The Effects Of Caffeine Caffeine And Nicotine - amazonia.fiocruz.br

The Effects Of Caffeine Caffeine And Nicotine Video

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Caffeine which is part of many beverages like tea, coffee, energy drinks, cola drinks and chocolates is one of the widely used stimulants by the human population all over the world. The consumption of caffeine varies across age groups. Generally adults follow a pattern in the consumption related to the time of the day, the sleep-wake cycle and other behavioral attributes. Caffeine acts as adenosine A 2A The Effects Of Caffeine Caffeine And Nicotine antagonist and the blockage of these receptors in striatal basal ganglia is said to be the cause of the stimulant effect of caffeine. Apart from the stimulant and subtle motor effects, caffeine also has several therapeutic effects in relation to its cellular mechanism. Caffeine can protect cells from skin cancer resulting from UV radiation since it is able to induce apoptosis of tumorigenic cells.

Caffeine therapy was found to Caffeinee effective in relief from apnea of prematurity in infants. When combined with PTEN treatment, caffeine has a synergistic effect in inducing the apoptosis of human colorectal cancer cells. There is a lot of scope to develop caffeine as a potent therapeutic drug and as part of other combinatorial therapies.

What is caffeine?

Caffeine is used as a recreational beverage in the form of coffee as well as a potent stimulator in form of energy drinks in all the parts of the world. Caffeine is a form of methyl xanthine and chemically it is 1,3,7-trimethyIxanthine. This stimulates the CNS. Based on the action of methylxanthines, 3 possible theories have been proposed regarding why does caffeine have effect on the CNS. Earlier it was thought that the effect of caffeine is due to the rise in levels of cyclic AMP, as caffeine inhibits the enzyme cAMP phosphodiesterase.

Caffeine was found to be more potent in the inhibition of adenosine receptors than in the inhibition of cAMP phosphodiesterase. Also, for the release of calcium ions in the skeletal muscles and to observe motor effects, very high concentrations of caffeine would be required. Striatal membrane of basal ganglia adenosine A 2A receptors lead to reduction in the affinity of D2 receptors for agonists. These antagonistic relationships affect striato-Gpe neurons which cause the indirect pathway. The biomarker used to assess the activity of striato-Gpe neurons is enkephalin mRNA in mice studies.

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Thus caffeine acts against the A 2A source, which in turn affects the dopamine D2 receptors increasing the motor activity. But some studies suggest that the dopamine D2 receptors Caffein not be involved and the A 2a receptors alone can cause the influence on motor activity. Caffeine counteracts against fatigue during exercise. This happens due to the blockade of A 1 receptorsand thus in turn leads to increase in dopamine concentration.

Caffeine does not act on the ventral striatum. Generally the blockage of A 2a receptors are more important in relation to the stimulant effect of caffeine.

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This was proved by the use of knockout mice in which A 2A receptor had been knocked out. After the administration of caffeine a lower locomotor activity was noticed in comparison to wild type mice. To study the role of dopamine in the action of caffeine, reserpine and also D1 and D2 receptor antagonists were used was used to study the effect.

Thus caffeine acts on striato-Gpe pathway and caffeine acts as an https://amazonia.fiocruz.br/scdp/essay/mormon-bank-utah/tutorial-2-professional-development.php A 2A receptor antagonist.]