CoChat
Sign Up
Cited by 483

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

The pattern of neurodegeneration in Huntington's disease: a comparative study of cannabinoid, dopamine, adenosine and GABAA receptor alterations in the human basal ganglia in Huntington's disease

Glass, M., Dragunow, M., Faull, R.L.M.·2000·Neuroscience
DOI 10.1016/s0306-4522(00)00008-7
Open this paper in CoChat — free account

Abstract

In order to investigate the sequence and pattern of neurodegeneration in Huntington's disease, the distribution and density of cannabinoid CB(1), dopamine D(1) and D(2), adenosine A(2a) and GABA(A) receptor changes were studied in the basal ganglia in early (grade 0), intermediate (grades 1, 2) and advanced (grade 3) neuropathological grades of Huntington's disease. The results showed a sequential pattern of receptor changes in the basal ganglia with increasing neuropathological grades of Huntington's disease. First, the very early stages of the disease (grade 0) were characterized by a major loss of cannabinoid CB(1), dopamine D(2) and adenosine A(2a) receptor binding in the caudate nucleus, putamen and globus pallidus externus and an increase in GABA(A) receptor binding in the globus pallidus externus. Second, intermediate neuropathological grades (grades 1, 2) showed a further marked decrease of CB(1) receptor binding in the caudate nucleus and putamen; this was associated with a loss of D(1) receptors in the caudate nucleus and putamen and a loss of both CB(1) and D(1) receptors in the substantia nigra. Finally, advanced grades of Huntington's disease showed an almost total loss of CB(1) receptors and the further depletion of D(1) receptors in the caudate nucleus, putamen and globus pallidus internus, and an increase in GABA(A) receptor binding in the globus pallidus internus. These findings suggest that there is a sequential but overlapping pattern of neurodegeneration o…

Overview

Integrity signals

Registry

Crossref · 10.1016/s0306-4522(00)00008-7

Cites

3 of 3 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The N-terminal fragment of hSREBP2 (1-482 aa) is the active form.

    “We obtained the AAV vector plasmid pZac-gfaABC1D-hSREBP2-tdTomato, expressing the active N-terminal fragment of hSREBP2 (1-482 aa) fused with tdTomato, starting from pZac2.1 gfaABC1D-tdTomato (from Addgene) and pcDNA3.1 hSREBP2(402)-eGFP (from T. Osborne) 61 .”

    From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [61]

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 65

  1. Albin, 1992, Preferential loss of striato-external pallidal projection neurons in presymptomatic Huntington's disease, Ann. Neurol., 31, 425, 10.1002/ana.410310412 · DOI
  2. Albin, 1989, The functional anatomy of basal ganglia disorders, Trends Neurosci., 12, 366, 10.1016/0166-2236(89)90074-X · DOI · Paper page
  3. Aubry, 1993, Co-expression of dopamine D2 and substance P (neurokinin-1) receptor messenger RNAs by a sub-population of cholinergic neurons in the rat caudate nucleus and putamen, Neuroscience, 53, 417, 10.1016/0306-4522(93)90205-T · DOI
  4. Augood, 1997, Dopamine D1 and D2 receptor gene expression in Huntington's disease caudate nucleus and putamen, Ann. Neurol., 42, 215, 10.1002/ana.410420213 · DOI
  5. Augood, 1996, Reduction in enkephalin and substance P messenger RNA in the caudate nucleus and putamen of early grade Huntington's disease: a detailed cellular in situ hybridization study, Neuroscience, 72, 1023, 10.1016/0306-4522(95)00595-1 · DOI
  6. Beckstead, 1986, Striatal axons to the globus pallidus entopenduncular nucleus and substantia nigra come mainly from separate cell populations in cat, Neuroscience, 19, 147, 10.1016/0306-4522(86)90012-6 · DOI
  7. Camps, 1989, Dopamine-receptors in human brain—autoradiographic distribution of D2 sites, Neuroscience, 28, 275, 10.1016/0306-4522(89)90179-6 · DOI
  8. Chan, 1998, Hippocampal neurotoxicity of delta(9)-tetrahydrocannabinol, J. Neurosci., 18, 5322, 10.1523/JNEUROSCI.18-14-05322.1998 · DOI
  9. Cortes, 1989, Dopamine-receptors in human brain—autoradiographic distribution of D1 sites, Neuroscience, 28, 263, 10.1016/0306-4522(89)90178-4 · DOI
  10. Dawbarn, 1985, Survival of basal ganglia neuropeptide-Y somatostatin neurons in Huntington's disease, Brain Res., 340, 251, 10.1016/0006-8993(85)90921-7 · DOI
  11. Dragunow, 1994, C-fos antisense inhibits basal expression of Krox 24 in rat caudate and neocortex, Cell. molec. Neurobiol., 14, 395, 10.1007/BF02088826 · DOI
  12. Enna, 1976, Alterations of brain neurotransmitter binding in Huntington's chorea, Brain Res., 16, 531, 10.1016/0006-8993(76)90502-3 · DOI
  13. Eshhar, 1993, HU-211, a non-psychotropic cannabinoid, rescues cortical-neurons from excitatory amino-acid toxicity in culture, NeuroReport, 5, 237, 10.1097/00001756-199312000-00013 · DOI
  14. Faull, 1986, Benzodiazepine receptors in the human spinal cord: a detailed anatomical and pharmacological study, Neuroscience, 17, 791, 10.1016/0306-4522(86)90045-X · DOI
  15. Faull, 1988, Multiple benzodiazepine receptors in the human basal ganglia: a detailed pharmacological and anatomical study, Neuroscience, 24, 433, 10.1016/0306-4522(88)90340-5 · DOI
  16. Faull, 1993, The distribution of GABAa-benzodiazepine receptors in the basal ganglia in Huntington's disease and in the quinolinic acid lesioned rat, Prog. Brain Res., 99, 105, 10.1016/S0079-6123(08)61341-2 · DOI
  17. Faull R. L. M., Waldvogel H. J., Nicholson L. F. B., Williams M. N. and Dragunow M. (1995) Huntington's disease and neural transplantation: GABAA receptor changes in the basal ganglia in Huntington's disease in the human brain and in the quinolinic acid lesioned rat model of the disease following fetal neuron transplants. In Neurotransmitters in the Human Brain. (eds Tracey D., Stone J. and Paxinos G.), pp. 173–198. Plenum, New York. · DOI
  18. Ferrante, 1987, Sparing of acetylcholinesterase-containing striatal neurons in Huntington's disease, Brain Res., 411, 162, 10.1016/0006-8993(87)90694-9 · DOI
  19. Ferrante, 1985, Selective sparing of a class of striatal neurons in Huntington's disease, Science, 230, 561, 10.1126/science.2931802 · DOI
  20. Ferre, 1991, Stimulation of high affinity adenosine A2 receptors decrease the affinity of dopamine D2 receptors in rat striatal membranes, Proc. natn. Acad. Sci. U.S.A., 88, 7238, 10.1073/pnas.88.16.7238 · DOI
  21. Fink, 1992, Molecular cloning of the rat A2 adenosine receptor: selective co-expression with D2 dopamine receptors in rat caudate nucleus and putamen, Molec. Brain Res., 14, 186, 10.1016/0169-328X(92)90173-9 · DOI
  22. Gimenez-Amaya, 1990, Compartmental origins of the striatopallidal projection in the primate, Neuroscience, 34, 111, 10.1016/0306-4522(90)90306-O · DOI
  23. Giuffrida, 1999, Dopamine activaton of endogenous cannabinoid signaling in dorsal caudate nucleus and putamen, Nature Neurosci., 2, 358, 10.1038/7268 · DOI
  24. Glass, 1993, Loss of cannabinoid receptors in the substantia nigra in Huntington's disease, Neuroscience, 56, 523, 10.1016/0306-4522(93)90352-G · DOI
  25. Glass, 1996, Localisation of the adenosine uptake site in the human brain: a comparison with the distribution of adenosine A1 receptors, Brain Res., 710, 79, 10.1016/0006-8993(95)01318-0 · DOI
  26. Graveland, 1985, Evidence for degenerative and regenerative changes in neostriatal spiny neurons in Huntington's desease, Science, 227, 770, 10.1126/science.3155875 · DOI
  27. Hedreen, 1995, Early loss of neostriatal striosome neurons in Huntington's disease, J. Neuropath. exp. Neurol., 54, 105, 10.1097/00005072-199501000-00013 · DOI
  28. Herkenham, 1990, Cannabinoid receptor localization in brain, Proc. natn. Acad. Sci. U.S.A., 87, 1932, 10.1073/pnas.87.5.1932 · DOI · Paper page
  29. Hill M. P., Di Marzo V., Bisogno T., Ambrosino G., Crossman A. R. and Brotchie J. M. (1999) Endocannabinoids and the control of movement and generation of symptoms in Parkinson's disease. Proceedings of the Symposium on the Cannabinoids, Burlington, Vermont, International Cannabinoid Research Society, p. 70.
  30. Hirsch, 1989, Striosomes and extrastiosomal matrix contain different amounts of immunoreactive choline acetyltransferase in the human caudate nucleus and putamen, Neurosci. Lett., 96, 145, 10.1016/0304-3940(89)90048-7 · DOI
  31. James, 1992, Adenosine receptors in post-mortem human brain, Br. J. Pharmac., 165, 238, 10.1111/j.1476-5381.1992.tb14240.x · DOI
  32. Le Moine, 1995, D1 and D2 dopamine receptor gene expression in the rat caudate nucleus and putamen: sensitive cRNA probes demonstrate prominent segregation of D1 and D2 mRNAs in distinct neuronal populations of the dorsal and ventral caudate nucleus and putamen, J. comp. Neurol., 35, 418, 10.1002/cne.903550308 · DOI
  33. Le Moine, 1991, Phenotypical characterization of the rat striatal neurons expressing the D1 dopamine receptor gene, Proc. natn. Acad. Sci. U.S.A., 88, 4205, 10.1073/pnas.88.10.4205 · DOI
  34. Leweke, 1999, Elevated endogenous cannabinoids in schizophrenia, NeuroReport, 10, 1665, 10.1097/00001756-199906030-00008 · DOI
  35. Mailleux, 1992, Localization of cannabinoid receptor in the human developing and adult basal ganglia. Higher levels in the striatonigral neurons, Neurosci. Lett., 148, 173, 10.1016/0304-3940(92)90832-R · DOI
  36. Martinez-Mir, 1991, Adenosine A2 receptors: selective localization in the human basal ganglia and alterations with disease, Neuroscience, 42, 697, 10.1016/0306-4522(91)90038-P · DOI
  37. Matsuda, 1990, Structure of cannabinoid receptor and functional expression of the cloned cDNA, Nature, 346, 561, 10.1038/346561a0 · DOI · Paper page
  38. Mayfield, 1993, Adenosine A2a receptor modulation of electrically evoked endogenous GABA release from slices of rat globus pallidus, J. Neurochem., 60, 2334, 10.1111/j.1471-4159.1993.tb03526.x · DOI
  39. Miller, 1995, Effects of a cannabinoid on spontaneous and evoked neuronal-activity in the substantia-nigra pars reticulata, Eur. J. Pharmac., 279, 179, 10.1016/0014-2999(95)00151-A · DOI
  40. Morton, 1993, Compartmental loss of NADPH diaphorase in the neuropil of the human caudate nucleus and putamen in Huntington's disease, Neuroscience, 53, 159, 10.1016/0306-4522(93)90294-P · DOI
  41. Myers, 1991, Decreased neuronal and increased oligodendroglial densities in Huntington's disease caudate nucleus, J. Neuropath. exp. Neurol., 50, 729, 10.1097/00005072-199111000-00005 · DOI
  42. Nadler, 1995, Ca-45 accumulation in rat-brain after closed-head injury—attenuation by the novel neuroprotective agent HU-211, Brain Res., 685, 1, 10.1016/0006-8993(95)00367-Y · DOI
  43. Oviedo, 1993, Chronic cannabinoid administration alters cannabinoid receptor binding in rat brain: a quantitative autoradiographic study, Brain Res., 616, 293, 10.1016/0006-8993(93)90220-H · DOI
  44. Parent, 1984, The striatopallidal and striatonigral projections: two distinct fibre systems in primate, Brain Res., 303, 385, 10.1016/0006-8993(84)91224-1 · DOI
  45. Penney, 1982, Quantitative autoradiography of neurotransmitter receptors in Huntington's disease, Neurology, 32, 1391, 10.1212/WNL.32.12.1391 · DOI
  46. Popoli, 1994, CGS 21680 antagonises motor hyperactivity in a rat model of Huntington's disease, Eur. J. Pharmac., 257, R5, 10.1016/0014-2999(94)90715-3 · DOI
  47. Reiner, 1988, Differential loss of striatal projection neurons in Huntington's disease, Proc. natn. Acad. Sci. U.S.A., 85, 5733, 10.1073/pnas.85.15.5733 · DOI · Paper page
  48. Reiner, 1990, The patterns of neurotransmiter and neuropeptide co-occurance among striatal neurons. Conclusions based on recent findings, Brain Res. Rev., 15, 251, 10.1016/0165-0173(90)90003-7 · DOI
  49. Reisine, 1980, Benzodiazepine receptors: the effect of GABA on their characteristics in human brain and their alterations in Huntington's disease, Brain Res., 199, 79, 10.1016/0006-8993(80)90231-0 · DOI
  50. Reynolds, 1990, Brain GABA levels in asymptomatic Huntington's disease, New Engl. J. Med., 287, 682
  51. Richfield, 1994, Selective vulnerability in Huntington's disease: preferential loss of cannabinoid receptors in lateral globus pallidus, Ann. Neurol., 36, 577, 10.1002/ana.410360406 · DOI
  52. Richfield, 1991, Heterogenous dopamine receptor changes in early and late Huntington's disease, Neurosci. Lett., 132, 121, 10.1016/0304-3940(91)90448-3 · DOI
  53. Sañudo-Peña, 1996, Effects of intranigral cannabinoids on rotational behaviour in rats: interactions with the dopaminergic system, Neurosci. Lett., 206, 21, 10.1016/0304-3940(96)12436-8 · DOI
  54. Sañudo-Peña, 1997, Role of the subthalamic nucleus in cannabinoid actions in the substantia nigra of the rat, J. Neurophysiol., 77, 1635, 10.1152/jn.1997.77.3.1635 · DOI
  55. Sañudo-Peña, 1998, Effects of intrapallidal cannabinoids on rotational behaviour in rats: interactions with dopaminergic systems, Synapse, 28, 27, 10.1002/(SICI)1098-2396(199801)28:1<27::AID-SYN4>3.0.CO;2-E · DOI
  56. Sapp, 1995, Evidence for a preferential loss of enkephalin immunoreactivity in the external globus-pallidus in low-grade Huntingtons disease using high-resolution image-analysis, Neuroscience, 64, 397, 10.1016/0306-4522(94)00427-7 · DOI
  57. Schiffman, 1991, Striatal restricted adenosine A2 receptor (RDC8) is expressed by enkephalin but not be substance P neurons: an in situ hybridization histochemistry study, J. Neurochem., 57, 1062, 10.1111/j.1471-4159.1991.tb08257.x · DOI
  58. Schiffmann, 1993, Adenosine A2 receptors regulate the gene expression of striatopallidal and striatonigral neurons, J. Neurosci., 13, 1080, 10.1523/JNEUROSCI.13-03-01080.1993 · DOI
  59. Spokes, 1980, Neurochemical alterations in Huntington's chorea—a study of postmortem brain tissue, Brain, 103, 179, 10.1093/brain/103.1.179 · DOI
  60. Steiner, 1999, Altered gene expression in striatal projection neurons in CB1 cannabinoid receptor knockout mice, Proc. natn. Acad. Sci. U.S.A., 96, 5786, 10.1073/pnas.96.10.5786 · DOI
  61. Storey, 1990, Neurochemical substrates of rigidity and chorea in Huntingtons-disease, Brain, 116, 1201, 10.1093/brain/116.5.1201 · DOI
  62. Szabo, 1998, Inhibition of GABAergic inhibitory postsynaptic currents by cannabinoids in rat corpus striatum, Neuroscience, 85, 395, 10.1016/S0306-4522(97)00597-6 · DOI
  63. Thibaut, 1990, Microtopography of D1 dopaminergic binding sites in the human substantia nigra: an autoradiographic study, Neuroscience, 37, 3873, 10.1016/0306-4522(90)90409-W · DOI
  64. Vonsattel, 1985, Neuropathological classification of Huntington's disease, J. Neuropath. exp. Neurol., 44, 559, 10.1097/00005072-198511000-00003 · DOI · Paper page
  65. Yoles, 1993, HU-211, a nonpsychotropic cannabinoid, produces short- and long-term neuroprotection after optic nerve axotomy, J. Neurotrauma, 13, 49, 10.1089/neu.1996.13.49 · DOI

Cited by

Sorted by citations

Metadata

Authors
Glass, M., Dragunow, M., & Faull, R. L. M.
Venue
Neuroscience
Publisher
Elsevier BV
Published
2000-05
Volume
97
Issue
3
Pages
505-519
ISSN
0306-4522
DOI
10.1016/s0306-4522(00)00008-7
Cited by
483
References
3
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review