- PKC delta expression increased in deep DCN neurons, and PKC gamma expression changed in specific cell populations within the DCN.
- VCN Purkinje-like cells (PLC) altered PKC isoform expression (gained PKC gamma) and calbindin D28k expression post-deafferentation.
Conclusions:
- PKC isoforms are differentially regulated in the cochlear nucleus in response to auditory deafferentation.
- These changes support a significant role for PKC signaling pathways in central auditory plasticity and neural adaptation.
