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Lesions of an avian forebrain nucleus prevent changes in protein kinase C levels associated with deafening‐induced vocal plasticity in adult songbirds
Author(s) -
Watanabe Aiko,
Li Rui,
Kimura Takeji,
Sakaguchi Hironobu
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.04763.x
Subject(s) - forebrain , neuroplasticity , auditory feedback , neuroscience , nucleus , protein kinase c , synaptic plasticity , lesion , biology , psychology , medicine , central nervous system , microbiology and biotechnology , signal transduction , receptor , pathology
We investigated the participation of protein kinase C (PKC) in the regulation of vocal plasticity in songbirds. Deafening of adult Bengalese finches causes initial song alteration, followed by stabilization. In parallel, the expression of PKC β1 increases transiently 2 weeks after deafening, and then decreases gradually in the robust nucleus of the arcopallium (RA) of Bengalese finches, similar to the pattern observed during developmental song learning. First, we showed that in adult zebra finches, whose songs change more gradually after auditory deprivation than those of Bengalese finches, PKC in RA also increased to an equal degree 2 weeks after deafening, despite the species difference. Second, double‐labeling with an anterograde tracer and PKC immunofluorescence revealed that PKC immunoreactivity in RA was detected on the synaptic terminals from a high premotor vocal nucleus (HVC), but not from the lateral magnocellular nucleus of the anterior nidopallium (LMAN). To determine what causes deafening‐induced PKC increases, we blocked signals from LMAN, the final output nucleus to RA in the anterior forebrain pathway (AFP), by a unilateral LMAN lesion prior to auditory deprivation of adult Bengalese finches. The PKC immunoreactivity increased in RA of the intact hemisphere; however, in RA on the lesioned side, it was less intense than that of the unlesioned side. Thus, the deafening‐induced PKC expression was suppressed by lesioning of LMAN. These results suggest that an output signal from the AFP via LMAN induces the increase in PKC activity on HVC‐RA synapses that may regulate song plasticity.