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Direct measurement of adenosine release during hypoxia in the CA1 region of the rat hippocampal slice

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UNSPECIFIED (2000) Direct measurement of adenosine release during hypoxia in the CA1 region of the rat hippocampal slice. JOURNAL OF PHYSIOLOGY-LONDON, 526 (1). pp. 143-155. ISSN 0022-3751

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Abstract

1.. We have used an enzyme-based, twin-barrelled sensor -to measure adenosine release during hypoxia in the CA1 region of rat hippocampal slices in conjunction with simultaneous extracellular field recordings of excitatory synaptic transmission. 2. When loaded with a combination of adenosine deaminase, nucleoside phosphorylase and xanthine oxidase, the sensor responded linearly to exogenous adenosine over the concentration range 10 nM to 20 mu M. 3. Without enzymes, the sensor when placed on the surface of hippocampal slices recorded a very small net signal during hypoxia of 40 +/- 43 pA (mean +/- S.E.M.; n = 7). Only when one barrel was loaded with the complete sequence of enzymes and the other with the last two in the cascade did the sensor record a large net difference signal during hypoxia (1226 +/- 423 pA; n = 7). 4. This signal increased progressively during the hypoxic episode, scaled with the hypoxic depression of the simultaneously recorded field excitatory postsynaptic potential and was greatly reduced (67 +/- 6.5%; n = 9) by coformycin (0.5-2 mu M), a selective inhibitor of adenosine deaminase, the first enzyme in the enzymic cascade within the sensor. 5. For 5 min hypoxic episodes, the sensor recorded a peak concentration of adenosine of 5.6 +/- 1.2 mu M (n = 16) with an IC50 for the depression of transmission of approximately 3 mu M. 6. In slices pre-incubated for 3-6 h in nominally Ca2+-free artificial cerebrospinal fluid, 5 min of hypoxia resulted in an approximately 9-fold greater release of adenosine (48.9 +/- 17.7 mu M; n = 6). 7. High extracellular Ca2+ (4 mM) both reduced the adenosine signal recorded by the sensor during hypoxia (3.5 +/- 0.6 mu M; n = 4) and delayed the hypoxic depression of excitatory synaptic transmission.

Item Type: Journal Article
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Q Science > QP Physiology
Journal or Publication Title: JOURNAL OF PHYSIOLOGY-LONDON
Publisher: CAMBRIDGE UNIV PRESS
ISSN: 0022-3751
Date: 1 July 2000
Volume: 526
Number: 1
Number of Pages: 13
Page Range: pp. 143-155
Publication Status: Published
URI: http://wrap.warwick.ac.uk/id/eprint/13180

Data sourced from Thomson Reuters' Web of Knowledge

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