Voie méso-limbique
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La voie mésolimbique, parfois appelée voie de la récompense, est une voie dopaminergique dans le cerveau[1]. La voie relie l'aire tegmentale ventrale du mésencéphale au striatum ventral des noyaux gris centraux du prosencéphale. Le striatum ventral comprend à la fois le noyau accumbens et le tubercule olfactif[2],[3]. La libération de dopamine de la voie mésolimbique dans le noyau accumbens régule la saillance des incitations (par exemple, la motivation et le désir de stimuli gratifiants) et facilite le renforcement et l'apprentissage des fonctions motrices liées à la récompense[4],[5],[6] ; elle peut également jouer un rôle dans la perception subjective du plaisir[4],[6].
Des troubles de la régulation de la voie mésolimbique et de ses neurones de sortie dans le noyau accumbens jouent un rôle important dans le développement et le maintien d'une dépendance[1],[7],[8],[9].
Étymologie
[modifier | modifier le code]Le préfixe méso dans le mot mésolimbique fait référence au cerveau moyen, puisque méso signifie moyen en grec.
Fonction
[modifier | modifier le code]La stimulation de l'aire tegmentaire ventrale produit une libération de dopamine dans le noyau accumbens.
Plusieurs études ont établi un lien entre les propriétés renforçantes de l'activation du système mésolimbique et la dépendance à plusieurs drogues. Les drogues, telles que les amphétamines, la cocaïne, la nicotine, les opiacés naturels et de synthèse (fentanyl, etc. ) ainsi que l'alcool, produisent des augmentations rapides et importantes du taux de dopamine dans le circuit de la récompense.
Notes et références
[modifier | modifier le code]- Dreyer JL, « New insights into the roles of microRNAs in drug addiction and neuroplasticity », Genome Med, vol. 2, no 12, , p. 92 (PMID 21205279, PMCID 3025434, DOI 10.1186/gm213
)
- Ikemoto S, « Brain reward circuitry beyond the mesolimbic dopamine system: a neurobiological theory », Neurosci Biobehav Rev, vol. 35, no 2, , p. 129–50 (PMID 20149820, PMCID 2894302, DOI 10.1016/j.neubiorev.2010.02.001) :
« Recent studies on intracranial self-administration of neurochemicals (drugs) found that rats learn to self-administer various drugs into the mesolimbic dopamine structures–the posterior ventral tegmental area, medial shell nucleus accumbens and medial olfactory tubercle. ... In the 1970s it was recognized that the olfactory tubercle contains a striatal component, which is filled with GABAergic medium spiny neurons receiving glutamatergic inputs form cortical regions and dopaminergic inputs from the VTA and projecting to the ventral pallidum just like the nucleus accumbens »
Figure 3: The ventral striatum and self-administration of amphetamine - Molecular Neuropharmacology : A Foundation for Clinical Neuroscience, New York, , 2e éd., 147–148, 154–157 (ISBN 978-0-07-148127-4), « Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin »
« Neurons from the SNc densely innervate the dorsal striatum where they play a critical role in the learning and execution of motor programs. Neurons from the VTA innervate the ventral striatum (nucleus accumbens), olfactory bulb, amygdala, hippocampus, orbital and medial prefrontal cortex, and cingulate cortex. VTA DA neurons play a critical role in motivation, reward-related behavior, attention, and multiple forms of memory… Thus, acting in diverse terminal fields, dopamine confers motivational salience (wanting) on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum).... DA has multiple actions in the prefrontal cortex. It promotes the cognitive control of behavior: the selection and successful monitoring of behavior to facilitate attainment of chosen goals. Aspects of cognitive control in which DA plays a role include working memory, the ability to hold information on line in order to guide actions, suppression of prepotent behaviors that compete with goal-directed actions, and control of attention and thus the ability to overcome distractions.(…) Noradrenergic projections from the LC thus interact with dopaminergic projections from the VTA to regulate cognitive control. »
- Malenka RC, Nestler EJ, Hyman SE, Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, New York, McGraw-Hill Medical, , 2nd éd., 147–148, 367, 376 (ISBN 978-0-07-148127-4) :
« VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience (“wanting”) on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum). In this example, dopamine modulates the processing of sensorimotor information in diverse neural circuits to maximize the ability of the organism to obtain future rewards. ...
The brain reward circuitry that is targeted by addictive drugs normally mediates the pleasure and strengthening of behaviors associated with natural reinforcers, such as food, water, and sexual contact. Dopamine neurons in the VTA are activated by food and water, and dopamine release in the NAc is stimulated by the presence of natural reinforcers, such as food, water, or a sexual partner. ...
The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement and the modulation of motoric responses to stimuli that satisfy internal homeostatic needs. The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine release in the shell than in the core of the NAc. » - Malenka RC, Nestler EJ, Hyman SE, Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, New York, McGraw-Hill Medical, , 2nd éd. (ISBN 978-0-07-148127-4), « Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu », p. 266 :
« Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward. »
- Berridge KC, Kringelbach ML, « Pleasure systems in the brain », Neuron, vol. 86, no 3, , p. 646–664 (PMID 25950633, PMCID 4425246, DOI 10.1016/j.neuron.2015.02.018) :
« To summarize: the emerging realization that many diverse pleasures share overlapping brain substrates; better neuroimaging maps for encoding human pleasure in orbitofrontal cortex; identification of hotspots and separable brain mechanisms for generating ‘liking’ and ‘wanting’ for the same reward; identification of larger keyboard patterns of generators for desire and dread within NAc, with multiple modes of function; and the realization that dopamine and most ‘pleasure electrode’ candidates for brain hedonic generators probably did not cause much pleasure after all. »
- Robison AJ, Nestler EJ, « Transcriptional and epigenetic mechanisms of addiction », Nat. Rev. Neurosci., vol. 12, no 11, , p. 623–637 (PMID 21989194, PMCID 3272277, DOI 10.1038/nrn3111) :
« ΔFosB has been linked directly to several addiction-related behaviors. (…) Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states. »
- Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M, « Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms », Journal of Psychoactive Drugs, vol. 44, no 1, , p. 38–55 (PMID 22641964, PMCID 4040958, DOI 10.1080/02791072.2012.662112) :
« It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues (2010) reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Next, the induction of c-Fos, a downstream (repressed) target of DeltaFosB, was measured in sexually experienced and naive animals. The number of mating-induced c-Fos-IR cells was significantly decreased in sexually experienced animals compared to sexually naive controls. Finally, DeltaFosB levels and its activity in the NAc were manipulated using viral-mediated gene transfer to study its potential role in mediating sexual experience and experience-induced facilitation of sexual performance. Animals with DeltaFosB overexpression displayed enhanced facilitation of sexual performance with sexual experience relative to controls. In contrast, the expression of DeltaJunD, a dominant-negative binding partner of DeltaFosB, attenuated sexual experience-induced facilitation of sexual performance, and stunted long-term maintenance of facilitation compared to DeltaFosB overexpressing group. Together, these findings support a critical role for DeltaFosB expression in the NAc in the reinforcing effects of sexual behavior and sexual experience-induced facilitation of sexual performance. ... both drug addiction and sexual addiction represent pathological forms of neuroplasticity along with the emergence of aberrant behaviors involving a cascade of neurochemical changes mainly in the brain's rewarding circuitry. »
- Olsen CM, « Natural rewards, neuroplasticity, and non-drug addictions », Neuropharmacology, vol. 61, no 7, , p. 1109–22 (PMID 21459101, PMCID 3139704, DOI 10.1016/j.neuropharm.2011.03.010)
