Behavioral and Side Effects of Caffeine

Behavioral and Side Effects of Caffeine

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Behavioral and Side Effects of Caffeine


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

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123helpme.com/search.asp?text=behavioral">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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Cameron, O.G., Modell, J.G., and Harinharan, M. (1990).
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