Layer-Specific Dilation of Penetrating Arteries Induced by Stimulation of the Nucleus Basalis of Meynert in the Mouse Frontal Cortex

Author:

Hotta Harumi1,Masamoto Kazuto23,Uchida Sae1,Sekiguchi Yuta4,Takuwa Hiroyuki2,Kawaguchi Hiroshi2,Shigemoto Kazuhiro5,Sudo Ryo4,Tanishita Kazuo4,Ito Hiroshi2,Kanno Iwao2

Affiliation:

1. Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan

2. Molecular Imaging Center, National Institute of Radiological Sciences, Chiba, Japan

3. Center for Frontier Science and Engineering, University of Electro-Communications, Tokyo, Japan

4. School of Integrated Design Engineering, Keio University, Yokohama, Japan

5. Department of Geriatric Medicine, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan

Abstract

To clarify mechanisms through which activation of the nucleus basalis of Meynert (NBM) increases cerebral cortical blood flow, we examined whether cortical parenchymal arteries dilate during NBM stimulation in anesthetized mice. We used two-photon microscopy to measure the diameter of single penetrating arteries at different depths (~800 μm, layers I to V) of the frontal cortex, and examined changes in the diameter during focal electrical stimulation of the NBM (0.5 ms at 30 to 50 μA and 50 Hz) and hypercapnia (3% CO2 inhalation). Stimulation of the NBM caused diameter of penetrating arteries to increase by 9% to 13% of the prestimulus diameter throughout the different layers of the cortex, except at the cortical surface and upper part of layer V, where the diameter of penetrating arteries increased only slightly during NBM stimulation. Hypercapnia caused obvious dilation of the penetrating arteries in all cortical layers, including the surface arteries. The diameters began to increase within 1 second after the onset of NBM stimulation in the upper cortical layers, and later in lower layers. Our results indicate that activation of the NBM dilates cortical penetrating arteries in a layer-specific manner in magnitude and latency, presumably related to the density of cholinergic nerve terminals from the NBM.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Neurology (clinical),Neurology

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