Pars compacta
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| Brain: Pars compacta | ||
|---|---|---|
| Gray's | subject #188 802 | |
| NeuroNames | hier-528 | |
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The pars compacta is a portion of the substantia nigra.
Anatomy
The pars compacta contains neurons which, in humans, are coloured black by the pigment neuromelanin that 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 area. 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 clear 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 subdivions 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.[1] The ventral tier is considered as A9v. The dorsal tier A9d is linked to an ensemble comprising also A8 and A10,[1] 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.[1] 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,[1] substantia nigra pars reticulata, and the subthalamic nucleus.[1]
Function
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".[1] 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 drugs of abuse, such as cocaine, mimic this reward response—providing an explanation for their addictive nature.
Pathology
Degeneration of pigmented neurons in this region is the principal pathology that underlies Parkinson's disease. 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.
References
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Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
