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The Journal of Neuroscience, June 6, 2007, 27(23):6268-6272; doi:10.1523/JNEUROSCI.4801-06.2007

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Brief Communications
Rapid Astrocyte Calcium Signals Correlate with Neuronal Activity and Onset of the Hemodynamic Response In Vivo

Ian R. Winship, Nathan Plaa, and Timothy H. Murphy

Department of Psychiatry, Brain Research Center, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3

Correspondence should be addressed to Dr. Timothy H. Murphy, 4N1-2255 Wesbrook Mall, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3. Email: thmurphy{at}interchange.ubc.ca

Elevation of intracellular Ca²⁺ in astrocytes can influence cerebral microcirculation and modulate synaptic transmission. Recently, in vivo imaging studies identified delayed, sensory-driven Ca²⁺ oscillations in cortical astrocytes; however, the long latencies of these Ca²⁺ signals raises questions in regards to their suitability for a role in short-latency modulation of cerebral microcirculation or rapid astrocyte-to-neuron communication. Here, using in vivo two-photon Ca²⁺ imaging, we demonstrate that 5% of sulforhodamine 101-labeled astrocytes in the hindlimb area of the mouse primary somatosensory cortex exhibit short-latency (peak amplitude 0.5 s after stimulus onset), contralateral hindlimb-selective sensory-evoked Ca²⁺ signals that operate on a time scale similar to neuronal activity and correlate with the onset of the hemodynamic response as measured by intrinsic signal imaging. The kinetics of astrocyte Ca²⁺ transients were similar in rise and decay times to postsynaptic neuronal transients, but decayed more slowly than neuropil Ca²⁺ transients that presumably reflect presynaptic transients. These in vivo findings suggest that astrocytes can respond to sensory activity in a selective manner and process information on a subsecond time scale, enabling them to potentially form an active partnership with neurons for rapid regulation of microvascular tone and neuron–astrocyte network properties.

Key words: astrocyte; calcium; synaptic transmission; blood flow; intrinsic optical signals; hindlimb; hyperemia

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Received Nov. 3, 2006; revised May 4, 2007; accepted May 6, 2007.

Correspondence should be addressed to Dr. Timothy H. Murphy, 4N1-2255 Wesbrook Mall, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3. Email: thmurphy{at}interchange.ubc.ca

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