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{{short description|Projection neurons in the brain that synthesize and release dopamine}}
[[File:Dopaminergic pathways.svg|thumb|right|The main dopaminergic pathways of the [[human brain]]]]
'''Dopaminergic pathways''' ('''dopamine pathways''', '''dopaminergic projections''') in the [[human brain]] are involved in both physiological and behavioral processes including [[motion|movement]], [[cognition]], [[executive functions]], [[Reward system|reward]], [[motivation]], and [[Neuroendocrine cell|neuroendocrine control]].<ref>{{cite journal | vauthors = Alcaro A, Huber R, Panksepp J | title = Behavioral functions of the mesolimbic dopaminergic system: an affective neuroethological perspective | journal = Brain Research Reviews | volume = 56 | issue = 2 | pages = 283–321 | date = December 2007 | pmid = 17905440 | pmc = 2238694 | doi = 10.1016/j.brainresrev.2007.07.014 }}</ref> Each pathway is a set of [[projection neuron|projection neurons]], consisting of individual dopaminergic neurons.

The four major dopaminergic pathways are the [[mesolimbic pathway]], the [[mesocortical pathway]], the [[nigrostriatal pathway]], and the [[tuberoinfundibular pathway]]. The mesolimbic pathway and the mesocortical pathway form the mesocorticolimbic system. Two other dopaminergic pathways to be considered are the [[hypothalamospinal tract]] and the [[incertohypothalamic pathway]].

[[Parkinson's disease]], [[attention deficit hyperactivity disorder]] (ADHD), [[substance use disorder]]s ([[addiction]]), and [[restless legs syndrome]] (RLS) can be attributed to dysfunction in specific dopaminergic pathways.

The dopamine neurons of the dopaminergic pathways synthesize and release the [[neurotransmitter]] [[dopamine]].<ref name="urlBeyond the Reward Pathway">{{cite web |title=Beyond the Reward Pathway | work = Learn Genetics | publisher = University of Utah |url=http://learn.genetics.utah.edu/content/addiction/reward/pathways.html|url-status=dead |archive-url= https://web.archive.org/web/20100209020641/http://learn.genetics.utah.edu/content/addiction/reward/pathways.html |archive-date=2010-02-09 |access-date=2009-10-23 }}</ref><ref name="projection">{{cite book | vauthors = Le Moal M | chapter = Mesocorticolimbic Dopaminergic Neurons: Functional and Regulatory Roles |url= http://www.acnp.org/g4/gn401000025/ch025.html|url-status=dead|archive-url= https://web.archive.org/web/20180205211300/http://www.acnp.org/g4/gn401000025/ch025.html |archive-date=5 February 2018 | veditors = Bloom FE, Kupfer DJ |title=Psychopharmacology: the fourth generation of progress |date=1995 |publisher=Raven Press |location=New York |isbn=978-0-7817-0166-2 }}</ref> Enzymes [[tyrosine hydroxylase]] and [[dopa decarboxylase]] are required for dopamine synthesis.<ref name = "Harsing_2000">{{cite book | vauthors = Harsing LG | chapter = Dopamine and the Dopaminergic Systems of the Brain |date=2008 | title = Handbook of Neurochemistry and Molecular Neurobiology|pages=149–170 | veditors = Lajtha A, Vizi ES |place=Boston, MA|publisher=Springer US |doi=10.1007/978-0-387-30382-6_7|isbn=978-0-387-30351-2 }}</ref> These enzymes are both produced in the [[Soma (biology)|cell bodies]] of dopamine neurons. Dopamine is stored in the cytoplasm and vesicles in axon terminals. Dopamine release from vesicles is triggered by action potential propagation-induced membrane depolarization.<ref name = "Harsing_2000" /> The [[axon]]s of dopamine neurons extend the entire length of their designated pathway.

== Pathways {{anchor|Mesocorticolimbic projection}} ==

=== Major ===

Six of the dopaminergic pathways are listed below.<ref name="Dopaminergic pathways and reward system review" /><ref name="NHM pathways" /><ref name="NHM tuberoinfundibular pathway">{{cite book | 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 = 9780071481274 | page = 249 | edition = 2nd | chapter = Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu | quote=Relationship of the hypothalamus and the pituitary gland. The anterior pituitary, or adenohypophysis, receives rich blood flow from the capillaries of the portal hypophyseal system. This system delivers factors released by hypothalamic neurons into portal capillaries at the median eminence. The figure shows one such projection, from the tuberal (arcuate) nuclei via the tuberoinfundibular tract to the median eminence.}}</ref>
{{clear}}
{| class="wikitable"
! scope="col" colspan="2"| Pathway name
! scope="col" | Description
! scope="col" | Associated processes
! scope="col" | Associated disorders
|- 
| rowspan="2" style="text-align:center;" | Mesocorticolimbic system
| {{center|[[mesolimbic pathway|Mesolimbic pathway]]}}
| The mesolimbic pathway transmits dopamine from the [[ventral tegmental area]] (VTA), which is located in the [[midbrain]], to the [[ventral striatum]], which includes both the [[nucleus accumbens]] and [[olfactory tubercle]].<ref name="Dopaminergic pathways and reward system review">{{cite journal | vauthors = Ikemoto S | title = Brain reward circuitry beyond the mesolimbic dopamine system: a neurobiological theory | journal = Neuroscience and Biobehavioral Reviews | volume = 35 | issue = 2 | pages = 129–50 | date = November 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 }} [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2894302/figure/F3/ Figure 3: The ventral striatum and self-administration of amphetamine]</ref><ref name="NHM pathways" /> The "meso" [[Prefix (linguistics)|prefix]] in the word "mesolimbic" refers to the midbrain, or "middle brain", since "meso" means "middle" in [[Greek language|Greek]].
|
*[[reward system|reward]]-related cognition
**[[incentive salience]] ("wanting")
**{{nowrap|[[pleasure]] ("liking") response from certain stimuli}}
**[[positive reinforcement]]
*aversion-related cognition
|
*[[ADHD]]
*[[addiction]]
*[[schizophrenia]]
|- 
| {{center|[[mesocortical pathway|Mesocortical pathway]]}} 
| The mesocortical pathway transmits dopamine from the VTA to the [[prefrontal cortex]]. The "meso" prefix in "mesocortical" refers to the VTA, which is located in the midbrain, and "cortical" refers to the cortex.
|
* [[executive function]]s
| 
*[[ADHD]]
*[[addiction]]
*[[schizophrenia]]
|- 
| colspan="2" style="text-align:center;" | [[Nigrostriatal pathway]] 
| The nigrostriatal pathway transmits dopaminergic neurons from the zona compacta of the substantia nigra<ref name=":02">{{cite book | vauthors = Hull EM, Rodríguez-Manzo G | chapter = Male Sexual Behavior |date=2017 | doi = 10.1016/b978-0-12-803592-4.00001-8 | title = Hormones, Brain and Behavior |pages=1–57 |publisher=Elsevier | isbn = 9780128036082 }}</ref> to the [[caudate nucleus]] and [[putamen]]. 
The [[substantia nigra]] is located in the midbrain, while both the caudate nucleus and putamen are located in the [[dorsal striatum]].
|
*motor function 
*[[reward system|reward]]-related cognition
*[[associative learning]]
|
*[[addiction]]
*[[chorea]]
*Huntington's disease
*Schizophrenia
*ADHD
*Tourette's Syndrome
*[[Parkinson's&nbsp;disease]]
|- 
| colspan="2" style="text-align:center;" | [[Tuberoinfundibular pathway]] || The tuberoinfundibular pathway transmits dopamine from the [[hypothalamus]] to the [[pituitary gland]].
This pathway controls the secretion of certain [[Hormone|hormones]], including [[prolactin]], from the pituitary gland.<ref>{{cite book | vauthors = Habibi M | chapter = Acetylcholine ☆ |date=2017 | doi = 10.1016/b978-0-12-809324-5.00464-8 | title = Reference Module in Neuroscience and Biobehavioral Psychology |publisher=Elsevier | isbn = 9780128093245 }}</ref>

"Infundibular" in the word "tuberoinfundibular" refers to the cup or [[Pituitary stalk|''infundibulum'']], out of which the pituitary gland develops.
|
*regulation of prolactin secretion<ref name="Hudepohl_2012">{{cite book | vauthors = Hudepohl NS, Nasrallah HA | chapter = Antipsychotic drugs |date=2012 | doi = 10.1016/b978-0-444-52002-9.00039-5 | title = Neurobiology of Psychiatric Disorders | series = Handbook of Clinical Neurology | volume = 106 |pages=657–667 |publisher=Elsevier | pmid = 22608650 | isbn = 9780444520029 | s2cid = 36698721 }}</ref>
|
*[[hyperprolactinaemia]]<ref name="Hudepohl_2012" />
|- 
| colspan="2" style="text-align:center;" | [[Hypothalamospinal tract]] || The tuberoinfundibular pathway not only regulates hormonal balance but also influences locomotor networks in the brainstem and spinal cord. Modulating motor control and coordination, showcasing the interconnected nature of neural circuits in the brain.
| 
*motor function.
| 
*[[restless legs syndrome]]
|- 
| colspan="2" style="text-align:center;" | [[Incertohypothalamic pathway]] || This pathway from the [[zona incerta]] influences the hypothalamus and locomotor centers in the brainstem.
| 
*visceral and sensorimotor activities.
| 
*[[tremor]]
|}

=== Minor ===
:Hypothalamospinal
:* [[Hypothalamus]] → [[Spinal cord]]
:Incertohypothalamic
:* [[Zona incerta]] → [[Hypothalamus]]
:* Zona incerta → [[Brainstem]] VTA → [[Amygdala]] (mesoamygdaloid pathway)<ref name="NHM pathways">{{cite book | 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 = 9780071481274 | pages = 147–148, 154–157 | edition = 2nd | 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>
:VTA → [[Hippocampus]]<ref name="NHM pathways" />
:VTA → [[Cingulate cortex]]<ref name="NHM pathways" />
:VTA → [[Olfactory bulb]]<ref name="NHM pathways" />
:SNc → [[Subthalamic nucleus]]<ref name="pmid15380000">{{cite journal | vauthors = Cragg SJ, Baufreton J, Xue Y, Bolam JP, Bevan MD | title = Synaptic release of dopamine in the subthalamic nucleus | journal = The European Journal of Neuroscience | volume = 20 | issue = 7 | pages = 1788–802 | date = October 2004 | pmid = 15380000 | doi = 10.1111/j.1460-9568.2004.03629.x | s2cid = 14698708 | doi-access = free }}</ref>
== Function ==

=== Mesocorticolimbic system ===
[[File:Mesocorticolimbic Circuit.png|thumb|The mesocorticolimbic pathway originates through the VTA and passes through the amygdala, nucleus accumbens, and hippocampus. These functions are relative to memory, emotional regulation, motivation, and reward.]]
The [[Mesocorticolimbic circuit|mesocorticolimbic system]] ([[mesocorticolimbic circuit]]) refers to both the [[mesocortical pathway|mesocortical]] and [[mesolimbic pathway|mesolimbic]] pathways.<ref name="projection" /><ref name="MEDRS-quality human review">{{cite journal | vauthors = Doyon WM, Thomas AM, Ostroumov A, Dong Y, Dani JA | title = Potential substrates for nicotine and alcohol interactions: a focus on the mesocorticolimbic dopamine system | journal = Biochemical Pharmacology | volume = 86 | issue = 8 | pages = 1181–93 | date = October 2013 | pmid = 23876345 | pmc = 3800178 | doi = 10.1016/j.bcp.2013.07.007 }}</ref> Both pathways originate at the ventral tegmental area (VTA) which is located in the midbrain. Through separate connections to the prefrontal cortex (mesocortical) and ventral striatum (mesolimbic), the mesocorticolimbic projection has a significant role in learning, motivation, reward, memory and movement.<ref>{{cite journal | vauthors = Yamaguchi T, Wang HL, Li X, Ng TH, Morales M | title = Mesocorticolimbic glutamatergic pathway | journal = The Journal of Neuroscience | volume = 31 | issue = 23 | pages = 8476–90 | date = June 2011 | pmid = 21653852 | pmc = 6623324 | doi = 10.1523/JNEUROSCI.1598-11.2011 }}</ref> Dopamine receptor subtypes, D1 and D2 have been shown to have complementary functions in the mesocorticolimbic projection, facilitating learning in response to both positive and [[negative feedback]].<ref>{{cite journal | vauthors = Verharen JP, Adan RA, Vanderschuren LJ | title = Differential contributions of striatal dopamine D1 and D2 receptors to component processes of value-based decision making | journal = Neuropsychopharmacology | volume = 44 | issue = 13 | pages = 2195–2204 | date = December 2019 | pmid = 31254972 | pmc = 6897916 | doi = 10.1038/s41386-019-0454-0 }}</ref> Both pathways of the mesocorticolimbic system are associated with [[ADHD]], [[schizophrenia]] and [[addiction]].<ref name="NHM-Cognitive Control">{{cite book|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=313–321|chapter=Chapter 13: Higher Cognitive Function and Behavioral Control|quote={{bull}} Executive function, the cognitive control of behavior, depends on the prefrontal cortex, which is highly developed in higher primates and especially humans. {{bull}} Working memory is a short-term, capacity-limited cognitive buffer that stores information and permits its manipulation to guide decision-making and behavior.&nbsp;... These diverse inputs and back projections to both cortical and subcortical structures put the prefrontal cortex in a position to exert what is often called “top-down” control or cognitive control of behavior.&nbsp;... The prefrontal cortex receives inputs not only from other cortical regions, including association cortex, but also, via the thalamus, inputs from subcortical structures subserving emotion and motivation, such as the amygdala (Chapter 14) and ventral striatum (or nucleus accumbens; Chapter 15).&nbsp;... In conditions in which prepotent responses tend to dominate behavior, such as in drug addiction, where drug cues can elicit drug seeking (Chapter 15), or in attention deficit hyperactivity disorder (ADHD; described below), significant negative consequences can result.&nbsp;... ADHD can be conceptualized as a disorder of executive function; specifically, ADHD is characterized by reduced ability to exert and maintain cognitive control of behavior. Compared with healthy individuals, those with ADHD have diminished ability to suppress inappropriate prepotent responses to stimuli (impaired response inhibition) and diminished ability to inhibit responses to irrelevant stimuli (impaired interference suppression).&nbsp;... Functional neuroimaging in humans demonstrates activation of the prefrontal cortex and caudate nucleus (part of the striatum) in tasks that demand inhibitory control of behavior.&nbsp;... Early results with structural MRI show thinning of the cerebral cortex in ADHD subjects compared with age-matched controls in prefrontal cortex and posterior parietal cortex, areas involved in working memory and attention.}}</ref><ref name="ADHD 2008 paper">{{cite journal | vauthors = Engert V, Pruessner JC | title = Dopaminergic and noradrenergic contributions to functionality in ADHD: the role of methylphenidate | journal = Current Neuropharmacology | volume = 6 | issue = 4 | pages = 322–8 | date = December 2008 | pmid = 19587853 | pmc = 2701285 | doi = 10.2174/157015908787386069 }}</ref><ref name=":0">{{cite journal | vauthors = Dreyer JL | title = New insights into the roles of microRNAs in drug addiction and neuroplasticity | journal = Genome Medicine | volume = 2 | issue = 12 | pages = 92 | date = December 2010 | pmid = 21205279 | pmc = 3025434 | doi = 10.1186/gm213 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Robison AJ, Nestler EJ | title = Transcriptional and epigenetic mechanisms of addiction | journal = Nature Reviews. Neuroscience | volume = 12 | issue = 11 | pages = 623–37 | date = October 2011 | pmid = 21989194 | pmc = 3272277 | doi = 10.1038/nrn3111 }}</ref>

==== Mesocortical pathway ====

The [[mesocortical pathway]] projects from the ventral tegmental area to the prefrontal cortex ([[Ventral tegmental area|VTA]] → [[Prefrontal cortex]]). This pathway is involved in cognition and the regulation of [[executive function]]s (e.g., attention, working memory, [[inhibitory control]], planning, etc.) This intricate neural circuit serves as a crucial communication route within the brain, facilitating the transmission of dopamine, a neurotransmitter associated with reward, motivation, and cognitive control.<ref>{{Cite journal |last=Keyser |first=J. De |date=1990 |title=The mesoneocortical dopamine neuron system |url=https://doi.org/10.1212/WNL.40.11.1660 |journal=Neurology |volume=40 |issue=11 |pages=1660–1662|doi=10.1212/WNL.40.11.1660 |pmid=2234421 |s2cid=12241566 }}</ref> The prefrontal cortex, being a central hub for executive functions, relies on the input from the mesocortical pathway to modulate and fine-tune cognitive processes essential for goal-directed behavior and decision-making.<ref>{{Cite journal |last1=Floresco |first1=Stan B. |last2=Magyar |first2=Orsolya |date=2006 |title=Mesocortical dopamine modulation of executive functions: beyond working memory |url=https://doi.org/10.1007/s00213-006-0404-5 |journal=Psychopharmacology |volume=188 |issue=4 |pages=567–585 |doi=10.1007/s00213-006-0404-5 |pmid=16670842 |s2cid=24568869 |via=SpringerLink}}</ref> Dysregulation of the neurons in this pathway has been connected to ADHD.<ref name="ADHD 2008 paper" />

==== Mesolimbic pathway ====

Referred to as the reward pathway, [[mesolimbic pathway]] projects from the ventral tegmental area to the ventral striatum ( VTA → [[Ventral striatum]] ([[nucleus accumbens]] and [[olfactory tubercle]]).<ref name=":0" /> When a reward is anticipated, the firing rate of dopamine neurons in the mesolimbic pathway increases.<ref name=":1">{{cite journal | vauthors = Salamone JD, Correa M | title = The mysterious motivational functions of mesolimbic dopamine | journal = Neuron | volume = 76 | issue = 3 | pages = 470–85 | date = November 2012 | pmid = 23141060 | pmc = 4450094 | doi = 10.1016/j.neuron.2012.10.021 }}</ref> The mesolimbic pathway is involved with [[incentive salience]], [[motivation]], reinforcement learning, fear and other cognitive processes.<ref name="NHM pathways" /><ref name="ADHD 2008 paper" /><ref>{{cite journal | vauthors = Pezze MA, Feldon J | title = Mesolimbic dopaminergic pathways in fear conditioning | journal = Progress in Neurobiology | volume = 74 | issue = 5 | pages = 301–20 | date = December 2004 | pmid = 15582224 | doi = 10.1016/j.pneurobio.2004.09.004 | s2cid = 36091832 }}</ref> In animal studies, depletion of dopamine in this pathway, or lesions at its site of origin, decrease the extent to which an animal is willing to go to obtain a reward (e.g., the number of lever presses for nicotine or time searching for food).<ref name=":1" /> Research is ongoing to determine the role of the mesolimbic pathway in the perception of pleasure.<ref name="Pleasure system">{{cite journal | vauthors = Berridge KC, Kringelbach ML | title = Pleasure systems in the brain | journal = Neuron | volume = 86 | issue = 3 | pages = 646–64 | date = May 2015 | pmid = 25950633 | pmc = 4425246 | 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. }}</ref><ref>{{cite journal | vauthors = Berridge KC, Kringelbach ML | title = Neuroscience of affect: brain mechanisms of pleasure and displeasure | journal = Current Opinion in Neurobiology | volume = 23 | issue = 3 | pages = 294–303 | date = June 2013 | pmid = 23375169 | pmc = 3644539 | doi = 10.1016/j.conb.2013.01.017 }}</ref><ref>{{Cite book| vauthors = Nestler EJ |url=https://www.worldcat.org/oclc/1191071328|title=Molecular neuropharmacology a foundation for clinical neuroscience|date=2020|others=Paul J. Kenny, Scott J. Russo, Anne, MD Schaefer|isbn=978-1-260-45691-2|edition=Fourth |location=New York|oclc=1191071328}}</ref><ref>{{cite journal | vauthors = Berridge KC, Kringelbach ML | title = Pleasure systems in the brain | journal = Neuron | volume = 86 | issue = 3 | pages = 646–64 | date = May 2015 | pmid = 25950633 | pmc = 4425246 | doi = 10.1016/j.neuron.2015.02.018 }}</ref>
[[File:Nigrostriatal Pathway.png|thumb|The nigrostriatal pathway is involved in behaviors relating to movement and motivation.]]

=== Nigrostriatal pathway ===
The [[nigrostriatal pathway]] is involved in behaviors relating to movement and motivation. The transmission of dopaminergic neurons to the [[dorsal striatum]] particularly plays a role in reward and motivation while movement is influenced by the transmission of dopaminergic neurons to the substantia nigra.<ref>{{cite journal | vauthors = Balleine BW, Delgado MR, Hikosaka O | title = The role of the dorsal striatum in reward and decision-making | journal = The Journal of Neuroscience | volume = 27 | issue = 31 | pages = 8161–8165 | date = August 2007 | pmid = 17670959 | pmc = 6673072 | doi = 10.1523/JNEUROSCI.1554-07.2007 }}</ref><ref>{{cite journal | vauthors = Mishra A, Singh S, Shukla S | title = Physiological and Functional Basis of Dopamine Receptors and Their Role in Neurogenesis: Possible Implication for Parkinson's disease | journal = Journal of Experimental Neuroscience | volume = 12 | pages = 1179069518779829 | date = 2018 | pmid = 29899667 | pmc = 5985548 | doi = 10.1177/1179069518779829 }}</ref> The nigrostriatal pathway is associated with conditions such as Huntington's disease, Parkinson's disease, ADHD, Schizophrenia, and Tourette's Syndrome. Huntington's disease, Parkinson's disease, and Tourette's Syndrome are conditions affected by motor functioning<ref>{{cite journal | vauthors = Mariani E, Frabetti F, Tarozzi A, Pelleri MC, Pizzetti F, Casadei R | title = Meta-Analysis of Parkinson's Disease Transcriptome Data Using TRAM Software: Whole Substantia Nigra Tissue and Single Dopamine Neuron Differential Gene Expression | journal = PLOS ONE | volume = 11 | issue = 9 | pages = e0161567 | date = 2016-09-09 | pmid = 27611585 | pmc = 5017670 | doi = 10.1371/journal.pone.0161567 | bibcode = 2016PLoSO..1161567M | doi-access = free }}</ref> while schizophrenia and ADHD are affected by reward and motivation functioning. This pathway also regulates associated learning such as classical conditioning and operant conditioning.<ref>{{cite book | vauthors = Carmack SA, Koob GF, Anagnostaras SG |chapter=Learning and Memory in Addiction |date=2017 | doi = 10.1016/b978-0-12-809324-5.21101-2 |title=Learning and Memory: A Comprehensive Reference |pages=523–538 |publisher= Elsevier |isbn=9780128052914 |url=https://escholarship.org/uc/item/9ww1p0g8 }}</ref>

[[File:Tuberoinfundibular Pathway.png|thumb|The tuberoinfundibular pathway transmits dopamine the hypothalamus to the pituitary gland.]]

=== Tuberoinfundibular pathway ===
The [[tuberoinfundibular pathway]] transmits dopamine from the [[hypothalamus]] to the [[pituitary gland]]. This neural circuit plays a pivotal role in the regulation of hormonal balance and, specifically, in modulating the secretion of prolactin from the pituitary gland, which is responsible for breast milk production in females. Hyperprolactinemia is an associated condition caused by an excessive amount of prolactin production that is common in pregnant women.<ref>{{cite journal | vauthors = Attaar A, Curran M, Meyenburg L, Bottner R, Johnston C, Roberts Mason K | title = Perioperative pain management and outcomes in patients who -discontinued or continued pre-existing buprenorphine therapy | journal = Journal of Opioid Management | volume = 17 | issue = 7 | pages = 33–41 | date = 2021-08-01 | pmid = 34520024 | doi = 10.5055/jom.2021.0640 | s2cid = 237507806 }}</ref> After childbirth, the tuberoinfundibular pathway resumes its role in regulating prolactin levels. The decline in estrogen levels postpartum contributes to the restoration of dopaminergic inhibition, preventing sustained hyperprolactinemia in non-pregnant and non-nursing individuals.<ref>{{Cite book |last1=Russell |first1=John A. |last2=Douglas |first2=Alison J. |last3=Ingram |first3=Colin D. |date=2001 |title=Brain preparations for maternity—adaptive changes in behavioral and neuroendocrine systems during pregnancy and lactation. An overview. |url=https://doi.org/10.1016/S0079-6123(01)33002-9 |series=Progress in Brain Research |volume=133 |pages=1–38 |doi=10.1016/S0079-6123(01)33002-9 |pmid=11589124 |via=Elsevier}}</ref>

=== Cortico-basal ganglia-thalamo-cortical loop ===

The dopaminergic pathways that project from the [[substantia nigra pars compacta]] (SNc) and [[ventral tegmental area]] (VTA) into the [[striatum]] (i.e., the nigrostriatal and mesolimbic pathways, respectively) form one component of a sequence of pathways known as the [[cortico-basal ganglia-thalamo-cortical loop]].<ref name="Reward system components and structure-specific functions">{{cite journal | vauthors = Taylor SB, Lewis CR, Olive MF | title = The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans | journal = Substance Abuse and Rehabilitation | volume = 4 | pages = 29–43 | year = 2013 | pmid = 24648786 | pmc = 3931688 | doi = 10.2147/SAR.S39684 | quote =  | doi-access = free }}</ref><ref name="Striatal efferents, afferents, and colocalized receptors in dMSNs and iMSNs">{{cite journal | vauthors = Yager LM, Garcia AF, Wunsch AM, Ferguson SM | title = The ins and outs of the striatum: role in drug addiction | journal = Neuroscience | volume = 301 | pages = 529–41 | date = August 2015 | pmid = 26116518 | pmc = 4523218 | doi = 10.1016/j.neuroscience.2015.06.033 | quote =  }}</ref> The nigrostriatal component of the loop consists of the SNc, giving rise to both inhibitory and excitatory pathways that run from the striatum into the [[globus pallidus]], before carrying on to the thalamus, or into the [[subthalamic nucleus]] before heading into the [[thalamus]]. The dopaminergic neurons in this circuit increase the magnitude of phasic firing in response to positive reward error, that is when the reward exceeds the expected reward. These neurons do not decrease phasic firing during a negative reward prediction (less reward than expected), leading to hypothesis that serotonergic, rather than dopaminergic neurons encode reward loss.{{source?|date=November 2023}} Dopamine phasic activity also increases during cues that signal negative events, however dopaminergic neuron stimulation still induces place preference, indicating its main role in evaluating a positive stimulus. From these findings, two hypotheses have developed, as to the role of the basal ganglia and nigrostiatal dopamine circuits in action selection. The first model suggests a "critic" which encodes value, and an actor which encodes responses to stimuli based on perceived value. However, the second model proposes that the actions do not originate in the basal ganglia, and instead originate in the cortex and are selected by the basal ganglia. This model proposes that the direct pathway controls appropriate behavior and the indirect suppresses actions not suitable for the situation. This model proposes that tonic dopaminergic firing increases the activity of the direct pathway, causing a bias towards executing actions faster.<ref name="pmid21270784">{{cite journal | vauthors = Maia TV, Frank MJ | title = From reinforcement learning models to psychiatric and neurological disorders | journal = Nature Neuroscience | volume = 14 | issue = 2 | pages = 154–62 | date = February 2011 | pmid = 21270784 | pmc = 4408000 | doi = 10.1038/nn.2723 }}</ref>

These models of the basal ganglia are thought to be relevant to the study of [[OCD]],<ref>{{cite journal | vauthors = Beucke JC, Sepulcre J, Talukdar T, Linnman C, Zschenderlein K, Endrass T, Kaufmann C, Kathmann N | display-authors = 6 | title = Abnormally high degree connectivity of the orbitofrontal cortex in obsessive-compulsive disorder | journal = JAMA Psychiatry | volume = 70 | issue = 6 | pages = 619–29 | date = June 2013 | pmid = 23740050 | doi = 10.1001/jamapsychiatry.2013.173 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Maia TV, Cooney RE, Peterson BS | title = The neural bases of obsessive-compulsive disorder in children and adults | journal = Development and Psychopathology | volume = 20 | issue = 4 | pages = 1251–83 | date = 1 January 2008 | pmid = 18838041 | pmc = 3079445 | doi = 10.1017/S0954579408000606 }}</ref> [[ADHD]], [[Tourette syndrome]], [[Parkinson's disease]], [[schizophrenia]], and [[addiction]]. For example, [[Parkinson's disease]] is hypothesized to be a result of excessive inhibitory pathway activity, which explains the slow movement and cognitive deficits, while Tourettes is proposed to be a result of excessive excitatory activity resulting in the tics characteristic of Tourettes.<ref name="pmid21270784" />

==Regulation==

The [[ventral tegmental area]] and [[substantia nigra pars compacta]] receive inputs from other neurotransmitters systems, including [[Glutamate (neurotransmitter)|glutaminergic]] inputs, [[GABAergic]] inputs, cholinergic inputs, and inputs from other monoaminergic nuclei. The VTA contains [[5-HT1A|5-HT1A receptor]]s that exert a biphasic effects on [[action potential|firing]], with low doses of 5-HT1A receptor agonists eliciting an increase in firing rate, and higher doses suppressing activity. The [[5-HT2A|5-HT2A receptor]]s expressed on dopaminergic neurons increase activity, while [[5-HT2C|5-HT2C receptor]]s elicit a decrease in activity.<ref name="5-ht da">{{cite book| vauthors = Adell A, Bortolozzi A, Díaz-Mataix L, Santana N, Celada P, Artigas F | chapter = Serotonin interaction with other transmitter systems. | veditors = Muller CP, Jacobs B | title = Handbook of Behavioral Neuroscience | date = January 2010 | volume = 21 | pages = 259-276 (262–264) |publisher=Academic|location=London|isbn=978-0-12-374634-4 }}</ref> The mesolimbic pathway, which projects from the VTA to the nucleus accumbens, is also regulated by [[muscarinic acetylcholine receptor]]s. In particular, the activation of [[muscarinic acetylcholine receptor M2]] and [[muscarinic acetylcholine receptor M4]] inhibits dopamine release, while [[muscarinic acetylcholine receptor M1]] activation increases dopamine release.<ref name="cholinergic">{{cite journal | vauthors = Shin JH, Adrover MF, Wess J, Alvarez VA | title = Muscarinic regulation of dopamine and glutamate transmission in the nucleus accumbens | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 112 | issue = 26 | pages = 8124–9 | date = June 2015 | pmid = 26080439 | pmc = 4491757 | doi = 10.1073/pnas.1508846112 | bibcode = 2015PNAS..112.8124S | doi-access = free }}</ref> GABAergic inputs from the striatum decrease dopaminergic neuronal activity, and glutaminergic inputs from many cortical and subcortical areas increase the firing rate of dopaminergic neurons. Endocannabinoids also appear to have a modulatory effect on dopamine release from neurons that project out of the VTA and SNc.<ref name="endocannabinoid inhibition">{{cite journal | vauthors = Melis M, Pistis M | title = Endocannabinoid signaling in midbrain dopamine neurons: more than physiology? | journal = Current Neuropharmacology | volume = 5 | issue = 4 | pages = 268–77 | date = December 2007 | pmid = 19305743 | pmc = 2644494 | doi = 10.2174/157015907782793612 | quote = Thus, it is conceivable that low levels of CB1 receptors are located on glutamatergic and GABAergic terminals impinging on DA neurons [127, 214], where they can fine-tune the release of inhibitory and excitatory neurotransmitter and regulate DA neuron firing. Consistently, in vitro electrophysiological experiments from independent laboratories have provided evidence of CB1 receptor localization on glutamatergic and GABAergic axon terminals in the VTA and SNc. }}</ref> [[Norepinephrine|Noradrenergic]] inputs deriving from the [[locus coeruleus]] have excitatory and inhibitory effects on the dopaminergic neurons that project out of the VTA and SNc.<ref name="da regulation">{{cite journal | vauthors = Morikawa H, Paladini CA | title = Dynamic regulation of midbrain dopamine neuron activity: intrinsic, synaptic, and plasticity mechanisms | journal = Neuroscience | volume = 198 | pages = 95–111 | date = December 2011 | pmid = 21872647 | pmc = 3221882 | doi = 10.1016/j.neuroscience.2011.08.023 }}</ref><ref name="Noradrenergic modulation of DA neurons - 2014 review" /> The excitatory [[orexin]]ergic inputs to the VTA originate in the [[lateral hypothalamus]] and may regulate the baseline [[Action potential|firing]] of VTA dopaminergic neurons.<ref name="Cannabinoid-Orexin systemic cross-talk" /><ref name="pmid19815001" />

{| class="wikitable"
|+ Inputs to the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc)
 |-
! scope="col" | [[Neurotransmitter]]
! scope="col" | Origin 
! scope="col" | Type of Connection
! scope="col" | Sources
|-
! scope="row" | [[Glutamate (neurotransmitter)|Glutamate]]
| 
*[[pedunculopontine nucleus]]
*[[subthalamic nucleus]]
*[[laterodorsal tegmental nucleus]]
*[[stria terminalis]]
*[[superior colliculus]]
*[[lateral hypothalamus]]
*[[preoptic area]]
*[[periaqueductal gray]]
*[[raphe nuclei]]
| Excitatory projections into the VTA and SNc
|<ref name="da regulation"/>
|-
! scope="row" | [[GABA]]
|
*[[rostromedial tegmental nucleus]]
*[[striatum]]
*local GABAergic inputs
| Inhibitory projections into the VTA and SNc
|<ref name="da regulation"/>
|-
!scope="row" | [[Serotonin]]
| 
*[[raphe nuclei]]
| Modulatory effect, depending on receptor subtype Produces a biphasic effect on VTA neurons
|<ref name="da regulation"/>
|-
!scope="row" | [[Norepinephrine]]
|
*[[locus coeruleus]]
*other noradrenergic nuclei
| Modulatory effect, depending on receptor subtype The excitatory and inhibitory effects of the {{abbr|LC|locus coeruleus}} on the VTA and SNc are time-dependent
|<ref name="da regulation"/><ref name="Noradrenergic modulation of DA neurons - 2014 review">{{cite journal | vauthors = Chandler DJ, Waterhouse BD, Gao WJ | title = New perspectives on catecholaminergic regulation of executive circuits: evidence for independent modulation of prefrontal functions by midbrain dopaminergic and noradrenergic neurons | journal = Frontiers in Neural Circuits | volume = 8 | pages = 53 | year = 2014 | pmid = 24904299 | pmc = 4033238 | doi = 10.3389/fncir.2014.00053 | quote = It has been shown that electrical stimulation of LC results in an excitation followed by a brief inhibition of midbrain dopamine (DA) neurons through an α1 receptor dependent mechanism (Grenhoff et al., 1993). | doi-access = free }}</ref>
|-
!scope="row" | [[Endocannabinoid]]s
|
*VTA dopamine neurons{{#tag:ref|At a [[Chemical synapse#Structure|chemical synapse]], neurotransmitters are normally released from the presynaptic [[axon terminal]] and signal through receptors that are located on the [[dendrite]]s of the postsynaptic neuron; however, in [[retrograde neurotransmission]], the dendrites of the postsynaptic neuron release neurotransmitters that signal through receptors that are located on the axon terminal of the presynaptic neuron.<ref name="Cannabinoid-Orexin systemic cross-talk" /> Endocannabinoids signal between neurons through retrograde neurotransmission at synapses;<ref name="Cannabinoid-Orexin systemic cross-talk" /> consequently, the dopaminergic neurons that project out of the VTA and SNc release endocannabinoids from their dendrites onto the axon terminals of their inhibitory GABAergic and excitatory glutamatergic inputs to inhibit their effects on dopamine neuronal firing.<ref name="endocannabinoid inhibition" /><ref name="Cannabinoid-Orexin systemic cross-talk" />|name="retrograde neurotransmission"|group="note"}}
*SNc dopamine neurons<ref name="retrograde neurotransmission" group="note" />
|Excitatory effect on dopaminergic neurons from inhibiting GABAergic inputs Inhibitory effect on dopaminergic neurons from inhibiting glutamatergic inputs May interact with orexins via [[cannabinoid receptor 1|CB1]]–[[orexin receptor|OX1]] [[GPCR oligomer|receptor heterodimer]]s to regulate neuronal firing
|<ref name="endocannabinoid inhibition" /><ref name="da regulation"/><ref name="Cannabinoid-Orexin systemic cross-talk" /><ref name="Human heterodimers: OX1–OX2 OX1–CB1 OX2–CB1" />
|-
!scope="row" | [[Acetylcholine]]
|
*[[pedunculopontine nucleus]]
*[[laterodorsal tegmental nuclei]]
| Modulatory effect, depending on receptor subtype
|<ref name="da regulation"/>
|-
!scope="row" | [[Orexin]]
|
*[[lateral hypothalamus]]
| Excitatory effect on dopaminergic neurons via signaling through [[orexin receptor]]s ([[orexin receptor 1|OX1]] and [[orexin receptor 2|OX2]]) Increases both tonic and phasic firing of dopaminergic neurons in the VTA May interact with endocannabinoids via [[cannabinoid receptor 1|CB1]]–[[orexin receptor|OX1]] [[GPCR oligomer|receptor heterodimer]]s to regulate neuronal firing
|<ref name="Cannabinoid-Orexin systemic cross-talk">{{cite journal | vauthors = Flores A, Maldonado R, Berrendero F | title = Cannabinoid-hypocretin cross-talk in the central nervous system: what we know so far | journal = Frontiers in Neuroscience | volume = 7 | pages = 256 | date = December 2013 | pmid = 24391536 | pmc = 3868890 | doi = 10.3389/fnins.2013.00256 | quote = Direct CB1-HcrtR1 interaction was first proposed in 2003 (Hilairet et al., 2003). Indeed, a 100-fold increase in the potency of hypocretin-1 to activate the ERK signaling was observed when CB1 and HcrtR1 were co-expressed&nbsp;... In this study, a higher potency of hypocretin-1 to regulate CB1-HcrtR1 heteromer compared with the HcrtR1-HcrtR1 homomer was reported (Ward et al., 2011b). These data provide unambiguous identification of CB1-HcrtR1 heteromerization, which has a substantial functional impact.&nbsp;... The existence of a cross-talk between the hypocretinergic and endocannabinoid systems is strongly supported by their partially overlapping anatomical distribution and common role in several physiological and pathological processes. However, little is known about the mechanisms underlying this interaction.&nbsp;... Acting as a retrograde messenger, endocannabinoids modulate the glutamatergic excitatory and GABAergic inhibitory synaptic inputs into the dopaminergic neurons of the VTA and the glutamate transmission in the NAc. Thus, the activation of CB1 receptors present on axon terminals of GABAergic neurons in the VTA inhibits GABA transmission, removing this inhibitory input on dopaminergic neurons (Riegel and Lupica, 2004). Glutamate synaptic transmission in the VTA and NAc, mainly from neurons of the PFC, is similarly modulated by the activation of CB1 receptors (Melis et al., 2004). | doi-access = free }} {{bull}}[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868890/figure/F1/ Figure 1: Schematic of brain CB1 expression and orexinergic neurons expressing OX1 (HcrtR1) or OX2 (HcrtR2)] {{bull}}[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868890/figure/F2/ Figure 2: Synaptic signaling mechanisms in cannabinoid and orexin systems] {{bull}}[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868890/figure/F3/ Figure 3: Schematic of brain pathways involved in food intake]</ref><ref name="pmid19815001">{{cite journal | vauthors = Aston-Jones G, Smith RJ, Sartor GC, Moorman DE, Massi L, Tahsili-Fahadan P, Richardson KA | title = Lateral hypothalamic orexin/hypocretin neurons: A role in reward-seeking and addiction | journal = Brain Research | volume = 1314 | pages = 74–90 | date = February 2010 | pmid = 19815001 | pmc = 2819557 | doi = 10.1016/j.brainres.2009.09.106 }}</ref><ref name="Human heterodimers: OX1–OX2 OX1–CB1 OX2–CB1">{{cite journal | vauthors = Jäntti MH, Mandrika I, Kukkonen JP | title = Human orexin/hypocretin receptors form constitutive homo- and heteromeric complexes with each other and with human CB1 cannabinoid receptors | journal = Biochemical and Biophysical Research Communications | volume = 445 | issue = 2 | pages = 486–90 | date = March 2014 | pmid = 24530395 | doi = 10.1016/j.bbrc.2014.02.026 | quote = Orexin receptor subtypes readily formed homo- and hetero(di)mers, as suggested by significant BRET signals. CB1 receptors formed homodimers, and they also heterodimerized with both orexin receptors.&nbsp;... In conclusion, orexin receptors have a significant propensity to make homo- and heterodi-/oligomeric complexes. However, it is unclear whether this affects their signaling. As orexin receptors efficiently signal via endocannabinoid production to CB1 receptors, dimerization could be an effective way of forming signal complexes with optimal cannabinoid concentrations available for cannabinoid receptors. }}</ref>
|}

== See also ==
*[[Dopaminergic cell groups]]

==Notes==
{{reflist|group=note}}

== References ==
{{reflist|2}}

[[Category:Central nervous system pathways]]
[[Category:Dopamine]]

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