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

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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.

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.) ----- Cocaine ----- Nicotine

Caffeine ----- Amphetamines ----- Cannabis ----- Ecstasy ----- Benzodiazepines

 

Alcohol

Alcohol passes directly from the digestive tract into the blood vessels. In minutes, the blood transports the alcohol to all parts of the body, including the brain.

Alcohol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate.

Click on the labels in the diagram to the right to see an animation about how alcohol affects a GABA synapse. GABA’s effect is to reduce neural activity by allowing chloride ions to enter the post-synaptic neuron. These ions have a negative electrical charge, which helps to make the neuron less excitable. This physiological effect is amplified when alcohol binds to the GABA receptor, probably because it enables the ion channel to stay open longer and thus let more Cl- ions into the cell.

The neuron’s activity would thus be further diminished, thus explaining the sedative effect of alcohol. This effect is accentuated because alcohol also reduces glutamate’s excitatory effect on NMDA receptors.

However, chronic consumption of alcohol gradually makes the NMDA receptors hypersensitive to glutamate while desensitizing the GABAergic receptors. It is this sort of adaptation that would cause the state of excitation characteristic of alcohol withdrawal.

Alcohol also helps to increase the release of dopamine, by a process that is still poorly understood but that appears to involve curtailing the activity of the enzyme that breaks dopamine down.

General links about alcohol:

 



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


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

 


History La consommation d·alcool au fil du temps Link :  Alcool, quand le cerveau est accro Link : How Alcohol Works Link : Booze Pleasure Center Identified Link : EFFETS DE L'ALCOOL Link : Reward Deficiency Syndrome Research : Researchers Study Mechanism of Alcohol's Effects·One Cell at a Time Link :  THP, TIQ, MAGNESIUM Link : Centres d'Action et de Libération du Mal-être Ethylique Link : Intoxicating Studies: The Effects of Alcohol on Social Behavior Link :  Booze and our brains Link :  Combien de verres, docteur? Lien :  Alcohol Lien :  Outpatient vs. Inpatient Addiction Treatment Link :  Combien de verres, docteur?

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