Contributions of structural connectivity and cerebrovascular parameters to functional magnetic resonance imaging signals in mice at rest and during sensory paw stimulation.
Previously, we reported widespread bilateral increases in stimulus-evoked functional magnetic resonance imaging signals in mouse brain to unilateral sensory paw stimulation. We attributed the pattern to arousal-related cardiovascular changes overruling cerebral autoregulation thereby masking specific signal changes elicited by local neuronal activity. To rule out the possibility that interhemispheric neuronal communication might contribute to bilateral functional magnetic resonance imaging responses, we compared stimulus-evoked functional magnetic resonance imaging responses to unilateral hindpaw stimulation in acallosal I/LnJ, C57BL/6, and BALB/c mice. We found bilateral blood-oxygenation-level dependent signal changes in all three strains, ruling out a dominant contribution of transcallosal communication as reason for bilaterality. Analysis of functional connectivity derived from resting-state functional magnetic resonance imaging, revealed that bilateral cortical functional connectivity is largely abolished in I/LnJ animals. Cortical functional connectivity in all strains correlated with structural connectivity in corpus callosum as revealed by diffusion tensor imaging. Given the profound influence of systemic hemodynamics on stimulus-evoked functional magnetic resonance imaging outcomes, we evaluated whether functional connectivity data might be affected by cerebrovascular parameters, i.e. baseline cerebral blood volume, vascular reactivity, and reserve. We found that effects of cerebral hemodynamics on functional connectivity are largely outweighed by dominating contributions of structural connectivity. In contrast, contributions of transcallosal interhemispheric communication to the occurrence of ipsilateral functional magnetic resonance imaging response of equal amplitude to unilateral stimuli seem negligible.
1 Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland.|2 Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland.
Aileen
A
Schroeter
1 Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland.|2 Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland.
Joanes
J
Grandjean
1 Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland.|2 Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland.
Felix
F
Schlegel
2 Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland.|3 Preclinical Laboratory for Translational Research into Affective Disorders, University of Zurich Hospital for Psychiatry, Zurich, Switzerland.
Bechara J
BJ
Saab
1 Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland.|2 Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland.|4 Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland.
Markus
M
Rudin
D000818:Animals; D001921:Brain / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D001931:Brain Mapping / Q000379:methods*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004558:Electric Stimulation; D005073:Evoked Potentials, Somatosensory / Q000502:physiology*; D005260:Female; D006339:Heart Rate / Q000502:physiology; D035002:Lower Extremity / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D012018:Reflex / Q000502:physiology
anesthesia; animal models; blood-oxygenation-level dependent contrast; brain imaging; cerebral blood flow; cerebral hemodynamics; diffusion tensor imaging; functional magnetic resonance imaging; imaging; magnetic resonance; magnetic resonance imaging; physiology