Somatic Ca 2+ signaling in cerebellar Purkinje neurons

Activity‐driven Ca 2+ signaling plays an important role in a number of neuronal functions, including neuronal growth, differentiation, and plasticity. Both cytosolic and nuclear Ca 2+ has been implicated in these functions. In the current study, we investigated membrane‐to‐nucleus Ca 2+ signaling in cerebellar Purkinje neurons in culture to gain insight into the pathways and mechanisms that can initiate nuclear Ca 2+ signaling in this neuronal type. Purkinje neurons are known to express an abundance of Ca 2+ signaling molecules such as voltage‐gated Ca 2+ channels, ryanodine receptors, and IP3 receptors. Results show that membrane depolarization evoked by brief stimulation with K + saline elicits a prominent Ca 2+ signal in the cytosol and nucleus of the Purkinje neurons. Ca 2+ influx through P/Q‐ and L‐type voltage‐gated Ca 2+ channels and Ca 2+ ‐induced Ca 2+ release (CICR) from intracellular stores contributed to the Ca 2+ signal, which spread from the plasma membrane to the nucleus. At strong K + stimulations, the amplitude of the nuclear Ca 2+ signal exceeded that of the cytosolic Ca 2+ signal, suggesting the involvement of a nuclear amplification mechanism and/or differences in Ca 2+ buffering in these two cellular compartments. An enhanced nuclear Ca 2+ signal was more prominent for Ca 2+ signals elicited by membrane depolarization than for Ca 2+ signals elicited by activation of the metabotropic glutamate receptor pathway (mGluR1), which is linked to Ca 2+ release from intracellular stores controlled by the IP3 receptor. © 2009 Wiley‐Liss, Inc.