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Pleasure and pain
Sub-Topics
Pleasure-Seeking Behaviour
Avoiding Pain

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HelpLinked Module: InfoFacts Index NIDALinked Module: National Institute on Drug Abuse NIDALinked Module: InfoFacts Index NIDA
Linked Module: Addictive Qualities of Popular DrugsLinked Module: Drug war factsLien : Neuropharmacology SummaryLien : Info-drogues

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.

Linked Module: chocolat
HOW DRUGS AFFECT NEUROTRANSMITTERS

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. Lien: Neurobiology of addiction and implications for treatment

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

 

Ecstasy

Ecstasy (MDMA) is a synthetic drug. It acts simultaneously as a stimulant and a hallucinogen because of its molecular structure, which is similar to that of both amphetamines and LSD. Like amphetamines and cocaine, ecstasy blocks the reuptake pumps for certain neurotransmitters, thus increasing their levels in the synaptic gap and their effect on the post-synaptic neurons’ receptors.

While ecstasy also potentiates the effects of norepinephrine and dopamine, it is distinguished from other psychostimulants by its strong affinity for serotonin transporters. The initial effect of ecstasy is thus an increased release of serotonin by the serotonergic neurons. The individual may then experience increased energy, euphoria, and the suppression of certain inhibitions in relating to other people.

A few hours later, there is a decrease in serotonin levels, amplified by the reduced activity of tryptophane hydroxylase, the enzyme responsible for synthesizing serotonin. This decrease can last much longer than the initial increase. Once again, an artificial increase in the level of a neurotransmitter exercises negative feedback on the enzyme that manufactures it. As a result, when intake of the drug ceases, the excess turns into a shortage.

Like all psychoactive drugs that produce a sensation of pleasure, ecstasy also increases the release of dopamine into the reward circuit. In addition, the extra serotonin produced by ecstasy leads indirectly to excitement of the dopaminergic neurons by the serotonergic neurons that connect to them.

The toxicity of ecstasy for humans has not been clearly established, but animal studies have shown that chronic high doses of MDMA lead to selective destruction of the terminal buttons of the serotonergic neurons.

 



For a description of the effects of ecstasy and the risks of dependency associated with it, click on the following links:


Linked Module: Drogues : savoir plus, risquer moins (Ecstasy)Linked Module: The Effects of Drugs on the Nervous System (Ecstasy)Linked Module: Ecstasy : des données biologiques et cliniques aux contextes d'usageLink: The Vaults of Erowid: MDMA (Ecstasy)Lien :  Politique des deux poids, deux mesures

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