Caffeine: Difference between revisions

Caffeine is a derivative of adenosine and is also called Trimethylxanthine. It is composed of purines; structurally it is polar, and water soluble. They antagonize or inhibit many of the adenosine receptors, like the A1 receptor mentioned above. Caffeine affects neurons and glial cells in the brain by binding to the same location that adenosine would bind and then induce a cascade of enzymatic downstream effects (Denoeud ''et al'' 2014).

A2A is a transmembrane protein coupled with a G protein in humans. Trimethylxanthine has a highly water soluble and thus when present in the system, interacts with the A2A receptor. In order for Trimethylxantine to bind to the receptor, the third and seventh transmembrane helical domains need to recognize the ligand. Trimethylxanthine can then bind. Trimethylxanthine, due to its similar structure and its purine alkaloid structure, can bind in place of adenosine. This binding will change the shape, but not initiate the cascade of downstream effects that adenosine does, like opening of ion channels and slowing its activity. The  concentrate of free adenosine increases extracellularly, when trimethylxanthine is bound (Xu and Stevens, 2011).

cAMP levels increase when adenosine is bound and are not effected when caffeine is bound. ERK1 and ERK2 are kinases, modify serine and threonine, of the GMGC group that regulation of cell growth and differentiation, and if adenosine was bound, this cascade of events would occur, but when Trimethylxanthine is bound, this regulation does not occur (Xu and Stevens, 2011).

== Conclusion  ==