Neuromelanin in the context of "Substantia nigra"

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👉 Neuromelanin in the context of Substantia nigra

The substantia nigra (SN) is a basal ganglia structure located in the midbrain that plays an important role in reward and movement. Substantia nigra is Latin for "black substance", reflecting the fact that parts of the substantia nigra appear darker than neighboring areas due to high levels of neuromelanin in dopaminergic neurons. Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta.

Although the substantia nigra appears as a continuous band in brain sections, anatomical studies have found that it actually consists of two parts with very different connections and functions: the pars compacta (SNpc) and the pars reticulata (SNpr). The pars compacta serves mainly as a projection to the basal ganglia circuit, supplying the striatum with dopamine. The pars reticulata conveys signals from the basal ganglia to numerous other brain structures.

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Neuromelanin in the context of Melanin

Melanin (/ˈmɛlənɪn/ ; from Ancient Greek μέλας (mélas) 'black, dark') is a family of biomolecules organized as oligomers or polymers, which among other functions provide the pigments of many organisms. Melanin pigments are produced in a specialized group of cells known as melanocytes.

There are five basic types of melanin: eumelanin, pheomelanin, neuromelanin, allomelanin and pyomelanin. Melanin is produced through a multistage chemical process known as melanogenesis, where the oxidation of the amino acid tyrosine is followed by polymerization. Pheomelanin is a cysteinated form containing polybenzothiazine portions that are largely responsible for the red or yellow tint given to some skin or hair colors. Neuromelanin is found in the brain. Research has been undertaken to investigate its efficacy in treating neurodegenerative disorders such as Parkinson's. Allomelanin and pyomelanin are two types of nitrogen-free melanin.

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Neuromelanin in the context of Lewy bodies

Lewy bodies are inclusion bodies – abnormal aggregations of protein – that develop inside neurons affected by Parkinson's disease, the Lewy body dementias (Parkinson's disease dementia and dementia with Lewy bodies (DLB)), and in several other disorders such as multiple system atrophy. The defining proteinaceous component of Lewy bodies is alpha-synuclein (α-synuclein), which aggregates to form Lewy bodies within neuronal cell bodies, and Lewy neurites in neuronal processes (axons or dendrites). In some disorders, alpha-synuclein also forms aggregates in glial cells that are referred to as 'glial cytoplasmic inclusions'; together, diseases involving Lewy bodies, Lewy neurites and glial cytoplasmic inclusions are called 'synucleinopathies'.

Lewy bodies appear as spherical masses in the neuronal cytoplasm that can displace other cellular components such as the nucleus and neuromelanin. A given neuron may contain one or more Lewy bodies. There are two main kinds of Lewy bodies – classical (brainstem-type) and cortical-type. Classical Lewy bodies occur most commonly in pigmented neurons of the brainstem, such as the substantia nigra and locus coeruleus, although they are not restricted to pigmented neurons. They are strongly eosinophilic structures ranging from 8-30 microns in diameter, and when viewed with a light microscope they are seen to consist of a dense core that is often surrounded by a pale shell. Electron microscopic analyses found that the core consists of a compact mass of haphazard filaments and various particles surrounded by a diffuse corona of radiating filaments. In contrast, cortical-type Lewy bodies are smaller, only faintly eosinophilic, and devoid of a surrounding halo with radial filaments. Cortical-type Lewy bodies occur in multiple regions of the cortex and in the amygdala. Cortical Lewy bodies are a distinguishing feature of dementia with Lewy bodies, but they may occasionally be seen in ballooned neurons characteristic of behavioural variant frontotemporal dementia and corticobasal degeneration, as well as in patients with other tauopathies.

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