量研学術機関リポジトリ「QST-Repository」は、国立研究開発法人 量子科学技術研究開発機構に所属する職員等が生み出した学術成果（学会誌発表論文、学会発表、研究開発報告書、特許等）を集積しインターネット上で広く公開するサービスです。 Welcome to QST-Repository where we accumulates and discloses the academic research results(Journal Publications, Conference presentation, Research and Development Report, Patent, etc.) of the members of National Institutes for Quantum Science and Technology.
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The effects of prolonged moderate hypoxia on the neurovascular coupling were examined in mice. One week before the experiments a cranial window was opened above the somatosensory cortex of C57BL/6J mice. The mice were slowly adapted (in 1.5 hours at first) into a hypoxia chamber (2.4 L) with two hypoxia levels (8% oxygen (n=6) and 10% oxygen (n=5)) for one month. Two of the 8% oxygen mice were further kept alive for another two months in room air. Cortical CBF responses to air puffs (10Hz for 20 sec) were weekly measured using LDF. All measurements were done in awake and the mice kept free motion on a floating ball. The cranial window was fixed to the stage of a two-photon microscope and 3D images with 0.5 micrometer x-y resolution were acquired individually at the same parenchymal location after intraperitoneal injection of sulforhodamine 101 as fluorescent dye. Hematocrit at week 1, 2 and one month was measured using separate mice of 8% oxygen. The 8% oxygen mice revealed a declined CBF responses week-by-week from 25% to < 5% in one month, though the 10% oxygen mice showed almost consistent CBF responses around 25% over one month. The two 8% oxygen mice kept alive for another two months in room air demonstrated sustained failure of CBF response. In 8% oxygen mice, the hematocrit was increased from 35 to 68 in one month. Since locomotion levels evoked by air-puffs were unchanged during the experiment period for both the 8% and 10% oxygen groups, it is plausible that the cortical neuronal function was intact during course of the experiment. Morphological change to the microvessels may not be a possible explanation for the decreased CBF response because the failure was sustained even when the microvessel diameter returned to the baseline level after the mice to room air for more than two months. However, the 8% oxygen mice demonstrated gradual increase in astroglia cell areas by 50%. Therefore, the failure of the neurovascular coupling might be caused by disruption of signal transmission between the neuron and the microvessel, e.g. malfunction in the pathways either from neuron to astroglia, from astroglia to the endothelium, or from endothelium to smooth muscle. Further experiments are necessary to confirm and clarify these questions, that is, measurements of cortical neuronal activity, and vascular responses to carbon dioxide (CO2) and/or to sodium nitroprusside (SNP; NO donor). In conclusion, circumstance to 8% oxygen for one month induced to fail the CBF response to somatosensory stimulation in mice. This could be used as a new model to study inhibition of the neurovascular coupling.
Persistent failure of neurovascular coupling induced by prolonged moderate hypoxia in the somatosensory cortex in mice
