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

Linked
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

 

Cannabis

The sensations of slight euphoria, relaxation, and amplified auditory and visual perceptions produced by marijuana are due almost entirely to its effect on the cannabinoid receptors in the brain. These receptors are present almost everywhere in the brain, and an endogenous molecule that binds to them naturally has been identified: anandamide. We are thus dealing with the same kind of mechanism as in the case of opiates that bind directly to the receptors for endorphins, the body’s natural morphines.

Anandamide is involved in regulating mood, memory, appetite, pain, cognition, and emotions. When cannabis is introduced into the body, its active ingredient, Delta-9-tetrahydrocannabinol (THC), can therefore interfere with all of these functions.

THC begins this process by binding to the CB1 receptors for anandamide. These receptors then modify the activity of several intracellular enzymes, including cAMP, whose activity they reduce. Less cAMP means less protein kinase A. The reduced activity of this enzyme affects the potassium and calcium channels so as to reduce the amount of neurotransmitters released. The general excitability of the brain’s neural networks is thus reduced as well.

However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons.

In chronic consumers of cannabis, the loss of CB1 receptors in the brain’s arteries reduces the flow of blood, and hence of glucose and oxygen, to the brain. The main results are attention deficits, memory loss, and impaired learning ability.

General links about cannabis:

Lien : Vizualisation of the endocannabinoid system Linked Module: The Brain's StashLinked Module: Basis for the actions of the cannabinoidsLinked Module: Pharmacology of endogenous cannabinoid substances
 



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


Linked Module: Drogues : savoir plus, risquer moins (Cannabis)Linked Module: The Effects of Drugs on the Nervous System (Cannabis)Linked Module: Health Canada: Canada’s Drug Strategy (Cannabis)Link: The Vaults of Erowid: Cannabis

 

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