Caffeine, probably the most widely used drug, is a potent pharmacological and psychotropic agent. The white, bitter-tasting, crystalline substance was first isolated from coffee in 1820.
The origins of the words, caffeine and coffee, reflect the spread of the beverage into Europe via Arabia and Turkey form North-East Africa, where coffee trees were cultivated in the 6th century. Coffee began to be popular in Europe in the 17th century, and plantation had been established in Indonesia and the West Indies by the 18th century.
Nowadays, it is a regular component of the diet for most people. Caffeine is considered as a cheap drug that could be found in many nature sources such as tea, chocolate, and cocoa.
What happen to the caffeine when it is ingested, and what are its consequences? In addressing these questions, there have been many contributors spent much time to prove that caffeine has been shown to behave as an adenosine antagonist to stimulate motor activity, mood and behavior.
This antagonist behavior is the basis for an increase in cholinergic and dopaminergic behavior after caffeine intake. Beside of that, the acute administration of caffeine has been reported by several laboratories to elevate brain level of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA).
This increase of serotonin may be associated with the improvement in good mood. Recent studies also show the higher caffeine intake to a lower suicide risk. In this paper, I will investigate the caffeine at a biochemical level and relate its effects on physiological behavior of human with information from the recent research.
For many years, the mechanism of caffeine was not yet clear. However, it was thought that the mechanism involves the response of hormone signals. When hormones cannot penetrate the cell directly, they bind to the hydrophilic surface of the cell membrane and activate adenylate cyclase, and enzyme that catalyzes ATP to cyclic AMP,a secondary messenger hormone.
Most of these hormones are catecholamines. This process, in turn, leads to cyclic AMP’s activation of protein kinases, which then active, catalyze a cascade of enzyme phosphorylation. The cascade leads to the releasing of other hormones which are responsible for physiological effects in brain.
In early studies, caffeine was thought to inhibit phosphodiesterase, an enzyme which is responsible for degrading cAMP. This inhibition leads to an increase of cAMP, which is known to have the effects on excitatory neurotransmitters such as norepinephrine and dopamine. Therefore, caffeine would lead to higher activity of the excitatory neurotransmitter causing the stimulatory effects psychomotor (Glass et al. 1996).
However, substantial inhibition of phosphodiesterases requires millimolar concentrations of caffeine, roughly 100 times the caffeine levels in the brain after ingestion of typical doses in man. Furthermore, some inhibitors of phosphodiesterase are 100-1000 times more potent than caffeine lack behavior effects.
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