Diabetes is well-known to cause both macrovascular and microvascular disease, but is increasingly associated with neurological dysfunction including dementia. Neurovascular coupling (increased regional cerebral blood flow in response to neural activation) is impaired in many neurological diseases including dementia. We therefore established a novel non-invasive zebrafish model allowing simultaneous quantification of cerebrovascular anatomy, neural activation, and cerebral vessel haemodynamics in response to visual stimulus and examined the effect of glucose exposure on cerebrovascular patterning and neurovascular coupling. Combining lightsheet microscopy and compound transgenics to simultaneously visualize neuronal calcium activity and blood flow, we find that zebrafish larvae exhibit neurovascular coupling by 8 days post fertilisation (n=40, p<0.0001 for neuronal calcium activations and p=0.0006 for RBC speed in response to visual stimulation). Using this model, we demonstrate continuous exposure to glucose at levels seen in the blood of poorly controlled diabetics (20mM or 360 mg/dL) impairs neurovascular coupling with reduced RBC speed (n=25, p=0.0008, two-way ANOVA) in the blood vessels of optic tectum (visual processing area in zebrafish). We also show associated cerebrovascular patterning defects such as reduced branch point number (n=20, p<0.0001), vessel length (n=20, p=0.0013) and vessel radius (n=20, p=0.0003), upon glucose treatment. Multiple reports show that nitric oxide (NO) generation is impaired by diabetes. Since both vascular development and neurovascular coupling are NO-dependent, we examined the effect of exposure to the NO donor, Sodium Nitroprusside (SNP), widely used to treat hypertension in humans. Administration of SNP resulted in a marked improvement in the impairment of neurovascular coupling induced by glucose exposure (n=20, p<0.0001) and prevented the glucose induced vascular defects (n=30, p<0.001). Our results establish the first non-mammalian model of neurovascular coupling and reveal a potential strategy to ameliorate the effects of hyperglycemia on cerebrovascular function.