Radially expanding transglial calcium waves in the intact cerebellum. Proc Natl Acad Sci USA

Department of Molecular Biology and Princeton Neuroscience Institute, Princeton University, Lewis Thomas Laboratory, Washington Road, Princeton, NJ 08544, USA.
Proceedings of the National Academy of Sciences (Impact Factor: 9.81). 03/2009; 106(9):3496-501. DOI: 10.1073/pnas.0809269106
Source: PubMed

ABSTRACT Multicellular glial calcium waves may locally regulate neural activity or brain energetics. Here, we report a diffusion-driven astrocytic signal in the normal, intact brain that spans many astrocytic processes in a confined volume without fully encompassing any one cell. By using 2-photon microscopy in rodent cerebellar cortex labeled with fluorescent indicator dyes or the calcium-sensor protein G-CaMP2, we discovered spontaneous calcium waves that filled approximately ellipsoidal domains of Bergmann glia processes. Waves spread in 3 dimensions at a speed of 4-11 microm/s to a diameter of approximately 50 microm, slowed during expansion, and were reversibly blocked by P2 receptor antagonists. Consistent with the hypothesis that ATP acts as a diffusible trigger of calcium release waves, local ejection of ATP triggered P2 receptor-mediated waves that were refractory to repeated activation. Transglial waves represent a means for purinergic signals to act with local specificity to modulate activity or energetics in local neural circuits.

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Available from: Werner Göbel, Aug 23, 2015
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    • "Yet, it was later acknowledged that astroglia exhibit a special form of excitability that is based on variations in the intracellular concentration of Ca 2+ ions (Charles et al., 1991; Cornell-Bell et al., 1990). Studies performed in acute brain slices and, more recently, in vivo allowed to determine that astrocytic [Ca 2+ ] i changes can occur spontaneously (Aguado et al., 2002; Hirase et al., 2004; Hoogland et al., 2009; Navarrete et al., 2013; Nett et al., 2002; Nimmerjahn et al., 2009; Panatier et al., 2011; Parri et al., 2001), or can be evoked in response to synaptic activity (Dani et al., 1992; Di Castro et al., 2011; Dombeck et al., 2007; Gourine et al., 2010; Jourdain et al., 2007; Nimmerjahn et al., 2009; Pasti et al., 1997; Paukert et al., 2014; Petzold et al., 2008; Porter and McCarthy, 1995a,b, 1996; Santello et al., 2011; Schummers et al., 2008; Wang et al., 2006; Winship et al., 2007). In addition, there is evidence indicating that they can be mediated also by transient receptor potential A1 channels (Shigetomi et al., 2012, 2013a). "
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    Progress in Neurobiology 04/2015; 29. DOI:10.1016/j.pneurobio.2015.04.003 · 10.30 Impact Factor
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    • "However, either trains of sustained stimulation of synaptic activity (Grosche et al., 1999; Matyash et al., 2001) or a large number of activated fibers (Honsek et al., 2012) are necessary to induce this type of astrocytic Ca 2+ activity. In vivo it has been suggested that astrocytes can synchronize their activity in clusters of 2–5 astrocytes (Hirase et al., 2004; Sasaki et al., 2011a) or spread through a network consisting of dozens to hundreds of astrocytes (Hoogland et al., 2009; Nimmerjahn et al., 2009; Kuga et al., 2011). "
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