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Optogenetic astrocyte activation evokes BOLD fMRI response with oxygen consumption without neuronal activity modulation
Author(s) -
Takata Norio,
Sugiura Yuki,
Yoshida Keitaro,
Koizumi Miwako,
Hiroshi Nishida,
Honda Kurara,
Yano Ryutaro,
Komaki Yuji,
Matsui Ko,
Suematsu Makoto,
Mimura Masaru,
Okano Hideyuki,
Tanaka Kenji F.
Publication year - 2018
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.23454
Subject(s) - astrocyte , neuroscience , optogenetics , premovement neuronal activity , functional magnetic resonance imaging , electrophysiology , biology , neuron , functional imaging , blood oxygenation , biological neural network , central nervous system
Functional magnetic resonance imaging (fMRI) based on the blood oxygenation level‐dependent (BOLD) signal has been used to infer sites of neuronal activation in the brain. A recent study demonstrated, however, unexpected BOLD signal generation without neuronal excitation, which led us to hypothesize the presence of another cellular source for BOLD signal generation. Collective assessment of optogenetic activation of astrocytes or neurons, fMRI in awake mice, electrophysiological measurements, and histochemical detection of neuronal activation, coherently suggested astrocytes as another cellular source. Unexpectedly, astrocyte‐evoked BOLD signal accompanied oxygen consumption without modulation of neuronal activity. Imaging mass spectrometry of brain sections identified synthesis of acetyl‐carnitine via oxidative glucose metabolism at the site of astrocyte‐, but not neuron‐evoked BOLD signal. Our data provide causal evidence that astrocytic activation alone is able to evoke BOLD signal response, which may lead to reconsideration of current interpretation of BOLD signal as a marker of neuronal activation.