Substantia Nigra Pars Reticulata (SNr)
Published: Jul 18, 2023
/
Updated: Aug 3, 2023
Written by Oseh Mathias
Founder, SpeechFit
The substantia nigra pars reticulata (SNr) is an important component of the basal ganglia system in the brain. Like the substantia nigra pars compacta (SNc), it is located in the midbrain, towards the base of the brain[1]. The substantia nigra as a whole, as its Latin name "black substance" suggests, is characterised by its dark colour due to high levels of neuromelanin in dopaminergic neurons. However, the SNr contains less of these pigmented cells compared to the SNc.
The SNr, along with the internal segment of the globus pallidus (GPi), is one of the main output nuclei of the basal ganglia. These output nuclei convey information from the basal ganglia to the thalamus, and from there, the information is relayed to the cerebral cortex. The output of the SNr is primarily inhibitory, utilising GABA (gamma-aminobutyric acid), the main inhibitory neurotransmitter in the brain[2].
Functionally, the SNr plays a significant role in motor control, sensory processing, and cognitive functions. By sending inhibitory signals to the thalamus, it helps regulate the initiation and cessation of voluntary movements. The SNr also receives input from numerous areas of the brain, including the striatum, subthalamic nucleus, and the pars compacta of the substantia nigra, which aids in its regulation of movement[3].
Furthermore, SNr neurons also project to the superior colliculus, a structure involved in the control of eye movements. Thus, the SNr also has a role in controlling saccadic eye movements, which are rapid movements of the eyes that abruptly change the point of fixation[4].
Pathological changes in the SNr, similar to changes in the SNc, have been implicated in movement disorders like Parkinson's disease[5]. The loss of inhibitory dopaminergic inputs from the SNc to the SNr can result in an over-activity of the SNr, leading to an excessive inhibition of the thalamus and a subsequent reduction in the excitatory drive to the motor cortex, which contributes to the hypokinetic features (like bradykinesia and rigidity) seen in Parkinson's disease[6].
Oseh is a software engineer, entrepreneur and founder of SpeechFit. Oseh is passionate about improving health and wellbeing outcomes for neurodiverse people and healthcare providers alike.
References
Gerfen, C. R., & Surmeier, D. J. (2011). Modulation of striatal projection systems by dopamine. Annual Review of Neuroscience, 34, 441–466.
Foster, N. N., Barry, J., Korobkova, L., et al. (2021). The mouse cortico–basal ganglia–thalamic network. Nature, 598, 188-194.
Kravitz, A. V., Freeze, B. S., Parker, P. R., Kay, K., Thwin, M. T., Deisseroth, K., & Kreitzer, A. C. (2010). Regulation of parkinsonian motor behaviours by optogenetic control of basal ganglia circuitry. Nature, 466(7306), 622–626.
Sparks, D. L. (2002). The brainstem control of saccadic eye movements. Nature Reviews Neuroscience, 3(12), 952–964.
Obeso, J. A., Rodríguez-Oroz, M. C., Goetz, C. G., Marin, C., Kordower, J. H., Rodriguez, M., Hirsch, E. C., Farrer, M., Schapira, A. H., & Halliday, G. (2010). Missing pieces in the Parkinson's disease puzzle. Nature Medicine, 16(6), 653–661.
DeLong, M. R., & Wichmann, T. (2007). Circuits and circuit disorders of the basal ganglia. Archives of Neurology, 64(1), 20–24.