Increased fMRI connectivity upon chemogenetic inhibition of the mouse prefrontal cortex
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Increased fMRI connectivity upon chemogenetic inhibition of the mouse prefrontal cortex. / Rocchi, Federico; Canella, Carola; Noei, Shahryar; Gutierrez-Barragan, Daniel; Coletta, Ludovico; Galbusera, Alberto; Stuefer, Alexia; Vassanelli, Stefano; Pasqualetti, Massimo; Iurilli, Giuliano; Panzeri, Stefano; Gozzi, Alessandro.
in: NAT COMMUN, Jahrgang 13, Nr. 1, 1056, 25.02.2022.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Increased fMRI connectivity upon chemogenetic inhibition of the mouse prefrontal cortex
AU - Rocchi, Federico
AU - Canella, Carola
AU - Noei, Shahryar
AU - Gutierrez-Barragan, Daniel
AU - Coletta, Ludovico
AU - Galbusera, Alberto
AU - Stuefer, Alexia
AU - Vassanelli, Stefano
AU - Pasqualetti, Massimo
AU - Iurilli, Giuliano
AU - Panzeri, Stefano
AU - Gozzi, Alessandro
N1 - © 2022. The Author(s).
PY - 2022/2/25
Y1 - 2022/2/25
N2 - While shaped and constrained by axonal connections, fMRI-based functional connectivity reorganizes in response to varying interareal input or pathological perturbations. However, the causal contribution of regional brain activity to whole-brain fMRI network organization remains unclear. Here we combine neural manipulations, resting-state fMRI and in vivo electrophysiology to probe how inactivation of a cortical node causally affects brain-wide fMRI coupling in the mouse. We find that chronic inhibition of the medial prefrontal cortex (PFC) via overexpression of a potassium channel increases fMRI connectivity between the inhibited area and its direct thalamo-cortical targets. Acute chemogenetic inhibition of the PFC produces analogous patterns of fMRI overconnectivity. Using in vivo electrophysiology, we find that chemogenetic inhibition of the PFC enhances low frequency (0.1-4 Hz) oscillatory power via suppression of neural firing not phase-locked to slow rhythms, resulting in increased slow and δ band coherence between areas that exhibit fMRI overconnectivity. These results provide causal evidence that cortical inactivation can counterintuitively increase fMRI connectivity via enhanced, less-localized slow oscillatory processes.
AB - While shaped and constrained by axonal connections, fMRI-based functional connectivity reorganizes in response to varying interareal input or pathological perturbations. However, the causal contribution of regional brain activity to whole-brain fMRI network organization remains unclear. Here we combine neural manipulations, resting-state fMRI and in vivo electrophysiology to probe how inactivation of a cortical node causally affects brain-wide fMRI coupling in the mouse. We find that chronic inhibition of the medial prefrontal cortex (PFC) via overexpression of a potassium channel increases fMRI connectivity between the inhibited area and its direct thalamo-cortical targets. Acute chemogenetic inhibition of the PFC produces analogous patterns of fMRI overconnectivity. Using in vivo electrophysiology, we find that chemogenetic inhibition of the PFC enhances low frequency (0.1-4 Hz) oscillatory power via suppression of neural firing not phase-locked to slow rhythms, resulting in increased slow and δ band coherence between areas that exhibit fMRI overconnectivity. These results provide causal evidence that cortical inactivation can counterintuitively increase fMRI connectivity via enhanced, less-localized slow oscillatory processes.
U2 - 10.1038/s41467-022-28591-3
DO - 10.1038/s41467-022-28591-3
M3 - SCORING: Journal article
C2 - 35217677
VL - 13
JO - NAT COMMUN
JF - NAT COMMUN
SN - 2041-1723
IS - 1
M1 - 1056
ER -