Hostname: page-component-76fb5796d-45l2p Total loading time: 0 Render date: 2024-04-26T13:18:03.469Z Has data issue: false hasContentIssue false
  • English
  • Français

Anatomy and Pathology of the Basal Ganglia

Published online by Cambridge University Press:  05 January 2016

P.L. McGeer ,
E.G. McGeer ,
S. Itagaki  and
K. Mizukawa
P.L. McGeer*
Affiliation:
Kinsmen Laboratory, Dept. of Psychiatry, University of British Columbia, Vancouver
E.G. McGeer
Affiliation:
Kinsmen Laboratory, Dept. of Psychiatry, University of British Columbia, Vancouver
S. Itagaki
Affiliation:
Kinsmen Laboratory, Dept. of Psychiatry, University of British Columbia, Vancouver
K. Mizukawa
Affiliation:
Kinsmen Laboratory, Dept. of Psychiatry, University of British Columbia, Vancouver
*
Kinsmen Laboratory, Dept. of Psychiatry, University of British Columbia, Vancouver, B.C., Canada V6T 1W5
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Neurotransmitters of the basal ganglia are of three types: I, amino acids; II, amines; and III, peptides. The amino acids generally act ionotropically while the amines and peptides generally act metabotropically. There are many examples of neurotransmitter coexistence in basal ganglia neurons. Diseases of the basal ganglia are characterized by selective neuronal degeneration. Lesions of the caudate, putamen, subthalamus and substantia nigra pars compacta occur, respectively, in chorea, dystonia, hemiballismus and parkinsonism. The differing signs and symptoms of these diseases constitute strong evidence of the functions of these various nuclei. Basal ganglia diseases can be of genetic origin, as in Huntington's chorea and Wilson's disease, of infectious origin as in Sydenham's chorea and postencephalitic parkinsonism, or of toxic origin as in MPTP poisoning. Regardless of the etiology, the pathogenesis is often regionally concentrated for reasons that are poorly understood. From studies on Parkinson and Huntington disease brains, evidence is presented that a common feature may be the expression of HLA-DR antigen on reactive microglia in the region where pathological neuronal dropout is occurring.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 14 , Issue S3 , August 1987 , pp. 363 - 372
Copyright
Copyright © Canadian Neurological Sciences Federation 1987

References

REFERENCES

1.McGeer, EG, Staines, WA, McGeer, PL. Neurotransmitters in the basal ganglia. Can J Neurol Sci 1984; 11: 89–99.CrossRefGoogle ScholarPubMed
2.McGeer, PL, Eccles, JC, McGeer, EG. eds. Molecular Biology of the Mammalian Brain. 2nd ed. New York: Plenum Press, 1987.CrossRefGoogle Scholar
3.McGeer, EG, McGeer, PL. Biochemical neuroanatomy of the basal ganglia. In: Calne, DB,ed. Drugs for the Treatment of Parkinson’s Disease. Berlin: Springer-Verlag (in press).Google Scholar
4.Husby, G, van de Rijn, I, Zabriskie, JB, et al. Antineuronal antibody in Sydenham’s chorea. Lancet 1977; 1: 1208.CrossRefGoogle ScholarPubMed
5.Brain, Lord, Walton, JN, eds. Brain’s Diseases of the Nervous System. 9th ed. London: Oxford University Press, 1985.Google Scholar
6.Burton, K, Farrell, K, Li, D, et al. Lesions of the putamen and dystonia: CT and magnetic resonance imaging. Neurol 1984; 34: 962–965.CrossRefGoogle ScholarPubMed
7.Burns, RS, Chiueh, CC, Markey, SP, et al. A primate model of parkinsonism: selective destruction of dopaminergic neurons in the pars compacta of the substantia nigra by N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Proc Natl Acad Sci USA 1983; 80: 4546–4550.CrossRefGoogle ScholarPubMed
8.Kamo, H, Kim, SU, McGeer, PL, et al. Transplantation of cultured human spinal cord cells into the rat motor cortex: use of phaseolus vulgaris leucoagglutinin as a cell marker. Neurosci Lett 1987; 76: 163–167.CrossRefGoogle ScholarPubMed
9.Kamo, H, Kim, SU, McGeer, PL, et al. Functional recovery in a rat model of Parkinson’s disease following transplantation of cultured human sympathetic neurons. Brain Res 1986; 397:372–376.CrossRefGoogle Scholar
10.Kamo, H, Kim, SU, McGeer, PL, et al. Transplantation of cultured fetal human adrenal chromaffin cells to rat brain. Neurosci Lett 1985; 57: 43–48.CrossRefGoogle ScholarPubMed
11.Kabat, EA, Wolf, A, Bezer, AE. The rapid production of acute disseminated encephalomyelitis in rhesus monkeys by injection of heterologous and homologous brain tissue with adjuvants. J Exp Med 1947; 85: 117.CrossRefGoogle ScholarPubMed
12.Husby, G, Wedege, E, Williams, RC Jr. Characterization of brain proteins reacting in vitro with anti-neuronal antibodies in patients with Huntington’s disease. Clin Immunol Immunopath 1978; 11: 131–141.CrossRefGoogle ScholarPubMed
13.Tonegawa, S.The molecules of the immune system. Scientific Amer 1985; 122–131.CrossRefGoogle ScholarPubMed
14.Penfield, W.Microglia and the process of phagocytosis in gliomas. Am J Pathol 1925; 1: 77–89.Google ScholarPubMed
15.Polak, M, DiAmelio, F, Johnson, JE Jr, et al. Microglial cells origins and reactions. In: Haymaker, W, Adams, RD, eds. Histology and Histopathology of the Nervous System. Springfield: Charles C Thomas, 1982; 481–559.Google Scholar
16.Dimitriu-Bona, A, Burmester, GR, Waters, SJ, et al. Human mononu-clear phagocyte differentiation antigens. I. Patterns of antigenic expression on the surface of human monocytes and macrophages defined by monoclonal antibodies. J Immunol 1983; 130: 145–152.CrossRefGoogle Scholar
17.Urdal, DL, March, CJ, Gillis, S, et al. Purification and chemical characterization of the receptor for interleukin 2 from activated human lymphocytes and from a human T-cell lymphoma cell line. Proc Natl Acad Sci USA 1984; 81: 6481–6485.CrossRefGoogle ScholarPubMed
18.Coyle, JT, McGeer, EG, McGeer, PL, et al. Neostriatal injections: a model for Huntington’s chorea. In: McGeer, EG, Olney, JW, McGeer, PL, eds. Kainic Acid as a Tool in Neurobiology. New York: Raven Press, 1978; 139–159.Google Scholar
19.McGeer, PL, McGeer, EG. Excitotoxic amino acids as tools in neurobiology. Rev Pure Appl Pharmacol Sci 1983; 4: 213–270.Google ScholarPubMed
20.Guttman, M, Seeman, P, Reynolds, GP, et al. Dopamine D2 receptor density remains constant in treated Parkinson’s disease. Ann Neurol 1986; 19: 487–492.CrossRefGoogle ScholarPubMed
21.Penney, JB Jr, Young, AB. Quantitative autoradiography of neuro- transmitter receptors in Huntington’s disease. Neurol 1982; 32: 1391–1395.CrossRefGoogle Scholar
22.Seizinger, BR, Liebisch, DC, Kish, SJ, et al. Opioid peptides in Huntington’s disease: alterations in prodynorphin and proen-kephalin system. Brain Res 1986; 378: 405–408.CrossRefGoogle ScholarPubMed
23.Ferrante, R, Kowall, N, Richardson, E Jr, et al. Topography of enkephalin, substance P and acetylcholinesterase staining in Huntington’s disease striatum. Neurosci Lett 1986; 71: 283–288.CrossRefGoogle ScholarPubMed
24.Zech, M, Bogerts, B.Methionine-enkephalin and substance P in the basal ganglia of normals, Parkinson patients, Huntington patients, and schizophrenics. Acta Neuropathol 1985; 68: 32–38.CrossRefGoogle ScholarPubMed
25.Kanazawa, I, Sasaki, H, Muramoto, O, et al. Studies on neurotrans- mitter markers and striatal neuronal cell density in Huntington’ disease and dentatorubropallidoluysian atrophy. J Neurol Sci 1985; 70: 151–165.CrossRefGoogle Scholar
26.Whitehouse, PJ, Trifiletti, RR, Jones, BE, et al. Neurotransmitter receptor alterations in Huntington’s disease: autoradiographic and homogenate studies with special reference to benzodiazepine receptor complexes. Ann Neurol 1985; 18: 202–210.CrossRefGoogle ScholarPubMed
27.Reynolds, GP, Garrett, NJ. Striatal dopamine and homovanillic acid in Huntington’s disease. J Neural Transm 1986; 151–155.Google ScholarPubMed
28.Cross, AJ, Slater, P, Reynolds, GP. Reduced high-affinity glutamate uptake sites in the brains of patients with Huntington’s disease. Neurosci Lett 1986; 67: 198–202.CrossRefGoogle ScholarPubMed
29.Greenamyre, JT, Penney, JB, Young, AB, et al. Alterations in L-glutamate binding in Alzheimer’s and Huntington’s diseases. Science 1985; 227: 1496–1499.CrossRefGoogle ScholarPubMed
30.Sadoul, JL, Checler, F, Kitabgi, P, et al. Loss of high affinity neurotensin receptors in substantia nigra from parkinsonian subjects. Biochem Biophys Res Commun 1984; 125: 395–404.CrossRefGoogle ScholarPubMed
31.Taquet, H, Javoy-Agid, F, Cesselin, F, et al. Microtopography of methionine-enkephalin, dopamine and noradrenaline in the ventral mesencephalon of human control and parkinsonian brains. Brain Res 1982; 235: 303–314.CrossRefGoogle ScholarPubMed
32.Garbarg, M, Javoy-Agid, F, Schwartz, JC, et al. Brain histidine decarboxylase activity in Parkinson’s disease. Lancet 1983i; 74–75.CrossRefGoogle ScholarPubMed
33.deMontis, G, Beaumont, K, Javoy-Agid, F, et al. Glycine receptors in the human substantia nigra as defined by [3H]strychnine binding. J Neurochem 1982; 38: 718–724.CrossRefGoogle Scholar
34.Gaspar, P, Javoy-Agid, F, Plaska, A, et al. Regional distribution of neurotransmitter synthesizing enzymes in the basal ganglia of human brain. J Neurochem 1980; 34: 278–283.CrossRefGoogle ScholarPubMed
35.Cash, R, Lasbennes, F, Sercombe, R, et al. Adrenergic receptors on cerebral microvessels in control and parkinsonian subjects. Life Sci 1985; 12: 531–536.CrossRefGoogle Scholar
36.Raisman, R, Cash, R and Agid, Y. Parkinson’s disease: decreased density of 3H-imipramine and 3H-paroxetine binding sites in putamen. Neurol 1986; 36: 556–560.Google ScholarPubMed
37.Reisine, TD, Fields, JZ, Yamamura, HI, et al. Neurotransmitter receptor alterations in Parkinson’s disease. Life Sci 1977; 21: 335–344.CrossRefGoogle ScholarPubMed
38.Guttman, M, Seeman, J.L-DOPA reverses the elevated density of D-2 dopamine receptors in Parkinson’s diseased striatum. J Neural Transm 1986; 64: 93–103.CrossRefGoogle Scholar
39.Schoemaker, H, Pimoule, C, Arbilla, S, et al. Sodium dependent [3H] cocaine binding associated with dopamine uptake sites in the rat striatum and human putamen decrease afterdopaminergic denervation and in Parkinson’s disease. Naunyn-Schmiedeberg’s Arch Pharmacol 1985; 329: 227–235.CrossRefGoogle Scholar
40.Pioro, EPJ, Hughes, JT, Cuello, AC. Loss of substance P and enkephalin immunoreactivity in the human substantia nigra after striato-pallidal infarction. Brain Res 1984; 292: 339–347.CrossRefGoogle ScholarPubMed
41.Nyberg, P, Gottfries, CG, Holmgren, G, et al. Advanced catechola-minergic disturbances in the brain in a case of Wilson’s disease. Acta Neurol Scandinav 1982; 65: 71–75.CrossRefGoogle Scholar
42.Bokobza, B, Rubert, M, Scatton, B, et al. [3H]Spiperone binding, dopamine and HVA concentrations in Parkinson’s disease and supranuclear palsy. Eur J Pharm 1984; 99: 167–175.CrossRefGoogle Scholar
43.Beal, M, Mazurek, M, Martin, J.Somatostatin immunoreactivity is reduced in Parkinson’s disease dementia with Alzheimer’s changes. Brain Res 1986; 397: 386–388.CrossRefGoogle ScholarPubMed
44.Ruberg, M, Ploska, A, Javoy-Agid, F, et al. Muscarinic binding and choline acetyltransferase activity in parkinsonian subjects with reference to dementia. Brain Res 1982; 232: 129–139.CrossRefGoogle ScholarPubMed
45.Marshall, PE, Landis, DMD, Zalneraitis, EL. Immunocytochemical studies of substance P and leucine-enkephalin in Huntington’s disease. Brain Res 1983; 289: 11–26.CrossRefGoogle ScholarPubMed
46.Tago, H, McGeer, PL, Bruce, G, et al. Distribution of choline acetyltransferase-containing neurons of the hypothalamus. Brain Res 1987 (in press).CrossRefGoogle ScholarPubMed