PV interneurons evoke astrocytic Ca2+ responses in awake mice, which contributes to neurovascular coupling.
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PV interneurons evoke astrocytic Ca2+ responses in awake mice, which contributes to neurovascular coupling. / Krogsgaard, Aske; Sperling, Leonora; Dahlqvist, Matilda; Thomsen, Kirsten; Vydmantaite, Gabriele; Li, Fangyuan; Thunemann, Martin; Lauritzen, Martin; Lind, Barbara Lykke.
In: Glia, Vol. 71, No. 8, 2023.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - PV interneurons evoke astrocytic Ca2+ responses in awake mice, which contributes to neurovascular coupling.
AU - Krogsgaard, Aske
AU - Sperling, Leonora
AU - Dahlqvist, Matilda
AU - Thomsen, Kirsten
AU - Vydmantaite, Gabriele
AU - Li, Fangyuan
AU - Thunemann, Martin
AU - Lauritzen, Martin
AU - Lind, Barbara Lykke
N1 - © 2023 The Authors. GLIA published by Wiley Periodicals LLC.
PY - 2023
Y1 - 2023
N2 - Neurovascular coupling (NVC) modulates cerebral blood flow to match increased metabolic demand during neuronal excitation. Activation of inhibitory interneurons also increase blood flow, but the basis for NVC caused by interneurons is unclear. While astrocyte Ca 2+ levels rise with excitatory neural transmission, much less is known with regards to astrocytic sensitivity to inhibitory neurotransmission. We performed two-photon microscopy in awake mice to examine the correlation between astrocytic Ca 2+ and NVC, evoked by activation of either all (VGAT IN ) or only parvalbumin-positive GABAergic interneurons (PV IN ). Optogenetic stimulation of VGAT IN and PV IN in the somatosensory cortex triggered astrocytic Ca 2+ increases that were abolished by anesthesia. In awake mice, PV IN evoked astrocytic Ca 2+ responses with a short latency that preceded NVC, whereas VGAT IN evoked Ca 2+ increases that were delayed relative to the NVC response. The early onset of PV IN evoked astrocytic Ca 2+ increases depended on noradrenaline release from locus coeruleus as did the subsequent NVC response. Though the relationship between interneuron activity and astrocytic Ca 2+ responses is complex, we suggest that the rapid astrocyte Ca 2+ responses to increased PV IN activity shaped the NVC. Our results underline that interneuron and astrocyte-dependent mechanisms should be studied in awake mice.
AB - Neurovascular coupling (NVC) modulates cerebral blood flow to match increased metabolic demand during neuronal excitation. Activation of inhibitory interneurons also increase blood flow, but the basis for NVC caused by interneurons is unclear. While astrocyte Ca 2+ levels rise with excitatory neural transmission, much less is known with regards to astrocytic sensitivity to inhibitory neurotransmission. We performed two-photon microscopy in awake mice to examine the correlation between astrocytic Ca 2+ and NVC, evoked by activation of either all (VGAT IN ) or only parvalbumin-positive GABAergic interneurons (PV IN ). Optogenetic stimulation of VGAT IN and PV IN in the somatosensory cortex triggered astrocytic Ca 2+ increases that were abolished by anesthesia. In awake mice, PV IN evoked astrocytic Ca 2+ responses with a short latency that preceded NVC, whereas VGAT IN evoked Ca 2+ increases that were delayed relative to the NVC response. The early onset of PV IN evoked astrocytic Ca 2+ increases depended on noradrenaline release from locus coeruleus as did the subsequent NVC response. Though the relationship between interneuron activity and astrocytic Ca 2+ responses is complex, we suggest that the rapid astrocyte Ca 2+ responses to increased PV IN activity shaped the NVC. Our results underline that interneuron and astrocyte-dependent mechanisms should be studied in awake mice.
U2 - 10.1002/glia.24370
DO - 10.1002/glia.24370
M3 - Journal article
C2 - 36994892
VL - 71
JO - GLIA
JF - GLIA
SN - 0894-1491
IS - 8
ER -
ID: 341262579