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Involvement of adenosine in depression of synaptic transmission during hypercapnia in isolated spinal cord of neonatal rats
Author(s) -
Otsuguro Kenichi,
Yamaji Yoshihiko,
Ban Masaaki,
Ohta Toshio,
Ito Shigeo
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.109660
Subject(s) - hypercapnia , adenosine , acidosis , anesthesia , reflex , endocrinology , medicine , adenosine kinase , adenosine receptor , adenosine deaminase , receptor , agonist
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% CO 2 , pH 6.7) reversibly depressed electrically evoked spinal reflex potentials. This depression was partially reversed by 8‐cyclopentlyl‐1,3‐dimethylxanthine (CPT), a selective A 1 adenosine receptor antagonist. Isohydric hypercapnia (20% CO 2 , pH 7.3), but not isocapnic acidosis (5% CO 2 , 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 A 1 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.