Theinternal globus pallidus(GPiormedial globus pallidus), and theexternal globus pallidus(GPe) make up theglobus pallidus.Inrodentsits homologue is known as theentopeduncular nucleus.The GPi is one of the outputnucleiof thebasal ganglia(the other being thesubstantia nigrapars reticulata). TheGABAergicneurons of the GPi send their axons to theventral anterior nucleus(VA) and theventral lateral nucleus(VL) in the dorsalthalamus,to thecentromediancomplex, and to thepedunculopontinecomplex.[1][2]
| Internal globus pallidus | |
|---|---|
 Internal globus pallidus (GPi) is seen in the 2nd image from the left | |
| Details | |
| Part of | Globus pallidus |
| Identifiers | |
| Latin | globus pallidus internus, globus pallidus medialis |
| Acronym(s) | GPi |
| NeuroNames | 233 |
| NeuroLexID | birnlex_1555 |
| TA98 | A14.1.09.511 |
| TA2 | 5572 |
| FMA | 61840 |
| Anatomical terms of neuroanatomy | |
The efferent bundle is constituted first of theansaandlenticular fasciculus,then crosses theinternal capsulewithin and in parallel to the Edinger's comb system then arrives at the laterosuperior corner of thesubthalamic nucleusand constitutes thefield H2of Forel,then H, and suddenly changes its direction to formfield H1that goes to the inferior part of the thalamus. The distribution of axonal islands is widespread in the lateral region of the thalamus. The innervation of the central region is done by collaterals.[3]
The internal globus pallidus containsGABAergicneurons, which allow for its inhibitory function. As the GPi, along with thesubstantia nigra pars reticulata,forms the output of the basal ganglia, these neurons extend to the thalamus, the centromedian complex and the pedunculopontine complex.[4]
Function
edit
The GPi acts to tonically inhibit theventral lateral nucleusandventral anterior nucleusof thethalamus.As these two nuclei are needed for movement planning, this inhibition restricts movement initiation and prevents unwanted movements.
Direct pathway
editThe GPi receives inhibitoryGABAergicsignals from thestriatumby way ofstriatopallidal fibres,when a movement requirement is signaled from thecerebral cortex.As the GPi is one of the direct output centers of thebasal ganglia,this causes disinhibition of thethalamus,increasing overall ease of initiating and maintaining movement. As this pathway only contains onesynapse(from the striatum to the internal globus pallidus), it is known as thedirect pathway.[5]
The direct pathway is modulated by stimulation of the GPi by theexternal globus pallidusandsubthalamic nucleus,via theindirect pathway.[6]
Clinical significance
editDysfunction of the internal globus pallidus has been correlated toParkinson's disease,[7]Tourette syndrome,[8]andtardive dyskinesia.[9]
The internal globus pallidus is the target ofdeep brain stimulation(DBS) for these diseases. Deep brain stimulation sends regulated electrical pulses to the target. In patients with tardive dyskinesia treated with DBS, most people reported more than a 50% improvement in symptoms.[9]Tourette syndrome patients have also benefited from this treatment, showing over 50% improvement inticseverity (compulsive disabling motor tics are symptoms of Tourette patients).[8]The GPi is also considered a "highly effective target for neuromodulation" when using deep brain stimulation on Parkinson's disease patients.[7] There is seen to be only some involvement inHuntington's disease[10]with mostly theexternal globus pallidusbeing affected.[11]
References
edit- ^Nauta WJ, Mehler WR (January 1966). "Projections of the lentiform nucleus in the monkey".Brain Res.1(1): 3–42.doi:10.1016/0006-8993(66)90103-X.PMID4956247.
- ^Percheron G, François C, Talbi B, Meder JF, Fenelon G, Yelnik J (1993). "The primate motor thalamus analysed with reference to subcortical afferent territories".Stereotact Funct Neurosurg.60(1–3): 32–41.doi:10.1159/000100588.PMID8511432.
- ^Yelnik J, François C, Percheron G, Tandé D (April 1996). "A spatial and quantitative study of the striatopallidal connection in the monkey".NeuroReport.7(5): 985–988.doi:10.1097/00001756-199604100-00006.PMID8804036.S2CID25425297.
- ^Schroll, Henning; Hamker, Fred H. (2013-01-01)."Computational models of basal-ganglia pathway functions: focus on functional neuroanatomy".Frontiers in Systems Neuroscience.7:122.doi:10.3389/fnsys.2013.00122.PMC3874581.PMID24416002.
- ^Morita, Makiko; Hikida, Takatoshi (2015-11-01). "[Distinct roles of the direct and indirect pathways in the basal ganglia circuit mechanism]".Nihon Shinkei Seishin Yakurigaku Zasshi = Japanese Journal of Psychopharmacology.35(5–6): 107–111.ISSN1340-2544.PMID26785520.
- ^Parent, André; Hazrati, Lili-Naz (1995-01-01). "Functional anatomy of the basal ganglia. II. The place of subthalamic nucleus and external pallidium in basal ganglia circuitry".Brain Research Reviews.20(1): 128–154.doi:10.1016/0165-0173(94)00008-D.PMID7711765.S2CID20808851.
- ^abAndrade, Pablo; Carrillo-Ruiz, José D.; Jiménez, Fiacro (2009-07-01). "A systematic review of the efficacy of globus pallidus stimulation in the treatment of Parkinson's disease".Journal of Clinical Neuroscience.16(7): 877–881.doi:10.1016/j.jocn.2008.11.006.ISSN0967-5868.PMID19398341.S2CID36080071.
- ^abDong, S.; Zhuang, P.; Zhang, X.-H.; Li, J.-Y.; Li, Y.-J. (2012-01-01)."Unilateral deep brain stimulation of the right globus pallidus internus in patients with Tourette's syndrome: two cases with outcomes after 1 year and a brief review of the literature".The Journal of International Medical Research.40(5): 2021–2028.doi:10.1177/030006051204000545.ISSN1473-2300.PMID23206487.
- ^abSpindler, Meredith A.; Galifianakis, Nicholas B.; Wilkinson, Jayne R.; Duda, John E. (2013-02-01)."Globus pallidus interna deep brain stimulation for tardive dyskinesia: case report and review of the literature".Parkinsonism & Related Disorders.19(2): 141–147.doi:10.1016/j.parkreldis.2012.09.016.ISSN1873-5126.PMID23099106.
- ^Waldvogel, Henry J.; Kim, Eric H.; Tippett, Lynette J.; Vonsattel, Jean-Paul G.; Faull, Richard LM (2014-01-01). Nguyen, Hoa Huu Phuc; Cenci, M. Angela (eds.).Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease.Current Topics in Behavioral Neurosciences. Vol. 22. Springer Berlin Heidelberg. pp. 33–80.doi:10.1007/7854_2014_354.ISBN9783662463437.PMID25300927.
- ^Walker, FO (20 January 2007). "Huntington's disease".Lancet.369(9557): 218–28.doi:10.1016/S0140-6736(07)60111-1.PMID17240289.S2CID46151626.