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In vivo and ex vivo dysfunction of neurovascular coupling in a mouse model of subarachnoid hemorrhage (676.3)
Author(s) -
Koide Masayo,
Dunn Kathryn,
Bulkeley Evelyn,
Nelson Mark,
Wellman George
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.676.3
Subject(s) - ex vivo , subarachnoid hemorrhage , vasoconstriction , neurovascular bundle , vasodilation , medicine , in vivo , arteriole , cerebral blood flow , anesthesia , neuroscience , subarachnoid space , cardiology , chemistry , anatomy , microcirculation , biology , cerebrospinal fluid , microbiology and biotechnology
Neurovascular coupling (NVC) represents activity‐dependent focal increases in cerebral blood flow (CBF) crucial for the enhanced delivery of nutrients to maintain brain function in regions of high metabolic demand. We have previously reported inversion of NVC, with neuronal activation causing vasoconstriction rather than vasodilation, in brain slices from subarachnoid hemorrhage (SAH) model rats (Koide et al , 2012). Here, we examined ex vivo NVC, in vivo functional hyperemia and sensory motor function using a mouse endovascular perforation SAH model. In brain slices, astroctyic endfoot Ca 2+ and adjoining parenchymal arteriolar diameter were measured using two‐photon and infrared‐differential interference contrast microscopy. Neuronal activation caused increased endfoot Ca 2+ that was followed by an inverted neurovascular response (i.e. vasoconstriction rather than vasodilation) in ~ 80% of brain slices from day 1 and day 2 SAH mice and ~ 30% of slices from SAH day 4 mice. In vivo functional hyperemia (whisker stimulation‐induced CBF increases) measured by laser Doppler flowmetry in SAH day 1 mice was also significantly attenuated. Consistent with impaired NVC, SAH mice showed a decreased ability to perform sensory motor tasks. These data demonstrate dysfunction of neurovascular coupling occurs both ex vivo and in vivo following SAH, which may contribute to the development of neuronal deficits.Grant Funding Source : Supported by Totman Research Trust, P. Martin Endowment, NIH P01HL095488, P30RR032135 & P30GM103498.