THE EFFECT OF CAFFIENE ON BRAIN IMAGING

咖啡因对大脑成像的影响

• 批准号: 7376711
• 负责人: Paul Laurienti
• 金额: $ 2.18万
• 依托单位: WAKE FOREST UNIVERSITY HEALTH SCIENCES
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-17 至 2007-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7376711
• 关键词: blood; brain; caffeine; purinergic receptor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for 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.

该子项目是利用 NIH/NCRR 资助的中心拨款提供的资源的众多研究子项目之一。子项目和研究者 (PI) 可能已从另一个 NIH 来源获得主要资金，因此可以在其他 CRISP 条目中出现。列出的机构是中心的机构，不一定是研究者的机构。咖啡因是世界上使用最广泛的神经兴奋剂，存在于各种食品和饮料中。咖啡因会阻断腺苷受体，不仅可以作为神经系统兴奋剂，还可以作为血管收缩剂。最近的研究表明，腺苷拮抗剂（例如咖啡因）可以增加功能磁共振（fMRI）研究中的血氧水平依赖性（BOLD）信号。有人提出，BOLD 信号的增强是由于静息脑血流量减少所致。然而，还有多项其他研究表明，大脑中基线血流量的变化并不能持续增强 BOLD 信号。众所周知，长期摄入咖啡因会导致腺苷受体数量增加，并且研究表明，在戒断状态下，一定剂量的咖啡因对静息脑血流量和BOLD信号变化有不同的影响。咖啡因对 BOLD fMRI 测量的影响引起了人们的极大关注，因为咖啡因会影响脑细胞活动和大脑血流。关于神经和血管腺苷反应对 BOLD 信号的贡献仍然存在重大的知识差距。这里提出的研究将澄清已发表的文献，并确定咖啡因是否是一种有效的 BOLD 信号增强剂（无论饮食中咖啡因的摄入量如何）。此外，这些研究将为腺苷受体子系统（神经与血管）提供急需的见解，这些子系统负责观察到的结果。