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Neurovascular 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 somato-sensory 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-haemoglobin. The results indicate a delicate balance that exists between GABA and NPY when n-NOS interneurons are activated mediated by NO. Whereas somato-sensory 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 substantiallyfrom the short pulses of 2 seconds as used in the above experiments.