open access

https://hdl.handle.net/2115/49925

Differential contributions of adenosine to hypoxia-evoked depressions of three neuronal pathways in isolated spinal cord of neonatal rats

英語

spinal cord

2011-09

Blackwell Publishing

British Journal of Pharmacology

164(1)

132-144

Background and purpose: Hypoxic effects on neuronal functions drastically vary with experimental conditions, but its mechanism is unclear. Adenosine has been reported to play a key role in depression of neuronal activities in the CNS during acute hypoxia. In this study, we examined the effect of acute hypoxia on different spinal reflex potentials and the contribution of adenosine to them. Experimental approach: Spinal reflex potentials, monosynaptic reflex potential (MSR), slow ventral root potential (sVRP) and dorsal root potential (DRP), were measured in the isolated spinal cord of the neonatal rat. Adenosine release was measured by using enzymatic biosensors. Key results: In the spinal cord preparation isolated from postnatal day 5-8 (P5-8) rats at 27℃, acute hypoxia released adenosine and depressed three reflex potentials. However, in postnatal day 0-3 (P0-3) rats at 27℃, the hypoxic adenosine release and depression of MSR were negligible, while the depression of sVRP and DRP were perceptible responses. In P0-3 rats at 33℃, hypoxia evoked adenosine release and depression of MSR. An adenosine A1 receptor selective antagonist and a high [Ca2+]o, which suppressed adenosine release, abolished the hypoxic depression of MSR but not those of sVRP and DRP. Conclusions and implications: These results indicate that the hypoxic depression of MSR depends on adenosine release, which is highly susceptible to age, temperature and [Ca2+]o. On the other hand, a large part of the depressions of DRP and sVRP were mediated via adenosine-independent mechanisms. This differential contribution of adenosine to depression is suggested to be an important factor for the varying influence of hypoxia on neuronal functions.

学術雑誌論文

Accepted Manuscript

The definitive version is available at www.interscience.wiley.com

0007-1188