Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 350-355 |
| Number of pages | 6 |
| Journal | Brain Research |
| Volume | 1537 |
| DOIs | |
| Publication status | Published - 2013 Nov 6 |
Fingerprint
Keywords
- Awake animal
- Cerebellar blood flow
- Crossed cerebellar diaschisis
- Neuronal deactivation
- Red blood cell concentration
- Red blood cell velocity
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Neurology
- Developmental Biology
- Molecular Biology
Cite this
Hemodynamic changes during neural deactivation in awake mice : A measurement by laser-Doppler flowmetry in crossed cerebellar diaschisis. / Takuwa, Hiroyuki; Tajima, Yosuke; Kokuryo, Daisuke; Matsuura, Tetsuya; Kawaguchi, Hiroshi; Masamoto, Kazuto; Taniguchi, Junko; Ikoma, Yoko; Seki, Chie; Aoki, Ichio; Tomita, Yutaka; Suzuki, Norihiro; Kanno, Iwao; Ito, Hiroshi.
In: Brain Research, Vol. 1537, 06.11.2013, p. 350-355.Research output: Contribution to journal › Article
}
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
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
UR - http://www.scopus.com/inward/record.url?scp=84887222742&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84887222742&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2013.09.023
DO - 10.1016/j.brainres.2013.09.023
M3 - Article
VL - 1537
SP - 350
EP - 355
JO - Brain Research
JF - Brain Research
SN - 0006-8993
ER -