Astrocytes amplify neurovascular coupling to sustained activation of neocortex in awake mice

Adam Institoris, Milène Vandal, Govind Peringod, Christy Catalano, Cam Ha Tran, Xinzhu Yu, Frank Visser, Cheryl Breiteneder, Leonardo Molina, Baljit S. Khakh, Minh Dang Nguyen, Roger J. Thompson and Grant R. Gordon ()
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Adam Institoris: University of Calgary
Milène Vandal: University of Calgary
Govind Peringod: University of Calgary
Christy Catalano: University of Calgary
Cam Ha Tran: University of Calgary
Xinzhu Yu: University of California Los Angeles
Frank Visser: University of Calgary
Cheryl Breiteneder: University of Calgary
Leonardo Molina: University of Calgary
Baljit S. Khakh: University of California Los Angeles
Minh Dang Nguyen: University of Calgary
Roger J. Thompson: University of Calgary
Grant R. Gordon: University of Calgary

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: Abstract Functional hyperemia occurs when enhanced neuronal activity signals to increase local cerebral blood flow (CBF) to satisfy regional energy demand. Ca2+ elevation in astrocytes can drive arteriole dilation to increase CBF, yet affirmative evidence for the necessity of astrocytes in functional hyperemia in vivo is lacking. In awake mice, we discovered that functional hyperemia is bimodal with a distinct early and late component whereby arteriole dilation progresses as sensory stimulation is sustained. Clamping astrocyte Ca2+ signaling in vivo by expressing a plasma membrane Ca2+ ATPase (CalEx) reduces sustained but not brief sensory-evoked arteriole dilation. Elevating astrocyte free Ca2+ using chemogenetics selectively augments sustained hyperemia. Antagonizing NMDA-receptors or epoxyeicosatrienoic acid production reduces only the late component of functional hyperemia, leaving brief increases in CBF to sensory stimulation intact. We propose that a fundamental role of astrocyte Ca2+ is to amplify functional hyperemia when neuronal activation is prolonged.

Date: 2022
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DOI: 10.1038/s41467-022-35383-2

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