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dc.contributor.authorDavid, Tim
dc.contributor.authorMorillo, Robin
dc.contributor.authorHowarth, Clare
dc.contributor.authorBerwick, Jason
dc.contributor.authorLee, Llywelyn
dc.date.accessioned2023-08-16T18:36:16Z
dc.date.available2023-08-16T18:36:16Z
dc.date.copyright12/14/2022 12:00:00 AM
dc.date.issued2022
dc.identifier.issn0148-0731
dc.identifier.otherbio_145_03_031007.pdf
dc.identifier.urihttp://yetl.yabesh.ir/yetl1/handle/yetl/4292200
dc.description.abstractNeurovascular coupling (NVC) is the ability to locally adjust vascular resistance as a function of neuronal activity. Recent experiments have illustrated that NVC is partially independent of metabolic signals. In addition, nitric oxide (NO) has been shown in some instances to provide an important mechanism in altering vascular resistance. An extension to the original model of NVC [1] has been developed to include the activation of both somatosensory neurons and GABAergic interneurons and to investigate the role of NO and the delicate balance of GABA and neuronal peptide enzymes (NPY) pathways. The numerical model is compared to murine experimental data that provides time-dependent profiles of oxy, de-oxy, and total-hemoglobin. The results indicate a delicate balance that exists between GABA and NPY when nNOS interneurons are activated mediated by NO. Whereas somatosensory neurons (producing potassium into the extracellular space) do not seem to be effected by the inhibition of NO. Further work will need to be done to investigate the role of NO when stimulation periods are increased substantially from the short pulses of 2 s as used in the above experiments.
dc.publisherThe American Society of Mechanical Engineers (ASME)
dc.titleThe Reversal Characteristics of GABAergic Neurons: A Neurovascular Model
dc.typeJournal Paper
dc.journal.volume145
dc.journal.issue3
dc.journal.titleJournal of Biomechanical Engineering
dc.identifier.doi10.1115/1.4056336
dc.journal.fristpage31007-1
dc.journal.lastpage31007-6
dc.page6
dc.treeJournal of Biomechanical Engineering:;2022:;volume( 145 ):;issue: 003
dc.contenttypeFulltext


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