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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

 

Benzodiazepines

Benzodiazepines, such as diazepam (Valium) and clonazepam (Rivotril) are anxiolytics that can also have hypnotic or amnesia-inducing effects. Like alcohol, these drugs increase the efficiency of synaptic transmission of the neurotransmitter GABA by acting on its receptors.

A GABA receptor is actually a macromolecular complex that, in addition to containing sites for binding GABA, also contains sites for binding other molecules such as benzodiazepines that modulate GABA’s activity.

When benzodiazepines bind to a specific site on a GABA receptor, they do not stimulate it directly. Instead, they make it more efficient by increasing the frequency with which the chlorine channel opens when GABA binds to its own site on this receptor (see animation). The resulting increase in the concentration of Cl- ions in the post-synaptic neuron immediately hyperpolarizes this neuron, thus making it less excitable.

Barbiturates bind to another site on the GABA receptor, with similar effects. But the advantage of benzodiazepines is that, unlike barbiturates, they do not open the Cl- channels directly, but instead act more subtly by potentiating the effect of GABA. Mixing benzodiazepines with alcohol is still very dangerous, however, because their respective effects on the Cl- channels can be additive.

We now know that benzodiazepines can cause a drug dependency even in what are considered therapeutic doses, and even in a short course of treatment.

General links about benzodiazepines:

Linked Module: Joan Gadsby a vécu 23 années de dépendance aux benzodiazépines - Les tranquillisants, une drogue légale aux effets ravageurs
 



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


Linked Module: Drogues : savoir plus, risquer moins (benzodiazépines)Linked Module: The Effects of Drugs on the Nervous System (Benzodiazepines)Linked Module: Health Canada: Canada’s Drug Strategy (Tranquilizers)Linked Module: The Vaults of Erowid: Diazepam (Valium)

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