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Somatic Ca2+ signaling in cerebellar Purkinje neurons
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Titel: |
Somatic Ca2+ signaling in cerebellar Purkinje neurons |
In: | Journal of Neuroscience Research, 88, 2010, 2, S. 275-289 |
veröffentlicht: |
Wiley
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Umfang: | 275-289 |
ISSN: |
0360-4012 1097-4547 |
DOI: | 10.1002/jnr.22204 |
Zusammenfassung: | <jats:title>Abstract</jats:title><jats:p>Activity‐driven Ca<jats:sup>2+</jats:sup> signaling plays an important role in a number of neuronal functions, including neuronal growth, differentiation, and plasticity. Both cytosolic and nuclear Ca<jats:sup>2+</jats:sup> has been implicated in these functions. In the current study, we investigated membrane‐to‐nucleus Ca<jats:sup>2+</jats:sup> signaling in cerebellar Purkinje neurons in culture to gain insight into the pathways and mechanisms that can initiate nuclear Ca<jats:sup>2+</jats:sup> signaling in this neuronal type. Purkinje neurons are known to express an abundance of Ca<jats:sup>2+</jats:sup> signaling molecules such as voltage‐gated Ca<jats:sup>2+</jats:sup> channels, ryanodine receptors, and IP3 receptors. Results show that membrane depolarization evoked by brief stimulation with K<jats:sup>+</jats:sup> saline elicits a prominent Ca<jats:sup>2+</jats:sup> signal in the cytosol and nucleus of the Purkinje neurons. Ca<jats:sup>2+</jats:sup> influx through P/Q‐ and L‐type voltage‐gated Ca<jats:sup>2+</jats:sup> channels and Ca<jats:sup>2+</jats:sup>‐induced Ca<jats:sup>2+</jats:sup> release (CICR) from intracellular stores contributed to the Ca<jats:sup>2+</jats:sup> signal, which spread from the plasma membrane to the nucleus. At strong K<jats:sup>+</jats:sup> stimulations, the amplitude of the nuclear Ca<jats:sup>2+</jats:sup> signal exceeded that of the cytosolic Ca<jats:sup>2+</jats:sup> signal, suggesting the involvement of a nuclear amplification mechanism and/or differences in Ca<jats:sup>2+</jats:sup> buffering in these two cellular compartments. An enhanced nuclear Ca<jats:sup>2+</jats:sup> signal was more prominent for Ca<jats:sup>2+</jats:sup> signals elicited by membrane depolarization than for Ca<jats:sup>2+</jats:sup> signals elicited by activation of the metabotropic glutamate receptor pathway (mGluR1), which is linked to Ca<jats:sup>2+</jats:sup> release from intracellular stores controlled by the IP3 receptor. © 2009 Wiley‐Liss, Inc.</jats:p> |
Format: | E-Article |
Quelle: | Wiley (CrossRef) |
Sprache: | Englisch |