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The Journal of Neuroscience, June 25, 2008, 28(26):6659-6663; doi:10.1523/JNEUROSCI.1717-08.2008

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Brief Communications
Two Forms of Astrocyte Calcium Excitability Have Distinct Effects on NMDA Receptor-Mediated Slow Inward Currents in Pyramidal Neurons

Eiji Shigetomi,^1,2 David N. Bowser,³ Michael V. Sofroniew,² and Baljit S. Khakh^1,2,3

Departments of ¹Physiology and ²Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095-1751, and ³Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 0QH, United Kingdom

Correspondence should be addressed to Baljit S. Khakh, Department of Physiology, University of California, Los Angeles, 10833 LeConte Avenue, 53-263 CHS, Los Angeles, CA 90095-1751. Email: bkhakh{at}mednet.ucla.edu

Astrocytes display excitability in the form of intracellular calcium concentration ([Ca²⁺]_i) increases, but the signaling impact of these for neurons remains debated and controversial. A key unresolved issue is whether astrocyte [Ca²⁺]_i elevations impact neurons or not. Here we report that in the CA1 region of the hippocampus, agonists of native P2Y₁ and PAR-1 receptors, which are preferentially expressed in astrocytes, equally elevated [Ca²⁺]_i levels without affecting the passive membrane properties of pyramidal neurons. However, under conditions chosen to isolate NMDA receptor responses, we found that activation of PAR-1 receptors led to the appearance of NMDA receptor-mediated slow inward currents (SICs) in pyramidal neurons. In stark contrast, activation of P2Y₁ receptors was ineffective in this regard. The PAR-1 receptor-mediated increased SICs were abolished by several strategies that selectively impaired astrocyte [Ca²⁺]_i excitability and function. Our studies therefore indicate that evoked astrocyte [Ca²⁺]_i transients are not a binary signal for interactions with neurons, and that astrocytes result in neuronal NMDA receptor-mediated SICs only when appropriately excited. The data thus provide a basis to rationalize recent contradictory data on astrocyte–neuron interactions.

Key words: astrocyte; calcium; SIC; gliotransmitter; astrocytic glutamate release; glia

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Received April 20, 2008; revised May 15, 2008; accepted May 16, 2008.

Correspondence should be addressed to Baljit S. Khakh, Department of Physiology, University of California, Los Angeles, 10833 LeConte Avenue, 53-263 CHS, Los Angeles, CA 90095-1751. Email: bkhakh{at}mednet.ucla.edu

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