Present address: Laboratory for Vocal Behavior Mechanisms, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.
Lesions of an avian forebrain nucleus prevent changes in protein kinase C levels associated with deafening-induced vocal plasticity in adult songbirds
Article first published online: 16 MAY 2006
European Journal of Neuroscience
Volume 23, Issue 9, pages 2447–2457, May 2006
How to Cite
Watanabe, A., Li, R., Kimura, T. and Sakaguchi, H. (2006), Lesions of an avian forebrain nucleus prevent changes in protein kinase C levels associated with deafening-induced vocal plasticity in adult songbirds. European Journal of Neuroscience, 23: 2447–2457. doi: 10.1111/j.1460-9568.2006.04763.x
- Issue published online: 16 MAY 2006
- Article first published online: 16 MAY 2006
- Received 19 September 2005, revised 16 February 2006, accepted 22 February 2006
- auditory feedback;
- basal ganglia;
- Bengalese finch;
- vocal behavior;
- zebra finch
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.