Caffeine is the most consumed psychoactive drug in the world
(Solinas et al, 2002). Caffeine has been known to have many side effects on hour external behavior and our internal physiological behavior. We use caffeine in our lives to sometimes stay awake to study or just get through the day.

Caffeine decreases the blood flow to the brain by constricting the blood vessels but can also increase blood flow after continuous intake that may cause headaches (Kalat, 2004).
Caffeine has a tendency to block adenosine (A1-, A2A-, A2B-,
A3), which increases throughout the day to allow us to sleep and then decreases as we sleep which allows us to wake. Thus, if caffeine blocks adenosine we are unable to sleep when feeling the urge or wanting to sleep, which may cause us to decrease our caffeine intake.

Caffeine acts to antagonize adenosine receptors, which then affects cell populations because it counteracts many adenosine effects. The caffeine mainly has an effect on the A2a adenosine receptors which then elevates the energy metabolism in the brain and also causes a decrease in cerebral blood flow
(Cameron,et.al, 1990; Ghelardini, et.al, 1997; Nehliget.al,1992;
Neuhauser-Berthold et.al, 1997). Along with caffeine affecting the adenosine it also has an effect on GABA receptors and the release of dopamine (Nehlig et.al, 1992).

Caffeine not only blockades adenosine it also releases intracellular calcium, inhibits phosphodiesterases and blockade or regulatory sites of GABAa-receptors (Gupta and Gupta, 1999).
Withdrawal symptoms of caffeine are headache, drowsiness, fatigue and lethargy (Gupta and Gupta, 1999).

Dopamine and glutamate neurotransmission is modulated by adenosine in the striatum. Adenosine A1 in the nerve terminals inhibits dopamine and glutamate from being released. Caffeine has an effect in this system by antagonizing of adenosine, which can then stimulate neurotransmitters to release dopamine and stimulate dopamine receptors (Solinas et al, 2002). A study done on rats showed that caffeine increased extracelluar concentrations of dopamine and glutamate in the shell of the nucleus accumbens (Solinas et al, 2002). These results of dopamine and glutamate in the shell of the nucleus accumbens might be related to the psycho stimulant effects of caffeine
(Solinas et al, 2002).

Studies show that Dopamine2 receptors are needed for caffeine activation in the brain (Zahniseret al, 2000).
Adenosine receptors, dopamine receptors and GABA have been shown in studies to be involved in behavioral hyperactivity due to caffeine intake which then induces locomotor activation
(Zahniser, et.al., 2000). Mice that have been injected with caffeine in studies have shown to be more active than mice that were injected with saline instead of caffeine due to the activation of Dopamine2 receptors (Zahniser, et.al., 2000).
The same study showed that caffeine-induced locomotion was mediated by the dopamine receptors that were being released to block the caffeine (Zahniser, et.al., 2000).

Studies have been done to test changes in ACh in the hippocampus in rats, which would then slow the blockade of presynaptic adenosine receptors, by caffeine. When ACh was paired with choline there was a synergistic effect that raised the ACh concentrations, thus the blockade of adenosine (Gupta and Gupta; 1999).

The inhibitions of transmitter release from the presynaptic cell and limit of the activity evoked membrane depolarization on postsynaptic cell are due to A1 receptors (Rudolphi et.al,
1992). A2 receptors are found in dopamine receptor rich areas of the brain and A1 receptors are in many areas of the brain but are found in large quantities in the neocortex (Fastbom, 1987;
Goodman, 1982). Caffeine binds with the A1 receptors, which then prevents inhibition thus causing excitation (Lesk and
Womble, 2004).

Caffeine in the central nervous system raises cerebrovascular resistance. In rats it has been shown that the rates of local cerebral blood flow (LCBF) decreases in the areas where it usually increases metabolism. In humans the cerebral blood flow also decreases but only by 20-30% and there are no decreases in any other regions (Gupta, Gupta; 1999). During these tests it showed that with the decreases in the cerebral blood flow that the patients (rats and humans) had an increased anxiety rating after the intake of caffeine (Gupta and Gupta,
1999).

Other studies have been done on rats with stress responses to coffee on the hippocampal serotonin and dopamine levels.
Coffee affects the brain in many ways such as it acts as a stimulant on the central nervous system, it increases the levels of serotonin and dopamine in the hippocampus and striatum. The hippocampus is mainly responsible for food intake, emotion and memory. Dopamine and serotonin is also released from the hippocampus when rats are exposed to restraint stress (Yomato,
2002). Studies on rats showed that when injected with some type of caffeine product while being restrained and then when released showed high levels of dopamine and serotonin but after an hour and forty minutes the levels of dopamine and serotonin went back to normal levels (Yomato et al, 2002). While the rats were being restrained the study found that the coffee/caffeine had suppressed the amount of serotonin that was released from the rats hippocampus (Yomato et al, 2002).

Studies have been done on caffeine drinks such as Red Bull and Rock Star to show the effects they have on the human and animal brain. Studies have shown that caffeine can interact with the neurotransmitters of the brain, which causes spontaneous firing rates of the cortical neurons (Specterman et al, 2005).

Caffeine has been shown by previous studies to increase alertness, increase visual vigilance and improve cognitive functioning (Fagan et al, 1998; Smith et al, 1992; Stein et.al,
1996; Loke and Meliska; 1984). Reaction time is also decreased in individuals who consume large amounts of caffeine (Leiberman et al, 1987).

A number of studies on caffeine and memory have shown that caffeine enhances memory performance. They have also shown that caffeine improves delay recall, recognition memory, semantic memory and verbal memory (Stein et al, 1996; Warburton, 1987;
Bowyer et.al, 1983; Jarris, 1993). Studies that showed an increase in performance in tasks such as short and long term memory retrieval, reading speed and encoding efficiency was due to caffeine having cholinergic properties (Greenburg and
Shapiro, 1987). However, even though there have been studies that show positive effects of caffeine there have been other studies that have shown the opposite effects, saying that caffeine decreases memory and recall (Gupta and Gupta, 1999).
Seeing that different studies have gotten opposite results other studies have been done to understand this and what was found was that the amount of recall and memory that an individual can exhibit with caffeine was due to the memory of the individual before (Andersen and Revelle, 1983).

People who chronically experience headaches usually take medications that have some type of caffeine, which causes the same effect that acetaminophen, would have. Those who suffer headaches from caffeine withdrawal can usually be relieved by in taking a small amount of caffeine (Nahlig, Daval, and Debry,
1992). During caffeine withdrawal headaches, in high caffeine consumers usually have headaches in the frontal regions of the brain. These headaches are due to the increase of cerebral blood flow. After these consumers have taken in some type of caffeine their cerebral blood flow decreases after about thirty minutes and then becomes normal again after approximately two hours (Couturier, Hering, and Steiner, 1992). Through these studies the brain and cerebral blood flow never adjust or evolve to caffeine intake (Gupta and Gupta, 1999).

Neurological changes are considered to be the central part of developing a dependence on drugs, which could then eventually lead to an outbreak in consumption of caffeine-containing beverages (Solinas et al, 2002).

In a study done to show if people who are habitual coffee drinkers become tolerant to caffeine showed that in both habitual and nonhabitual coffee drinkers when caffeine was infused into the system their sympathetic nerve active and blood pressure increased. In nonhabitual coffee drinkers their systolic blood pressure increased and did not in habitual drinker thus indicating that habitual coffee drinkers may develop a tolerance to caffeine (Corti et.al, 2003). In the study decaffeinated and caffeinated coffee was tested and showed that decaffeinated coffee also increased the sympathetic nerve activity and blood pressure as did with caffeinated coffee in nonhabitual coffee drinkers. The study also showed that the up regulation of adenosine receptors is the reason for caffeine tolerance but there may be other substances that may contribute to the effects of coffee (Corti et.al, 2003).

Caffeine has a large effect on adenosine receptors in the brain and can cause many different types of reactions from increased stress, anxiety, alertness, insomnia (due to large in take of caffeine), and effects on the hippocampus and can even have some dependence effects. The effect that caffeine has on people is different for each person. One person may have no effects to caffeine and another person may have strong effects.
However, caffeine does affect your brain no matter what your tolerance to it may be.

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