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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
Nicotine
in Tobacco
Nicotine imitates the action of a
natural neurotransmitter called acetylcholine and binds
to a particular type of acetylcholine receptor, known as
the nicotinic receptor.
Whether it is acetylcholine or nicotine that binds to this
receptor, it responds in the same way: it changes its conformation,
which causes its associated ion channel to open for a few
milliseconds. This channel then allows sodium ions to enter
the neuron, depolarizing the membrane and exciting the
cell. Then the channel closes again, and the nicotinic
receptor becomes temporarily unresponsive to any neurotransmitters.
It is this state of desensitization that is artificially
prolonged by continual exposure to nicotine.
Tobacco dependency, which then develops very quickly, arises
because nicotinic receptors are present on the neurons
of the ventral tegmental area which project their terminations
into the nucleus accumbens. In smokers, repeated nicotine
stimulation thus increases the amount of dopamine released
in the nucleus accumbens. Between cigarettes, however,
chronic smokers maintain a high enough concentration of
nicotine to deactivate the receptors and slow down their
recovery. This is why smokers develop a tolerance to nicotine
and experience reduced pleasure from it.
After a brief period without smoking (a night’s sleep,
for example), the baseline concentration of nicotine drops
again, and some of the receptors regain their sensitivity.
When all these receptors become functional again, cholinergic
neurotransmission is raised to an abnormally high level
that affects all the cholinergic pathways in the brain.
Smokers then experience the agitation and discomfort that
leads them to smoke another cigarette.
Another substance in tobacco smoke, not yet clearly identified,
inhibits monoamine oxydase B (MAO B), an enzyme that breaks
down dopamine after its reuptake. The result is a higher
concentration of dopamine in the reward circuit, which
also contributes to the smoker’s dependency.
General links about nicotine:
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