{{위키데이터 속성 추적}}
[[파일:Vias dopaminergicas.png|섬네일]]
'''중뇌-변연계 경로'''({{llang|en|mesolimbic pathway}}) 또는 '''보상 경로'''({{llang|en|reward pathway}})는 [[뇌]]의 [[도파민시스템|도파민 경로]] 중 하나이다.<ref name="pmid21205279">{{저널 인용| vauthors = Dreyer JL | title = New insights into the roles of microRNAs in drug addiction and neuroplasticity | journal = Genome Med | volume = 2 | issue = 12 | pages = 92 | year = 2010 | pmid = 21205279 | pmc = 3025434 | doi = 10.1186/gm213 }}</ref> [[중뇌]]의 [[배쪽 피개부]]와 [[전뇌]] [[기저핵]]의 배쪽 [[선조체]]를 연결한다. 배쪽 선조체에는 [[기댐핵]]과 [[후각결절]] 등이 포함된다.<ref name="Dopaminergic pathways and reward system review">{{저널 인용| vauthors = Ikemoto S | title = Brain reward circuitry beyond the mesolimbic dopamine system: a neurobiological theory | journal = Neurosci Biobehav Rev | volume = 35 | issue = 2 | pages = 129–50 | year = 2010 | pmid = 20149820 | pmc = 2894302 | doi = 10.1016/j.neubiorev.2010.02.001 | quote = 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.&nbsp;... 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}}<br />[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2894302/figure/F3/ Figure 3: The ventral striatum and self-administration of amphetamine]</ref>

중뇌-변연계 경로에서 기댐핵으로의 도파민 분비는 [[유인적 현저성]](incentive salience, [[보상 자극]]에 대한 동기와 욕구)을 조절하고 [[강화 (심리학)|강화]]와 보상에 관련된 운동 기능 학습을 촉진한다.<ref name="NAcc function" /><ref name="Malenka NAcc">{{서적 인용|vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-148127-4 | page = 266 | edition = 2nd | chapter = Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu | quote = Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward.}}</ref><ref name="Pleasure system" /> 또한 주관적인 쾌감의 인식에도 영향을 줄 가능성이 있다.<ref name="NAcc function">{{서적 인용|vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-148127-4 | pages = 147–148, 367, 376 | edition = 2nd | quote= 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.&nbsp;...<br />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.&nbsp;...<br />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.}}</ref><ref name="Pleasure system">{{저널 인용| vauthors = Berridge KC, Kringelbach ML | title = Pleasure systems in the brain | journal = Neuron | volume = 86 | issue = 3 | pages = 646–664 | date = May 2015 | pmid = 25950633 | doi = 10.1016/j.neuron.2015.02.018 | quote = 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.| pmc=4425246}}</ref> 중뇌-변연계 경로 및 그에 연결된 기댐핵 신경세포의 조절곤란은 [[탐닉]]의 형성과 유지에 중요한 역할을 한다.<ref name="pmid21205279" /><ref name="Nestler2">{{저널 인용|vauthors=Robison AJ, Nestler EJ|date=November 2011|title=Transcriptional and epigenetic mechanisms of addiction|journal=Nat. Rev. Neurosci.|volume=12|issue=11|pages=623–637|doi=10.1038/nrn3111|pmc=3272277|pmid=21989194|quote=ΔFosB has been linked directly to several addiction-related behaviors&nbsp;...  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.}}</ref><ref name="ΔFosB reward2">{{저널 인용|vauthors=Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M|year=2012|title=Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms|journal=Journal of Psychoactive Drugs|volume=44|issue=1|pages=38–55|doi=10.1080/02791072.2012.662112|pmc=4040958|pmid=22641964|quote=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.&nbsp;... 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.}}</ref><ref name="Natural and drug addictions2">{{저널 인용|author=Olsen CM|date=December 2011|title=Natural rewards, neuroplasticity, and non-drug addictions|journal=Neuropharmacology|volume=61|issue=7|pages=1109–22|doi=10.1016/j.neuropharm.2011.03.010|pmc=3139704|pmid=21459101}}</ref>

== 구조 ==
[[파일:Mesolimbic pathway.svg|섬네일|중뇌-변연계 경로와 다른 [[도파민시스템|도파민 경로]]의 위치]]
중뇌-변연계 경로는 [[배쪽 피개부]](VTA)에서 뻗어나와 [[기댐핵]](NAcc)과 [[후각결절]]을 포함하는 [[배쪽 선조체]]로 가는 도파민신경세포들의 모임이다.<ref name="Dopaminergic pathways and reward system review2">{{저널 인용|vauthors=Ikemoto S|year=2010|title=Brain reward circuitry beyond the mesolimbic dopamine system: a neurobiological theory|journal=Neurosci Biobehav Rev|volume=35|issue=2|pages=129–50|doi=10.1016/j.neubiorev.2010.02.001|pmc=2894302|pmid=20149820|quote=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.&nbsp;... 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}}[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2894302/figure/F3/ Figure 3: The ventral striatum and self-administration of amphetamine]</ref> [[뇌자극보상]]을 매개하는 신경 경로들의 모임인 [[안쪽앞뇌다발]]에 속한다.<ref name="pmid117207862">{{저널 인용|vauthors=You ZB, Chen YQ, Wise RA|year=2001|title=Dopamine and glutamate release in the nucleus accumbens and ventral tegmental area of rat following lateral hypothalamic self-stimulation|journal=Neuroscience|volume=107|issue=4|pages=629–39|doi=10.1016/s0306-4522(01)00379-7|pmid=11720786}}</ref>

[[중뇌]]에 위치한 배쪽 피개부는 [[도파민]]·[[감마 아미노뷰티르산|GABA]]·[[글루탐산]] 신경세포들로 이루어져 있다.<ref name="Pierce2">{{저널 인용|vauthors=Pierce RC, Kumaresan V|year=2006|title=The mesolimbic dopamine system: The final common pathway for the reinforcing effect of drugs of abuse?|journal=Neuroscience and Biobehavioral Reviews|volume=30|issue=2|pages=215–38|doi=10.1016/j.neubiorev.2005.04.016|pmid=16099045}}</ref> 이 부위의 도파민신경세포는 [[대뇌다리교뇌핵]]과 [[등가쪽 피개핵]]의 콜린성신경세포로부터 자극을 전달받고, [[전전두엽]] 등 다른 부위의 글루탐산신경세포로부터도 자극을 받는다. [[배쪽 선조체]]에 위치한 기댐핵과 후각결절은 주로 [[중간크기 가시뉴런]](MSN)으로 이루어져 있다.<ref name="Dopaminergic pathways and reward system review2" /><ref name="Zhang2">{{저널 인용|vauthors=Zhang TA, Maldve RE, Morrisett RA|year=2006|title=Coincident signaling in mesolimbic structures underlying alcohol reinforcement|journal=[[Biochemical Pharmacology (journal)|Biochemical Pharmacology]]|volume=72|issue=8|pages=919–27|doi=10.1016/j.bcp.2006.04.022|pmid=16764827}}</ref><ref name="Purves2">Purves D et al. 2008. Neuroscience. Sinauer 4ed. 754-56</ref> 기댐핵은 각각 변연기능과 운동기능에 관련된 NAcc 껍질(NAcc shell)과 NAcc 핵심(NAcc core)의 두 부분으로 나뉜다.<ref name="Pierce2" /> 기댐핵의 중간크기 가시뉴런은 배쪽 피개부의 도파민신경세포와 [[해마 (뇌)|해마]]·[[편도체]]·안쪽전전두엽의 글루탐산신경세포로부터 자극을 전달받는다. 이러한 자극을 받고 활성화된 중간크기 가시뉴런은 [[배쪽 창백핵]]으로 GABA를 분비한다.<ref name="Pierce2" />

== 기능 ==
중뇌-변연계 경로는 [[유인적 현저성]], 동기부여, 강화학습, 공포 등등 여러 인지 과정을 조절한다.<ref name="NHM pathways2">{{서적 인용|title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience|vauthors=Malenka RC, Nestler EJ, Hyman SE|publisher=McGraw-Hill Medical|year=2009|isbn=9780071481274|veditors=Sydor A, Brown RY|edition=2nd|location=New York|pages=147–148, 154–157|chapter=Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin|quote=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.&nbsp;... 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).&nbsp;... 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.&nbsp;... Noradrenergic projections from the LC thus interact with dopaminergic projections from the VTA to regulate cognitive control.}}</ref><ref name="ADHD 2008 paper2">{{저널 인용|last1=Engert|first1=Veronika|last2=Pruessner|first2=Jens C|date=9 January 2017|title=Dopaminergic and Noradrenergic Contributions to Functionality in ADHD: The Role of Methylphenidate|journal=Current Neuropharmacology|volume=6|issue=4|pages=322–328|doi=10.2174/157015908787386069|issn=1570-159X|pmc=2701285|pmid=19587853}}</ref><ref>{{저널 인용|last1=Pezze|first1=Marie A.|last2=Feldon|first2=Joram|date=1 December 2004|title=Mesolimbic dopaminergic pathways in fear conditioning|journal=Progress in Neurobiology|volume=74|issue=5|pages=301–320|doi=10.1016/j.pneurobio.2004.09.004|issn=0301-0082|pmid=15582224}}</ref>

중뇌-변연계 경로는 [[동기 부여]]의 인지에 관여한다. 이 경로에 도파민이 고갈되거나 그 시작 부위에 병변이 생기면, 동물이 보상을 얻으려 행동하는 정도가 줄어든다. 예를 들어 쥐가 니코틴 정맥 주입을 받으려고 손잡이를 누르는 횟수나 먹이를 찾으러 돌아다니는 시간이 감소하는 것을 관찰할 수 있다. 도파민성 약물은 동물이 보상을 얻으려 행동하는 정도를 증가시킬 수 있다. 나아가, 보상을 기대하는 동안에는 중뇌-변연계 경로 신경세포의 발화율이 증가하는데, 이는 갈망(craving)의 기전에 대한 설명이 될 수 있다.<ref>{{저널 인용|last1=Salamone|first1=John D.|last2=Correa|first2=Mercè|year=2012|title=The Mysterious Motivational Functions of Mesolimbic Dopamine|journal=Neuron|volume=76|issue=3|pages=470–485|doi=10.1016/j.neuron.2012.10.021|pmc=4450094|pmid=23141060}}</ref> 과거에 중뇌-변연계 경로의 도파민 분비는 쾌감의 주된 매개체로 생각되었으나, 현재는 쾌감의 지각에 있어 중뇌-변연계의 역할은 부차적일 뿐이라고 여겨진다.<ref name="Pleasure system2">{{저널 인용|vauthors=Berridge KC, Kringelbach ML|date=May 2015|title=Pleasure systems in the brain|journal=Neuron|volume=86|issue=3|pages=646–664|doi=10.1016/j.neuron.2015.02.018|pmc=4425246|pmid=25950633|quote=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.}}</ref><ref>{{저널 인용|last1=Berridge|first1=Kent C|last2=Kringelbach|first2=Morten L|date=1 June 2013|title=Neuroscience of affect: brain mechanisms of pleasure and displeasure|journal=Current Opinion in Neurobiology|volume=23|issue=3|pages=294–303|doi=10.1016/j.conb.2013.01.017|pmc=3644539|pmid=23375169}}</ref>

== 임상적 중요성 ==
=== 탐닉 기전 ===
중뇌-변연계 경로와 그 출력을 받는 특정 종류의 신경세포(예: 기댐핵의 D1-유형 [[중간크기 가시뉴런]])은 [[탐닉]]의 신경생물학에서 핵심 역할을 한다.<ref name="Nestler2"/><ref name="ΔFosB reward2"/><ref name="Natural and drug addictions2"/> 약물 탐닉은 습관적 약물 사용에 따른 뇌 신경회로의 화학적 변화 때문에 생기는 병이다.<ref>{{서적 인용|url=https://www.ncbi.nlm.nih.gov/books/NBK424849/|title=THE NEUROBIOLOGY OF SUBSTANCE USE, MISUSE, AND ADDICTION|last=Administration (US)|first=Substance Abuse and Mental Health Services|last2=General (US)|first2=Office of the Surgeon|date=November 2016|publisher=US Department of Health and Human Services}}</ref> [[코카인]], [[알코올]], [[니코틴]] 등 흔히 접할 수 있는 중독성 물질은 중뇌-변연계 경로, 특히 기댐핵에서 세포외 도파민 농도를 높이는 것으로 드러났다. 그 기전은 약물의 유형에 따라 다르다. 예를 들어 코카인은 시냅스전 도파민 전달체를 차단하여 시냅스 도파민의 재흡수를 막는다. 또다른 자극제인 [[암페타민]]은 시냅스소포의 도파민 분비를 촉진한다. 자극제가 아닌 약물의 경우 [[리간드 개폐 통로]]나 [[G 단백질 연결 수용체]]와 결합하는 경우가 많은데, 알코올, 니코틴, [[테트라하이드로카나비놀]](THC) 등이 그 예이다.<ref>{{저널 인용|last=Adinoff|first=Bryon|date=2004|title=Neurobiologic Processes in Drug Reward and Addiction|journal=Harvard Review of Psychiatry|volume=12|issue=6|pages=305–320|doi=10.1080/10673220490910844|issn=1067-3229|pmc=1920543|pmid=15764467}}</ref>

이처럼 중뇌-변연계 경로가 활성화되어 도파민을 분비하면 보상을 인지하게 된다. 이렇게 형성된 자극과 보상의 연결은 [[소거 (심리학)|소거]]에 저항성이 있으며, 보상을 준 행동을 똑같이 반복하려는 동기의 정도를 높인다.<ref>{{저널 인용|last=Di Chiara|first=Gaetano|last2=Bassareo|first2=Valentina|date=2007-02-01|title=Reward system and addiction: what dopamine does and doesn't do|journal=Current Opinion in Pharmacology|series=Neurosciences|volume=7|issue=1|pages=69–76|doi=10.1016/j.coph.2006.11.003|pmid=17174602|issn=1471-4892}}</ref>

2017년의 한 연구는 감정적·신체적·성적 학대와 부정적 생애사건은 코카인에 대한 변연계의 높은 반응 수준과 상관관계가 있다고 보고했다. 즉, 학대를 경험한 사람은 코카인 등 약물 사용에 빠지기 쉬운 뇌 신경회로를 가질 확률이 더 높다는 것이다.<ref>Regier PS, Monge ZA, Franklin TR, Wetherill RR, Teitelman AM, Jagannathan K, et al. Emotional, physical and sexual abuse are associated with a heightened limbic response to cocaine cues. Addiction Biology. 2017 Nov;22(6):1768-177. doi: 10.1111/adb.12445</ref>

=== 신경 및 심리 장애와의 관계 ===
중뇌-변연계 경로는 [[조현병]], [[주요 우울 장애|우울증]],<ref name="Van2">{{저널 인용|author=Van, den Heuval DMA, Pasterkamp RJ|year=2008|title=Getting connected in the dopamine system|journal=Progress in Neurobiology|volume=85|issue=1|pages=75–93|doi=10.1016/j.pneurobio.2008.01.003|pmid=18304718}}</ref><ref name="Laviolette2">{{저널 인용|author=Laviolette SR|year=2007|title=Dopamine modulation of emotional processing in cortical and subcortical neural circuits: evidence for a final common pathway in schizophrenia?|journal=Schizophrenia Bulletin|volume=33|issue=4|pages=971–981|doi=10.1093/schbul/sbm048|pmc=2632330|pmid=17519393}}</ref><ref name="Diaz2">Diaz J. 1996. How Drugs Influence Behavior: A Neurobehavorial Approach. Prentice Hall</ref> [[파킨슨병]]과 관련이 있다.<ref>{{저널 인용|last=Nyberg|first=Eric M.|last2=Tanabe|first2=Jody|last3=Honce|first3=Justin M.|last4=Krmpotich|first4=Theodore|last5=Shelton|first5=Erika|last6=Hedeman|first6=Jessica|last7=Berman|first7=Brian D.|date=2015-05-01|title=Morphologic changes in the mesolimbic pathway in Parkinson's disease motor subtypes|journal=Parkinsonism & Related Disorders|volume=21|issue=5|pages=536–540|doi=10.1016/j.parkreldis.2015.03.008|pmid=25817514|pmc=4424152|issn=1353-8020}}</ref><ref>{{저널 인용|last=Caminiti|first=Silvia Paola|last2=Presotto|first2=Luca|last3=Baroncini|first3=Damiano|last4=Garibotto|first4=Valentina|last5=Moresco|first5=Rosa Maria|last6=Gianolli|first6=Luigi|last7=Volonté|first7=Maria Antonietta|last8=Antonini|first8=Angelo|last9=Perani|first9=Daniela|date=2017-01-01|title=Axonal damage and loss of connectivity in nigrostriatal and mesolimbic dopamine pathways in early Parkinson's disease|journal=NeuroImage: Clinical|volume=14|pages=734–740|doi=10.1016/j.nicl.2017.03.011|pmid=28409113|pmc=5379906|issn=2213-1582}}</ref> 또 전자 매체 과용에도 관련돼 있다는 주장이 있다.<ref>{{웹 인용|url=http://sitn.hms.harvard.edu/flash/2018/dopamine-smartphones-battle-time/|title=Dopamine, Smartphones & You: A battle for your time|date=2018-05-01|website=Science in the News|access-date=2019-05-10}}</ref> 각각의 장애는 중뇌-변연계의 서로 다른 구조적 변화를 동반한다.<ref name="Van2" />

== 다른 도파민 경로 ==
{{본문|도파민시스템}}
* [[중뇌-피질 경로]]
* [[흑색질-선조체 경로]]
* [[결절-누두체 경로]]

== 같이 보기 ==
* [[항정신병제제]]
* [[지연성 운동장애]]
* [[내성 (약물)]]
* [[금단 증상]]

== 각주 ==
{{각주|2}}

== 외부 링크 ==
{{위키공용분류}}

{{보강장애}}

[[분류:중추신경계]]
[[분류:탐닉]]
[[분류:도파민]]
[[분류:중추신경계 경로]]