Er... at least two persons read this blag! Awesome!
And on top of that, at least one of them can explain blood oxygen level dependent fMRI signals better than I can:
The BOLD fMRI signal observed in brain activation is from a measurement of the relative quantities of oxy and deoxyhemoglobin. Vasodilation increases blood flow in the activated regions and that changed oxy/deoxy ratio is what is observed.You can't sum it more simply and accurately than that. I looked at Baylor College's "What is fMRI?" page and found a slightly more detailed summary. It works on the principal of neurovascular coupling - basically, when an area of your brain becomes active, the blood vessels in that area dilate (presumably in order to get more fuel - food and oxygen - to the active cells). When the blood vessels dilate, more oxygenated blood rushes into that area. The relatively higher concentrations of oxygenated blood compared to deoxygenated blood in that area can be detected with a functional magnetic resonance imaging device - an fMRI.
But wait! There's more!
Vasodilation is controlled by NO.NO, or Nitric Oxide, is a gaseous chemical messenger in your body. It is well-known (to dorks like me) as the endothelium-derived relaxing factor. Now if you knew that the endothelium is the technical name for the tissue lining your blood vessels, you could reason that NO is produced by your blood vessels and "relaxes". Which is absolutely spot-on.
The regions of activation observed in BOLD fMRI are actually regions of NO, where the prompt neurogenic NO release is high enough to cause vasodilation by activating sGC. That NO does things besides vasodilation. Those things are not understood. I think that those things are actually more important than the increased O2 consumption.
It is well established that the O2 delivery by the increased blood flow exceeds the metabolic requirements of the activated region.
Production of NO in this specific context can be set off by a bunch of factors, mainly the ones that would indicate that you needed more blood-flow capacity (strain, certain immune system factors). It seems to act by setting off a G-protein cascade ending with phosphorylating a handful of proteins, with the effect (very generally speaking) of relaxing the smooth muscle around the blood vessel, and thus dilating the vessel.
NO does have differing effects on different tissues (as could be said about pretty much any substance), and it is certainly true that we do not know all of NO's possible effects.
There is apparently an international conference on NO/cGMP interactions, with a lot of stuff posted online if you'd care to slog through it. The takeaway message is: physiology is fuckin' complicated.
While poking around the internet pondering this, I found this paper from the Journal of Neuroscience online. The experiments involved neurovascular coupling, and one focuses on NO specifically as a modulator. The result: when NO is removed (by inhibiting its production), you see only vasodilation in rat retinal neurons. In this case NO acts to cause vasoconstriction in neural blood vessels.
That may sound weird, but the mechanism for how blood vessels dilate in the body may be drastically different from how blood vessels dilate in the brain. Mostly because the brain has special needs. Delicate system of interconnected neurons, and all that. Maybe couldn't handle the strains if the blood vessels just regulated themselves willy-nilly. The paper suggests that glia, the support cells in the brain, have an important role in regulating blood flow.
NO is itself a used as a neurotransmitter both in the brain and in the rest of your body. And it has a buttload of known or hypothesized effects, which you could peruse at your leisure if you're so inclined.
Thank you for the comment, daedalus2u!