TY - JOUR
T1 - Hemodynamic changes during neural deactivation in awake mice
T2 - A measurement by laser-Doppler flowmetry in crossed cerebellar diaschisis
AU - Takuwa, Hiroyuki
AU - Tajima, Yosuke
AU - Kokuryo, Daisuke
AU - Matsuura, Tetsuya
AU - Kawaguchi, Hiroshi
AU - Masamoto, Kazuto
AU - Taniguchi, Junko
AU - Ikoma, Yoko
AU - Seki, Chie
AU - Aoki, Ichio
AU - Tomita, Yutaka
AU - Suzuki, Norihiro
AU - Kanno, Iwao
AU - Ito, Hiroshi
N1 - Funding Information:
The assistance of members of the National Institute of Radiological Sciences in performing the LDF experiments is gratefully acknowledged. This work was partially supported by a Grant-in-Aid for Scientific Research to T. M. from the Japan Society for the Promotion of Science . The authors thank Sayaka Shibata, Aiko Sekita and Nobuhiro Nitta for the MRI experiments.
PY - 2013/11/6
Y1 - 2013/11/6
N2 - Crossed cerebellar diaschisis (CCD) caused by contralateral supratentorial lesions can be considered a condition of neural deactivation, and hemodynamic changes in CCD were investigated with positron emission tomography (PET) in humans. In the present study, to investigate the effects of neural deactivation on hemodynamics, we developed a new mouse model of CCD, which was caused by middle cerebral artery occlusion (MCAO), and measured changes in cerebellar blood flow (CbBF), red blood cell (RBC) velocity and concentration due to CCD using laser-Doppler flowmetry (LDF) in awake mice. The ratio of the CCD side to the unaffected side in the cerebellum for CbBF 1 day after MCAO was decreased by -18% compared to baseline (before CCD). The ratio of the CCD side to the unaffected side for RBC concentration 1 day after MCAO was decreased by -23% compared to baseline. However, no significant changes in the ratio of the CCD side to the unaffected side were observed for RBC velocity. The present results indicate that the reduction of CbBF induced by neural deactivation was mainly caused by the decrease in RBC concentration. In contrast, our previous study showed that RBC velocity had a dominant role in the increase in cerebral blood flow (CBF) induced by neural activation. If RBC concentration can be considered an indicator of cerebral blood volume (CBV), hemodynamic changes due to neural activation and deactivation measured by LDF in mice might be in good agreement with human PET studies.
AB - Crossed cerebellar diaschisis (CCD) caused by contralateral supratentorial lesions can be considered a condition of neural deactivation, and hemodynamic changes in CCD were investigated with positron emission tomography (PET) in humans. In the present study, to investigate the effects of neural deactivation on hemodynamics, we developed a new mouse model of CCD, which was caused by middle cerebral artery occlusion (MCAO), and measured changes in cerebellar blood flow (CbBF), red blood cell (RBC) velocity and concentration due to CCD using laser-Doppler flowmetry (LDF) in awake mice. The ratio of the CCD side to the unaffected side in the cerebellum for CbBF 1 day after MCAO was decreased by -18% compared to baseline (before CCD). The ratio of the CCD side to the unaffected side for RBC concentration 1 day after MCAO was decreased by -23% compared to baseline. However, no significant changes in the ratio of the CCD side to the unaffected side were observed for RBC velocity. The present results indicate that the reduction of CbBF induced by neural deactivation was mainly caused by the decrease in RBC concentration. In contrast, our previous study showed that RBC velocity had a dominant role in the increase in cerebral blood flow (CBF) induced by neural activation. If RBC concentration can be considered an indicator of cerebral blood volume (CBV), hemodynamic changes due to neural activation and deactivation measured by LDF in mice might be in good agreement with human PET studies.
KW - Awake animal
KW - Cerebellar blood flow
KW - Crossed cerebellar diaschisis
KW - Neuronal deactivation
KW - Red blood cell concentration
KW - Red blood cell velocity
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U2 - 10.1016/j.brainres.2013.09.023
DO - 10.1016/j.brainres.2013.09.023
M3 - Article
C2 - 24076448
AN - SCOPUS:84887222742
VL - 1537
SP - 350
EP - 355
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
ER -