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Pleasure and pain
Pleasure-Seeking Behaviour

Help Sommes-nous tous des drogués ? DOPAMINE NEUROTRANSMISSION WHEN OPIATES ARE ADDED Influence of the endogenous opioid system on high alcohol consumption and genetic predisposition to alcoholism

Some addictions do not involve drugs. Instead, the brain becomes dependent on substances that it secretes naturally during certain activities.
For instance, you can become “hooked” on endorphins–the endogenous opiates that the brain produces when you are working or engaging in sports. The stress of these activities causes the norepinephrine-producing neurons in the brain to become overactive. To counteract the excess norepinephrine, the brain produces more endorphins, which eliminate the sense of discomfort caused by the norepinephrine and can even create a feeling of euphoria. But once you stop the activity that raised your endorphin levels, there are no longer enough endorphins in your system to control the secretion of norepinephrine. As a result, you will experience feelings both of deprivation (from lack of endorphins) and discomfort (from the excess norepinephrine). You will therefore again seek out those activities that flood your brain with its own endogenous morphines.


In addition to being influenced by dopamine, the reward circuit is modulated by endogenous opiates, such as enkephalins, b-endorphin, and dynorphin.

In the ventral tegmental area (VTA), endorphins act on mu receptors on the dendrites of GABAergic interneurons. Normally, these interneurons inhibit the dopaminergic neurons that project from the VTA to the nucleus accumbens. But if you engage in a sport or other activity that raises your natural endorphin level (or if you take an exogenous opiate), it suppresses the release of GABA and thus removes the GABAergic inhibition on these dopaminergic neurons. Consequently, the nucleus accumbens is even more stimulated by the dopamine from the dopaminergic neurons of the VTA, which creates a positive reinforcement.

Conversely, dynorphins, another type of endogenous opiate, bind to kappa receptors to inhibit the release of dopamine in the nucleus accumbens. The stimulation of the nucleus accumbens is thereby reduced, which creates an aversive effect.


Normally, endorphins bind to the neurons involved in controlling pain and hyperpolarize them, thus reducing the amount of neurotransmitters released. Endorphins also inhibit the effect of the norepinephrinergic neurons involved in vigilance and feelings of uneasiness.

Exogenous opiates such as heroin and morphine have a similar structure to endogenous enkephalins and attach to the same receptors when they reach the brain. In response to this artificial surplus, the enkephalin-producing neurons reduce their activity.

But once the drug has left the system, the reduced enkephalin output of these neurons no longer suffices to contain the activity of the neurons that they were inhibiting.

For example, in the VTA, the GABAergic interneurons are less inhibited, and so are more effective in reducing the release of dopamine in the nucleus accumbens. In these circumstances, drug addicts experience the feelings of displeasure and general physical distress that typify drug dependency.


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