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Nearly 15% of all men and 30% of all women admit to a craving for chocolate.
Over 300 substances have been identified in chocolate. Some of these, including caffeine and theobromine (another, less powerful stimulant) could actually cause dependency effects. But the amounts of these substances in chocolate are too small to really have any effect.
The same goes for phenylethylamine, a substance related to a family of stimulants called amphetamines. For example, chocolate contains less phenylethylamine than goat cheese.
Anandamide, a neurotransmitter produced naturally by the brain, has also been isolated in chocolate. The neural receptors for anandamide are the same ones to which THC, the main active ingredient in cannabis, binds. The anandamide in chocolate might therefore contribute to the feeling of well-being reported by “chocoholics” (though you would have to eat well over 30 kilos of chocolate to experience effects comparable to one dose of cannabis!).
Be that as it may, many scientists agree that dependency on chocolate could simply be due to its taste, which causes a sensation of intense pleasure that people want to repeat.
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| HOW DRUGS AFFECT NEUROTRANSMITTERS |
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Dopamine appeared
very early in the course of evolution and is involved in many functions
that are essential for survival of the organism, such as motricity,
attentiveness, motivation, learning,
and memorization. But most of all, dopamine is a key element
in identifying natural rewards for the organism. These natural
stimuli such as food and water cause individuals to engage in approach
behaviours. Dopamine is also involved in unconscious memorization
of signs associated with these rewards.
It has now been established that all substances that trigger dependencies
in human beings increase the release of a neuromediator, dopamine,
in a specific area of the brain: the
nucleus accumbens. 
But not all drugs increase dopamine levels in the brain in the
same way.
- Some substances imitate natural
neuromediators and take their place on their receptors. Morphine,
for example, binds to the receptors for endorphin (a natural "morphine" produced
by the brain), while nicotine binds to the receptors for acetylcholine.
- Other substances increase the secretion of
natural neuromediators. Cocaine, for example, mainly increases
the amount of dopamine in the synapses, while ecstasy mainly
increases the amount of serotonin.
- Still other substances block a natural neuromediator.
Alcohol, for example, blocks the NMDA receptors.
Click on the names of each of the
following drugs to read about how they work and what effects
they have.
Alcohol ----- Opiates
(heroin, morphine, etc.) ----- Cocaïne ----- Nicotine
Caffeine ----- Amphetamines ----- Cannabis ----- Ecstasy ----- Benzodiazepines
Opiates (heroin,
morphine, etc.)
The human body naturally produces
its own opiate-like substances and uses them as neurotransmitters.
These substances include endorphins, enkephalins, and dynorphin,
often collectively known as endogenous opioids. Endogenous
opioids modulate our reactions to painful stimuli. They
also regulate vital functions such as hunger and thirst
and are involved in mood control, immune response, and
other processes.
The reason that opiates such as heroin and morphine affect
us so powerfully is that these exogenous substances bind
to the same receptors as our endogenous opioids. There
are three kinds of receptors widely distributed throughout
the brain: mu, delta, and kappa receptors.
These receptors, through second messengers, influence the
likelihood that ion channels will open, which in certain
cases reduces the excitability of neurons. This reduced
excitability is the likely source of the euphoric effect
of opiates and appears to be mediated by the mu and delta
receptors.
This euphoric effect also appears to involve another mechanism
in which the GABA-inhibitory interneurons of the ventral
tegmental area come into play. By attaching to their mu
receptors, exogenous opioids reduce the amount of GABA
released (see animation). Normally, GABA reduces the amount
of dopamine released in the nucleus accumbens. By inhibiting
this inhibitor, the opiates ultimately increase the amount
of dopamine produced and the amount of pleasure felt.
Chronic consumption of opiates inhibits the production
of cAMP, but this inhibition is offset in the long run
by other cAMP production mechanisms. When no opiates are
available, this increased cAMP production capacity comes
to the fore and results in neural hyperactivity and the
sensation of craving the drug.
General links about opiates:
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