Neural computation is highly energy demanding: the brain consumes 20% of the body’s resting energy production despite being only 2% of its mass. To use the available energy efficiently the brain has evolved mechanisms, termed neurovascular coupling, which increase the blood flow, and hence the energy supply, specifically to regions where there are active neurons. Control of blood flow occurs at the arteriole level mediated by smooth muscle, but may also occur at the capillary level mediated by isolated contractile cells called pericytes. I will report experiments on rat cerebellar slices investigating the signalling pathways by which neurons and astrocytes control blood flow at the capillary level, and studying how pericytes malfunction in diseases such as stroke. Application of noradrenaline constricts cerebellar capillaries at pericyte locations, and superimposing glutamate (to mimic neuronal activity) causes a dilation. The dilation evoked by glutamate is inhibited by blocking nitric oxide synthase (with L-nitroarginine) but unaffected by blocking guanylate cyclase (with ODQ) implying that glutamate and NO do not dilate via the cGMP pathway. The effect of NO synthase block was abolished by inhibiting production of 20-HETE (using HET0016), and glutamate-evoked dilation was still seen with NO and 20-HETE production blocked. Thus, NO acts by suppressing production of 20-HETE. Blocking EET production (with MSPPOH) had no effect on the glutamate-evoked dilation while blocking prostaglandin EP4 receptors (with L-161,982) abolished it. These data suggest that glutamate dilates capillaries via a prostaglandin pathway, but also requires NO release to suppress release of vasoconstricting 20-HETE. Patch-clamping cerebellar molecular layer pericytes revealed that glutamate or parallel fibre stimulation evoked an outward current that would be expected to hyperpolarize the cell and thus evoke dilation. Parallel fibre stimulation (12 Hz for 10 sec) evoked a capillary dilation with an onset (in 20% O2) after 4.5 sec and a maximum after 22 sec. Some pericytes constrict in ischaemia. We found that an hour’s simulated ischaemia of cerebellar slices led to ~90% of pericytes dying. Blocking either NMDA receptors with 50 μM D-AP5, MK-801 and 5-chlorokynurenate, or AMPA/kainate receptors with NBQX, reduced the death by half. These data suggest that death of pericytes, while they are in rigor after an ischaemia-evoked [Ca2+]i rise, may contribute to the long-lasting decrease of cerebral blood flow that occurs after ischaemia even when an occluded vessel is made patent again.