Substantia nigra



A basal ganglia structure located in the midbrain that plays an important role in reward and movement.

Appears darker than neighboring areas due to high levels of neuromelanin in dopaminergic neurons.

Loss of dopaminergic neurons in the substantia nigra pars compacta is found in Parkinson’s disease

Appears as a continuous band in brain sections, but actually consists of two parts with different connections and functions: the pars compacta and the pars reticulata

The substantia nigra is critical in the development of many diseases and syndromes, including parkinsonism.

Parkinson’s disease is a neurodegenerative disease characterized, in part, by the death of dopaminergic neurons in the substantial nigra pars compacta.

The cause of death of dopaminergic neurons in the substantia nigra pars compacta is unknown.

Dopaminergic neurons show abnormalities in mitochondrial complex 1.

Dopaminergic neurons in the pars compacta contain less calbindin than other dopaminergic neurons.

Calbindin is a protein involved in calcium ion transport within cells.

Excessive calcium in cells is toxic, explaining the high cytotoxicity of Parkinson’s in the substantia nigra compared to the ventral tegmental area.

Parkinsonian symptoms do not appear until up to 50–80% of pars compacta dopaminergic neurons have died.

At the neurochemical level, dopamine transport systems are slowed, allowing dopamine to linger for longer periods of time delaying onset of symptom.

Patients with Parkinson’s consistently have a smaller substantia nigra, specifically in the substantia nigra pars reticulata.

The small volume of this region may be responsible for motor impairments which may result in tremors found in Parkinson’s disease patients.

Increased levels of dopamine in the substantia nigra have been implicated in the development of schizophrenia.

The Wooden chest, or fentanyl chest wall rigidity syndrome, is a rare side effect of synthetic opioids such as Fentanyl resulting in a generalized increase in skeletal muscle tone.

The Wooden chest, or fentanyl chest wall rigidity syndrome, is thought to be via increased dopamine release and decreased GABA release in the nerves of the substantia nigra/striatum.

Multiple system atrophy characterized by neuronal degeneration in the striatum and substantia nigra

Amphetamine and trace amines increase the concentrations of dopamine in the synaptic cleft, heightening the response of the post-synaptic neuron.

It is the target for the treatment of Parkinson’s disease, with Levodopa, the dopamine precursor.

Levodopa crosses the blood–brain barrier and increases dopamine levels in the substantia nigra, alleviating the symptoms of Parkinson’s disease.

The pars reticulata bears a strong resemblance to the internal part of the globus pallidus, the two are sometimes considered parts of the same structure.

The neurons in pars reticulata are mainly GABAergic, like the globus pallidus.

The main input to the substantial nigra pars reticulate comes from the striatum in direct and indirect pathways.

Striatal activity via the direct pathway exerts an inhibitory effect on neurons in the substantial nigra pars reticulata but an excitatory effect via the indirect pathway.

The substantia nigra is important in brain function such as eye movement, motor planning, reward-seeking, learning, and addiction.

Many of the substantia nigra’s effects are mediated through the striatum.

The pars reticulata of the substantia nigra is an important processing center in the basal ganglia, as its GABAergic neurons convey the final processed signals of the basal ganglia to the thalamus and superior colliculus.

The GABAergic neurons of the pars reticulata spontaneously fire action potentials that inhibit targets of the basal ganglia, and decreases in inhibition are associated with movement.

The subthalamic nucleus gives excitatory input that modulates the rate of firing of these spontaneous action potentials.

Altered patterns of pars reticulata firing are found in Parkinson’s disease and epilepsy.

The Pars compacta’s major function is motor control by indirect; electrical stimulation of the substantia nigra mediating the striatum in the nigra.

The pars compacta sends excitatory input to the striatum that excites and activates the striatum, resulting in the release of GABA onto the globus pallidus to inhibit its inhibitory effects on the thalamic nucleus.

The pars compacta causes the thalamocortical pathways to become excited and transmits motor neuron signals to the cerebral cortex to allow the initiation of movement.

In Parkinson’s disease, the lack of pars compacta neurons has a large influence on movement.

The motor role of the pars compacta may involve fine motor control.

The pars compacta is involved in learned responses to stimuli, and is important in spatial learning, the observations about one’s environment and location in space.

The pars compacta also plays a role in temporal processing, and suspected of regulating the sleep-wake cycle,

One reply on “Substantia nigra”

Does the loss of pars compacta 50% to 80% happen quickly or gradually?
Would a blow to the head prompt it faster such as falling and hitting your head?
Is there a drug or medicine that can slow the loss of pars compacta
or help it to be not as severe?

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