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This Article Full Text Full Text (PDF) All Versions of this Article: 574/3/835    most recent jphysiol.2006.109660v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Otsuguro, K.-i. Articles by Ito, S. Search for Related Content PubMed PubMed Citation Articles by Otsuguro, K.-i. Articles by Ito, S. Related Collections Neuroscience

¹ Laboratory of Pharmacology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan

Adenosine is one of the most important neuromodulators in the CNS, both under physiological and pathological conditions. In the isolated spinal cord of the neonatal rat in vitro, acute hypercapnic acidosis (20% CO₂, pH 6.7) reversibly depressed electrically evoked spinal reflex potentials. This depression was partially reversed by 8-cyclopentlyl-1,3-dimethylxanthine (CPT), a selective A₁ adenosine receptor antagonist. Isohydric hypercapnia (20% CO₂, pH 7.3), but not isocapnic acidosis (5% CO₂, pH 6.7), depressed the reflex potentials, which were also reversed by CPT. An ecto-5'-nucleotidase inhibitor did not affect the hypercapnic acidosis-evoked depression. An inhibitor of adenosine kinase, but not deaminase, mimicked the inhibitory effect of hypercapnic acidosis on the spinal reflex potentials. Accumulation of extracellular adenosine and inhibition of adenosine kinase activity were caused by hypercapnic acidosis and isohydric hypercapnia, but not isohydric acidosis. These results indicate that the activation of adenosine A₁ receptors is involved in the hypercapnia-evoked depression of reflex potentials in the isolated spinal cord of the neonatal rat. The inhibition of adenosine kinase activity is suggested to cause the accumulation of extracellular adenosine during hypercapnia.

(Received 13 March 2006; accepted after revision 28 May 2006; first published online 1 June 2006)
Corresponding author K. Otsuguro: Laboratory of Pharmacology, Graduate School of Veterinary Medicine, Hokkaido University, Kita 18, Nishi 9, Kita-ku, Sapporo 060-0818, Japan. Email: otsuguro{at}vetmed.hokudai.ac.jp

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