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The Journal of Neuroscience, January 31, 2007, 27(5):1167-1175; doi:10.1523/JNEUROSCI.3535-06.2007

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Cellular/Molecular
Regulation of Postsynaptic Ca²⁺ Influx in Hippocampal CA1 Pyramidal Neurons via Extracellular Carbonic Anhydrase

Nataliya Fedirko, Marat Avshalumov, Margaret E. Rice, and Mitchell Chesler

Department of Neurosurgery and Department of Physiology and Neuroscience, New York University School of Medicine, New York, New York 10016

Correspondence should be addressed to Dr. Mitchell Chesler, Department of Physiology and Neuroscience, New York University School of Medicine, 550 First Avenue, New York, NY 10016. Email: mitch.chesler{at}med.nyu.edu

Synchronous neural activity causes rapid changes of extracellular pH (pH_e) in the nervous system. In the CA1 region of the hippocampus, stimulation of the Schaffer collaterals elicits an alkaline pH_e transient in stratum radiatum that is limited by extracellular carbonic anhydrase (ECA). When interstitial buffering is diminished by inhibition of ECA, the alkalosis is enhanced and NMDA receptor (NMDAR)-mediated postsynaptic currents can be augmented. Accordingly, the dendritic influx of Ca²⁺ elicited by synaptic excitation may be expected to increase if ECA activity were blocked. We tested this hypothesis in the CA1 stratum radiatum of hippocampal slices from juvenile rats, using extracellular, concentric pH- and Ca²⁺-selective microelectrodes with response times of a few milliseconds, as well as Fluo-5F imaging of intracellular Ca²⁺ transients. Brief stimulation of the Schaffer collaterals elicited an alkaline pH_e transient, a transient decrease in free extracellular Ca²⁺ concentration ([Ca²⁺]_e), and a corresponding transient rise in free intracellular Ca²⁺ concentration ([Ca²⁺]_i). Inhibition of ECA with benzolamide caused a marked amplification and prolonged recovery of the pH_e and [Ca²⁺]_e responses, as well as the dendritic [Ca²⁺]_i transients. The increase in amplitude caused by benzolamide did not occur in the presence of the NMDAR antagonist APV, but the decay of the responses was still prolonged. These results indicate that ECA can shape dendritic Ca²⁺ dynamics governed by NMDARs by virtue of its regulation of concomitant activity-dependent pH_e shifts. The data also suggest that Ca²⁺ transients are influenced by additional mechanisms sensitive to shifts in pH_e.

Key words: benzolamide; Fluo-5F; ion-selective microelectrode; stratum radiatum; NMDA receptor; APV

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Received Aug. 15, 2006; revised Dec. 8, 2006; accepted Dec. 25, 2006.

Correspondence should be addressed to Dr. Mitchell Chesler, Department of Physiology and Neuroscience, New York University School of Medicine, 550 First Avenue, New York, NY 10016. Email: mitch.chesler{at}med.nyu.edu

This article has been cited by other articles:

				S. Makani and M. Chesler Endogenous Alkaline Transients Boost Postsynaptic NMDA Receptor Responses in Hippocampal CA1 Pyramidal Neurons J. Neurosci., July 11, 2007; 27(28): 7438 - 7446. [Abstract] [Full Text] [PDF]

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