중뇌변연계 경로: 두 판 사이의 차이

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새 문서: '''중뇌-변연계 경로'''({{llang|en|mesolimbic pathway}}) 또는 '''보상 경로'''({{llang|en|reward pathway}})는 뇌의 도파민경로 중 하나...
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2021년 4월 21일 (수) 18:32 판

중뇌-변연계 경로(영어: mesolimbic pathway) 또는 보상 경로(영어: reward pathway)는 뇌의 도파민경로 중 하나이다.[1] 중뇌의 배쪽 피개부와 전뇌 기저핵의 배쪽 선조체를 연결한다. 배쪽 선조체에는 기댐핵과 후각결절 등이 포함된다.[2]

중뇌-변연계 경로에서 기댐핵으로의 도파민 분비는 유인적 현저성(incentive salience, 보상 자극에 대한 동기와 욕구)을 조절하고 [[강화 (심리학)|]와 보상에 관련된 운동 기능 학습을 촉진한다.[3][4][5] 또한 주관적인 쾌감의 인식에도 영향을 줄 가능성이 있다.[3][5] 중뇌-변연계 경로 및 그에 연결된 기댐핵 신경세포의 조절곤란은 탐닉(addiction)의 형성과 유지에 중요한 역할을 한다.[1][6][7][8]

구조

The mesolimbic pathway and its positioning in relation to the other dopaminergic pathways

The mesolimbic pathway is a collection of dopaminergic (i.e., dopamine-releasing) neurons that project from the ventral tegmental area (VTA) to the ventral striatum, which includes the nucleus accumbens (NAcc) and olfactory tubercle.[9] It is one of the component pathways of the medial forebrain bundle, which is a set of neural pathways that mediate brain stimulation reward.[10]

The VTA is located in the midbrain and consists of dopaminergic, GABAergic, and glutamatergic neurons.[11] The dopaminergic neurons in this region receive stimuli from both cholinergic neurons in the pedunculopontine nucleus and the laterodorsal tegmental nucleus as well as glutamatergic neurons in other regions such as the prefrontal cortex. The nucleus accumbens and olfactory tubercle are located in the ventral striatum and are primarily composed of medium spiny neurons.[9][12][13] The nucleus accumbens is subdivided into limbic and motor subregions known as the NAcc shell and NAcc core.[11] The medium spiny neurons in the nucleus accumbens receive input from both the dopaminergic neurons of the VTA and the glutamatergic neurons of the hippocampus, amygdala, and medial prefrontal cortex. When they are activated by these inputs, the medium spiny neurons' projections release GABA onto the ventral pallidum.[11]

기능

각주

  1. ↑ 가 나 Dreyer JL (2010). “New insights into the roles of microRNAs in drug addiction and neuroplasticity”. 《Genome Med》 2 (12): 92. doi:10.1186/gm213. PMC 3025434. PMID 21205279. 
  2. ↑ Ikemoto S (2010). “Brain reward circuitry beyond the mesolimbic dopamine system: a neurobiological theory”. 《Neurosci Biobehav Rev》 35 (2): 129–50. doi:10.1016/j.neubiorev.2010.02.001. PMC 2894302. PMID 20149820. 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
  3. ↑ 가 나 Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY, 편집. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 2판. New York: McGraw-Hill Medical. 147–148, 367, 376쪽. 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.     
  4. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). 〈Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu〉. Sydor A, Brown RY. 《Molecular Neuropharmacology: A Foundation for Clinical Neuroscience》 2판. New York: McGraw-Hill Medical. 266쪽. ISBN 978-0-07-148127-4. Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward. 
  5. ↑ 가 나 Berridge KC, Kringelbach ML (May 2015). “Pleasure systems in the brain”. 《Neuron》 86 (3): 646–664. doi:10.1016/j.neuron.2015.02.018. PMC 4425246. PMID 25950633. 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. 
  6. ↑ Robison AJ, Nestler EJ (November 2011). “Transcriptional and epigenetic mechanisms of addiction”. 《Nat. Rev. Neurosci.》 12 (11): 623–637. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. 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. 
  7. ↑ Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M (2012). “Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms”. 《Journal of Psychoactive Drugs》 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC 4040958. PMID 22641964. 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. 
  8. ↑ Olsen CM (December 2011). “Natural rewards, neuroplasticity, and non-drug addictions”. 《Neuropharmacology》 61 (7): 1109–22. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101. 
  9. ↑ 가 나 Ikemoto S (2010). “Brain reward circuitry beyond the mesolimbic dopamine system: a neurobiological theory”. 《Neurosci Biobehav Rev》 35 (2): 129–50. doi:10.1016/j.neubiorev.2010.02.001. PMC 2894302. PMID 20149820. 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
  10. ↑ You ZB, Chen YQ, Wise RA (2001). “Dopamine and glutamate release in the nucleus accumbens and ventral tegmental area of rat following lateral hypothalamic self-stimulation”. 《Neuroscience》 107 (4): 629–39. doi:10.1016/s0306-4522(01)00379-7. PMID 11720786. 
  11. ↑ 가 나 다 Pierce RC, Kumaresan V (2006). “The mesolimbic dopamine system: The final common pathway for the reinforcing effect of drugs of abuse?”. 《Neuroscience and Biobehavioral Reviews》 30 (2): 215–38. doi:10.1016/j.neubiorev.2005.04.016. PMID 16099045. 
  12. ↑ Zhang TA, Maldve RE, Morrisett RA (2006). “Coincident signaling in mesolimbic structures underlying alcohol reinforcement”. 《Biochemical Pharmacology》 72 (8): 919–27. doi:10.1016/j.bcp.2006.04.022. PMID 16764827. 
  13. ↑ Purves D et al. 2008. Neuroscience. Sinauer 4ed. 754-56
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