This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Caffeine is the most widely used neurostimulant in the world and is found in a variety of foods and beverages. Caffeine blocks adenosine receptors and acts not only as a nervous system stimulant but also as a vasoconstrictor. Recent studies have suggested that adenosine antagonists, such as caffeine, increase the blood oxygenation level dependent (BOLD) signal in functional magnetic resonance (fMRI) studies. It has been proposed that this enhancement of the BOLD signal is due to a decrease in resting brain blood flow. However, there are multiple other studies demonstrating that changes in baseline blood flow in the brain do not consistently strengthen the BOLD signal. It is well known that chronic caffeine use causes an increase in the number of adenosine receptors, and it has been shown that in a withdrawal state, a dose of caffeine has different effects on resting cerebral blood flow and BOLD signal changes. The effects of caffeine on BOLD fMRI measures are of considerable interest because caffeine affects both brain cell activity and blood flow in the brain. There remains a significant knowledge gap concerning the contribution of neural and vascular adenosine responses to the BOLD signal. The studies proposed here will clarify the published literature and determine if caffeine is an effective BOLD signal enhancer (regardless of dietary caffeine consumption). In addition, these studies will provide much needed insights into the adenosine receptor sub-system (neural vs. vascular) that are responsible for the observed findings.
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