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Globus Pallidus Externus (GPe)

Published: Jul 17, 2023
  /  
Updated: Jul 25, 2023

Written by Oseh Mathias

Founder, SpeechFit

The external segment of the globus pallidus, or globus pallidus externus (GPe), is a key component of the basal ganglia, a group of nuclei in the brain associated with a variety of functions, including control of voluntary motor movements, habit formation, and procedural learning[1].

The GPe serves as a nexus within the basal ganglia circuitry, with various inputs and outputs. Its principal neurons are GABAergic, meaning they use gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter in the central nervous system, to transmit signals[2].

image within the content - in line image
Location of the Globus Pallidus externus (GPe). Tseng, Y-T., Khosravani, S., Mahnan, A., & Konczak, J. (2017).[3] I have removed some of the labels for clarity.

In terms of inputs, the GPe mainly receives inhibitory projections from the striatum, specifically the D2 receptor-expressing medium spiny neurons involved in the indirect pathway of motor control. It also receives excitatory inputs from the subthalamic nucleus (STN)[4].

The GPe has two main sets of outputs:

  1. Firstly, it sends inhibitory GABAergic projections to the subthalamic nucleus (STN), helping to regulate the activity of the STN.

  2. Secondly, it sends inhibitory projections to the internal segment of the globus pallidus (GPi), which plays a significant role in controlling the final output of the basal ganglia[5].

Within the context of the basal ganglia motor circuits, the GPe plays a critical role in the indirect pathway. In this pathway, activation of the GPe by the striatum inhibits the STN, which reduces excitation of the GPi, leading to decreased inhibition of the thalamus and, ultimately, decreased motor activity[6].

Through these connections and its involvement in the direct and indirect pathways, the GPe contributes to the regulation of movement. It helps maintain balance in the system by adjusting and modulating signals, which is crucial for smooth, coordinated voluntary movements[7]. Disruptions or dysfunctions within this system can lead to movement disorders, like Parkinson's disease and dystonia[8].


Author

Oseh Mathias

SpeechFit Founder

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
  • Graybiel, A. M. (2000). The basal ganglia. Current Biology, 10(14), R509-R511. doi: 10.1016/S0960-9822(00)00593-5

  • Tritsch, N. X., & Sabatini, B. L. (2012). Dopaminergic modulation of synaptic transmission in cortex and striatum. Neuron, 76(1), 33-50. doi: 10.1016/j.neuron.2012.09.023

  • Tseng, Y-T., Khosravani, S., Mahnan, A., & Konczak, J. (2017). Overview of the neuroanatomy of the basal ganglia. In Exercise as Medicine for the Treatment of Brain Dysfunction: Evidence for Cortical Stroke, Cerebellar Ataxia, and Parkinson’s Disease. Retrieved from https://www.researchgate.net/figure/Overview-of-the-neuroanatomy-of-the-basal-ganglia-A-The-basal-ganglia-are-comprised_fig1_313960410

  • Smeal, R. M., Gaspar, R. C., Keefe, K. A., & Wilcox, K. S. (2007). A rat brain slice preparation for characterizing both thalamostriatal and corticostriatal afferents. Journal of Neuroscience Methods, 159(2), 224-235. doi: 10.1016/j.jneumeth.2006.07.018

  • Mastro, K. J., Bouchard, R. S., Holt, H. A. K., & Gittis, A. H. (2014). Transgenic mouse lines subdivide external segment of the globus pallidus (GPe) neurons and reveal distinct GPe output pathways. Journal of Neuroscience, 34(6), 2087–2099. doi: 10.1523/JNEUROSCI.4646-13.2014

  • Obeso, J. A., Rodríguez-Oroz, M. C., Benitez-Temino, B., Blesa, F. J., Guridi, J., Marin, C., & Rodriguez, M. (2008). Functional organization of the basal ganglia: therapeutic implications for Parkinson's disease. Movement Disorders, 23(S3), S548-S559. doi: 10.1002/mds.22062

  • Nambu, A. (2008). Seven problems on the basal ganglia. Current Opinion in Neurobiology, 18(6), 595-604. doi: 10.1016/j.conb.2008.11.001

  • Vitek, J. L. (2002). Pathophysiology of dystonia: a neuronal model. Movement Disorders, 17(S3), S49-S62. doi: 10.1002/mds.10175