Funding for this site is provided by readers like you.
Pleasure and pain
Pleasure-Seeking Behaviour
Avoiding Pain

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

A neuroscientist gets drunk to explain alcohol’s effects on the brain

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

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


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:


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

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

Axons Play Unexpected Role in Processing Information

Lien :  Nicotine Lien :  The Pleasure Principle : Back to FreudLien : How Nicotine WorksLien : Nicotine Rewires Brain's Reward SystemLien : Nicotine and the BrainLien : Physical and pharmacological effects of nicotineLien : "Alternative" Cigarettes Not Safer Than Regular Cigarettes
Lien : A Small Part of the Brain, and Its Profound EffectsLien : Nursing Your Lungs
  Presentations | Credits | Contact | Copyleft