Caffeine has been reported to cause a dose-dependent (30-75 mg/kg) increase in dopamine in the striatum (Morgan and Vestal, 1989). Adenosine A1 receptors (in contrast to adenosine A2A receptors) have been shown to influence dopamine release in slices of the striatum (Jin et al., 1993 Jin and Fredholm, 1997).

Thus, an inhibition of A2A receptors by caffeine would be expected to increase transmission via dopamine at D2 receptors (Ferré et al., 1992īesides the direct effects on striatopallidal neurons mediated via an antagonism of A2A receptors, caffeineat least at high doseshas been reported to influence the turnover of dopamine. The interaction between adenosine A2A and dopamine D2 receptors highlighted above could provide a mechanism for several actions of caffeine and some of its metabolites on dopaminergic activity. Activation of Dopaminergic Transmission and Effects on Motor Behavior Finally, we will briefly comment upon the similarities and dissimilarities between caffeine and known addictive drugs such as cocaine, morphine, and nicotine.Ī. Below we will briefly consider a set of such responses and attempt to relate them to the primary actions of caffeine. Nonetheless, some specific aspects need to be brought forward as they relate directly or indirectly to the issue at hand. It would clearly be outside the scope of this review to cover all aspects of caffeine action in the CNS. This in turn will influence a large number of different physiological functions. Even though the primary action of caffeine may be to block adenosine receptors this leads to very important secondary effects on many classes of neurotransmitters, including noradrenaline, dopamine, serotonin, acetylcholine, glutamate, and GABA (Daly, 1993). Withdrawal symptoms typically begin 12 to 24 hours after the last caffeine dose, peak after one to two days of abstinence, and may last up to nine days.Having discussed the molecular and neuronal actions of caffeine, especially as they relate to a primary effect on adenosine receptors, it is important to consider some actions at a more integrated level. Flu-like symptoms such as nausea and muscle pain.Symptoms of caffeine withdrawal can include: Since caffeine affects different people in different ways, the definition of 'overuse' can vary.Īlthough some research suggests that regular use of caffeine is more of a habit than an addiction, the fact that overuse causes physical and psychological symptoms and that withdrawal symptoms develop when people stop drinking caffeinated beverages indicates the substance has addictive qualities. Overuse can lead to what is called 'caffeine intoxication,' which involves restlessness, nervousness, excitement, flushed facial skin, insomnia, increased urine production, gastrointestinal upset, irregular heartbeat, muscle twitching, jumpiness, or shakiness, or any combination of these symptoms. The American Medical Association Council on Scientific Affairs concludes, 'Moderate tea or coffee drinkers probably have no concern for their health relative to their caffeine consumption provided other lifestyle habits ( diet, alcohol consumption) are moderate as well.' The effects of caffeine on health have been widely studied-in particular, its effects on fibrocystic breast disease, conditions of the heart and blood vessels, birth defects, reproductive function, and behavior in children. It is excreted in the urine hours after it has been consumed. Caffeine does not accumulate in the bloodstream nor is it stored in the body. After absorption, it passes into the brain. Once ingested, caffeine is absorbed and distributed quickly. Similarly, caffeine should never be given to a frostbite or hypothermia victim. Contrary to common myth, coffee will not sober up an inebriated person instead, it typically causes agitation. As a stimulant, caffeine can cause the heart to beat faster and hasten the effects of cold temperatures on the body. Caffeine functions as a central nervous system stimulant and also a diuretic.

Adenosine caffeine structure