Activation of protein kinase C by the error signal from a basal ganglia-forebrain circuit in the zebra finch song control nuclei.

An error signal from the anterior forebrain pathway (AFP) in the songbird brain is necessary for juvenile song learning and adult song maintenance. It induces the expression of protein kinase C (PKC) which is related to the plasticity in the robust nucleus of the archistriatum (RA), one of the song control nuclei in the forebrain. The glutamatergic inputs from the AFP activate mainly the NMDA receptors of the RA neurons. In order to clarify the molecular mechanism of error signal-induced PKC activation, two experiments were carried out. First, Ca 2+ concentration was measured in a brain slice preparation from zebra finches using the fluorescent Ca 2+ indicator Fura 2-AM. Glutamate increased the intracellular Ca 2+ concentration ([Ca 2+ ] i ) in RA neurons. This increase was inhibited by the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid (AP5). Second, we examined the expression of PKC in the RA slice preparation after stimulation with glutamate for 10 min using PKCβl fluorescence immunohistochemistry. Glutamate induced the activation of PKC as the translocation from the cytosol to the cell membrane, and the translocation was inhibited by APS. These results indicate that the translocation of the PKC caused by the [Ca 2+ ] ι elevation through NMDA receptors is concerned with the initial stage of error signal-induced plasticity in the RA.