title: Pial arteries respond earlier than penetrating arterioles to neural activation in the somatosensory cortex in awake mice exposed to chronic hypoxia: an additional mechanism to proximal integration signaling?
abstract: The pial and penetrating arteries have a crucial role in regulating cerebral blood flow (CBF) to meet neural demand in the cortex. Here, we examined the longitudinal effects of chronic hypoxia on the arterial diameter responses to single whisker stimulation in the awake mouse cortex, where activity-induced responses of CBF were gradually attenuated. The vasodilation responses to whisker stimulation under prehypoxia normal conditions were 8.1% and 12% relative to their baselines in the pial arteries and penetrating arterioles, respectively. After 3 weeks of hypoxia, however, these responses were significantly reduced to 5.5% and 4.1%, respectively. The CBF response, measured using laser-Doppler flowmetry (LDF), induced by the same whisker stimulation was also attenuated (14% to 2.6%). A close linear correlation was found for the responses between the penetrating arteriolar diameter and LDF, and their temporal dynamics. After 3 weeks of chronic hypoxia, the initiation of vasodilation in the penetrating arterioles was significantly extended, but the pial artery responses remained unchanged. These results show that vasodilation of the penetrating arterioles followed the pial artery responses, which are not explainable in terms of proximal integration signaling. The findings therefore indicate an additional mechanism for triggering pial artery dilation in the neurovascular coupling.
authors: 1] School of Integrated Design Engineering, Keio University, Yokohama, Japan [2] Molecular Imaging Center, National Institute of Radiological Sciences, Inage, Chiba, Japan.
authors: Yuta
authors: Y
authors: Sekiguchi
authors: Molecular Imaging Center, National Institute of Radiological Sciences, Inage, Chiba, Japan.
authors: Hiroyuki
authors: H
authors: Takuwa
authors: Molecular Imaging Center, National Institute of Radiological Sciences, Inage, Chiba, Japan.
authors: Hiroshi
authors: H
authors: Kawaguchi
authors: Department of Electronics and Electrical Engineering, Keio University, Yokohama, Japan.
authors: Takahiro
authors: T
authors: Kikuchi
authors: Department of Electronics and Electrical Engineering, Keio University, Yokohama, Japan.
authors: Eiji
authors: E
authors: Okada
authors: Molecular Imaging Center, National Institute of Radiological Sciences, Inage, Chiba, Japan.
authors: Iwao
authors: I
authors: Kanno
authors: Molecular Imaging Center, National Institute of Radiological Sciences, Inage, Chiba, Japan.
authors: Hiroshi
authors: H
authors: Ito
authors: Department of Neurology, School of Medicine Keio University, Shinjuku, Tokyo, Japan.
authors: Yutaka
authors: Y
authors: Tomita
authors: Department of Neurology, School of Medicine Keio University, Shinjuku, Tokyo, Japan.
authors: Yoshiaki
authors: Y
authors: Itoh
authors: Department of Neurology, School of Medicine Keio University, Shinjuku, Tokyo, Japan.
authors: Norihiro
authors: N
authors: Suzuki
authors: 1] School of Integrated Design Engineering, Keio University, Yokohama, Japan [2] Department of System Design Engineering, Keio University, Yokohama, Japan.
authors: Ryo
authors: R
authors: Sudo
authors: 1] School of Integrated Design Engineering, Keio University, Yokohama, Japan [2] Department of System Design Engineering, Keio University, Yokohama, Japan.
authors: Kazuo
authors: K
authors: Tanishita
authors: 1] Molecular Imaging Center, National Institute of Radiological Sciences, Inage, Chiba, Japan [2] Brain Science Inspired Life Support Research Center, University of Electro-Communications, Chofu, Tokyo, Japan.
authors: Kazuto
authors: K
authors: Masamoto
mesh_terms: D000818:Animals; D001160:Arterioles / Q000502:physiology; D001783:Blood Flow Velocity / Q000502:physiology; D002536:Cerebral Arteries / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D009474:Neurons / Q000378:metabolism; D013003:Somatosensory Cortex / Q000098:blood supply* / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*; D014851:Wakefulness / Q000502:physiology*