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Substantia nigra pars compacta

Pars compacta
Latin Pars compacta substantiae nigrae
Part of substantia nigra
Gray's p.802
NeuroNames hier-528
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Anatomical terms of neuroanatomy

The pars compacta is a portion of the substantia nigra, located in midbrain. It is formed by dopaminergic neuron and located medial to pars reticulata. Parkinson's disease is characterized by the death of dopaminergic neurons in this region.[1]


In humans, the nerve cell bodies of the pars compacta are coloured black by the pigment neuromelanin. The degree of pigmentation increases with age. This pigmentation is visible as a distinctive black stripe in brain sections and is the origin of the name given to this volume of the brain. The neurons have particularly long and thick dendrites (François et al.). The ventral dendrites, particularly, go down deeply in the pars reticulata. Other similar neurons are more sparsely distributed in the mesencephalon and constitute "groups" with no well-defined borders, although continuous to the pars compacta, in a prerubral position. These have been given, in early works in rats (with not much respect for the anatomical subdivisions), the name of "area A8" and "A10". The pars compacta itself ("A9") is usually subdivided into a ventral and a dorsal tier, the last being calbindin positive.[2] The ventral tier is considered as A9v. The dorsal tier A9d is linked to an ensemble comprising also A8 and A10,[3] A8, A9d and A10 representing 28% of dopaminergic neurons. The long dendrites of compacta neurons receive striatal information. This cannot be the case for the more posterior groups that are located outside the striato-pallidonigral bundle territory. Neurons of the pars compacta receive inhibiting signals from the collateral axons from the neurons of the pars reticulata.[4] All these neurons send their axons along the nigrostriatal pathway to the striatum where they release the neurotransmitter dopamine. There is an organization in which dopaminergic neurons of the fringes (the lowest) go to the sensorimotor striatum and the highest to the associative striatum. Dopaminergic axons also innervate other elements of the basal ganglia system including the lateral and medial pallidum,[5] substantia nigra pars reticulata, and the subthalamic nucleus.[6]


The function of the dopamine neurons in the substantia nigra pars compacta is complex. Contrary to what was thought initially it is not directly linked to movements. "Dopamine neurons are activated by novel, unexpected stimuli, by primary rewards in the absence of predictive stimuli and during learning".[7] Dopamine neurons are thought to be involved in learning to predict which behaviours will lead to a reward (for example food or sex). In particular, it is suggested that dopamine neurons fire when a reward is greater than that previously expected; a key component of many reinforcement learning models. This signal can then be used to update the expected value of that action. Many recreational drugs, such as cocaine, mimic this reward response—providing an explanation for their addictive nature.


Degeneration of pigmented neurons in this region is the principal pathology that underlies Parkinson's disease and this depigmentation can be visualized in vivo with Neuromelanin MRI.[8] In a few people, the cause of Parkinson's disease is genetic, but in most cases, the reason for the death of these dopamine neurons is unknown. Parkinsonism can also be produced by viral infections such as encephalitis or a number of toxins, such as MPTP, an industrial toxin which can be mistakenly produced during synthesis of the meperidine analog MPPP. Many such toxins appear to work by producing reactive oxygen species. Binding to neuromelanin by means of charge transfer complexes may concentrate radical-generating toxins in the substantia nigra.

Pathological changes to the dopaminergic neurons of the pars compacta are also thought to be involved in schizophrenia (see the dopamine hypothesis of schizophrenia) and psychomotor retardation sometimes seen in clinical depression.


  1. ^ Kim, S. J.; Sung, JY; Um, JW; Hattori, N; Mizuno, Y; Tanaka, K; Paik, SR; Kim, J; Chung, KC (2003). "Parkin Cleaves Intracellular -Synuclein Inclusions via the Activation of Calpain". Journal of Biological Chemistry 278 (43): 41890–9. PMID 12917442. doi:10.1074/jbc.M306017200. 
  2. ^ Francois, C.; Yelnik, J.; Tande, D.; Agid, Y. & Hirsch, E.C. (1999). "Dopaminergic cell group A8 in the monkey: anatomical organization and projections to the striatum". Journal of Comparative Neurology 414 (3): 334–347. PMID 10516600. doi:10.1002/(SICI)1096-9861(19991122)414:3<334::AID-CNE4>3.0.CO;2-X. 
  3. ^ Feigenbaum Langer, L.; Jimenez-Castellanos, J. & Graybiel, A.M. (1991). "The substantia nigra and its relations with the striatum in the monkey". Progress in Brain Research 87: 81–99. PMID 1678193. doi:10.1016/S0079-6123(08)63048-4. 
  4. ^ Hajos, M. & Greenfield, S.A. (1994). "Synaptic connections between pars compacta and pars reticulata neurones: electrophysiological evidence for functional modules within the substantia nigra". Brain Research 660 (2): 216–224. PMID 7820690. doi:10.1016/0006-8993(94)91292-0. 
  5. ^ Lavoie, B., Smith, Y., Parent, A. (1989). "Dopaminergic innervation of the basal ganglia in the squirrel monkey as revealed by tyrosine hydroxylase immunohistochemistry". The Journal of Comparative Neurology 289 (1): 36–52. PMID 2572613. doi:10.1002/cne.902890104. 
  6. ^ Cragg S.J.; Baufreton J.; Xue Y.; Bolam J.P.; & Bevan M.D. (2004). "Synaptic release of dopamine in the subthalamic nucleus". European Journal of Neuroscience 20 (7): 1788–1802. PMID 15380000. doi:10.1111/j.1460-9568.2004.03629.x. 
  7. ^ Schultz, W. (1992). "Activity of dopamine neurons in the behaving primate". Seminar in Neuroscience 4 (2): 129–138. doi:10.1016/1044-5765(92)90011-P. 
  8. ^ Sasaki M, Shibata E, Tohyama K, Takahashi J, Otsuka K, Tsuchiya K, Takahashi S, Ehara S, Terayama Y, Sakai A (July 2006). "Neuromelanin magnetic resonance imaging of locus ceruleus and substantia nigra in Parkinson's disease". NeuroReport 17 (11): 1215–8. PMID 16837857. doi:10.1097/01.wnr.0000227984.84927.a7.