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Journal of Experimental Biology, Vol 198, Issue 7 1621-1628, Copyright © 1995 by Company of Biologists

JOURNAL ARTICLES

Role of adenosine in NMDA receptor modulation in the cerebral cortex of an anoxia-tolerant turtle (Chrysemys picta belli)

LT Buck and PE Bickler
Department of Anesthesia, University of California, San Francisco 94143-0542, USA.

Accumulation of the neuromodulator adenosine in the anoxia-tolerant turtle brain may play a key role in a protective decrease in excitatory neurotransmission during anoxia. Since excitatory neurotransmission is mediated largely by Ca2+ entry through N-methyl-D-aspartate (NMDA) receptors, we measured the effect of adenosine on NMDA-mediated Ca2+ transients in normoxic and anoxic turtle cerebrocortical sheets. Intracellular [Ca2+] was measured fluorometrically with the Ca2+-sensitive dye Fura-2. Baseline intracellular [Ca2+] and [ATP] were also measured to assess cortical sheet viability and potential toxic effects of NMDA. Baseline [Ca2+] did not change significantly under any condition, ranging from 109 +/- 22 to 187 +/- 26 nmoll-1. Throughout normoxic and 2h anoxic protocols, and after single and multiple NMDA exposures, [ATP] did not change significantly, ranging from 16.0 +/- 1.9 to 25.3 +/- 4.9 nmol ATP mg-1 protein. Adenosine caused a reduction in the normoxic NMDA-mediated increase in [Ca2+] from a control level of 287 +/- 35 to 103 +/- 22 nmoll-1 (64%). This effect is mediated by the A1 receptor since 8-phenyltheophylline (a specific A1 antagonist) effectively blocked the adenosine effect and N6-cyclopentyladenosine (a specific A1 agonist) elicited a similar decrease in the NMDA-mediated response. Cortical sheets exposed to anoxia alone exhibited a 52% decrease in the NMDA-mediated [Ca2+] rise, from 232 +/- 30 to 111 +/- 9 nmoll-1. The addition of adenosine had no further effect and 8-phenyltheophylline did not antagonize the observed decrease. Therefore, the observed down-regulation of NMDA receptor activity during anoxia must involve additional, as yet unknown, mechanisms.

This article has been cited by other articles:

				P. E. Bickler, P. H. Donohoe, and L. T. Buck Hypoxia-Induced Silencing of NMDA Receptors in Turtle Neurons J. Neurosci., May 15, 2000; 20(10): 3522 - 3528. [Abstract] [Full Text] [PDF]

				G Krumschnabel, C Biasi, and W Wieser Action of adenosine on energetics, protein synthesis and K(+) homeostasis in teleost hepatocytes J. Exp. Biol., January 9, 2000; 203(17): 2657 - 2665. [Abstract] [PDF]

				H. S. Ghai and L. T. Buck Acute reduction in whole cell conductance in anoxic turtle brain Am J Physiol Regulatory Integrative Comp Physiol, September 1, 1999; 277(3): R887 - R893. [Abstract] [Full Text] [PDF]

				H. Le Corronc, B. Hue, and R. M. Pitman Ionic Mechanisms Underlying Depolarizing Responses of an Identified Insect Motor Neuron to Short Periods of Hypoxia J Neurophysiol, January 1, 1999; 81(1): 307 - 318. [Abstract] [Full Text] [PDF]

				P. E. Bickler Reduction of NMDA receptor activity in cerebrocortex of turtles (Chrysemys picta) during 6 wk of anoxia Am J Physiol Regulatory Integrative Comp Physiol, July 1, 1998; 275(1): R86 - R91. [Abstract] [Full Text] [PDF]