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Selective Sparing of Human Nucleus Accumbens in Aging and Anoxia

Published online by Cambridge University Press:  18 September 2015

Ke-Wei Huang*
Affiliation:
Neuropathology Laboratory, Chinese PLA General Hospital, Beijing
Yan Zhao
Affiliation:
Neuropathology Laboratory, Chinese PLA General Hospital, Beijing
*
Neuropathology Laboratory, Chinese PLA General Hospital, Beijing, 100853, People’s Republic of China
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Abstract

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Objective

To investigate the effects of aging and anoxia on the nucleus accumbens.

Methods

The number of neurons in nucleus accumbens and caudate neucleus in 35 patients over 65 and 35 under 65 years, all without neurological or psychiatric diseases were counted.

Results

There was no statistically significant difference between the number of neurons in the accumbens in the two groups, but there was a decrease in the number of neurons in the elderly group. There was no reduction in volume of the neuronal nucleoli of the accumbens measured in 12 elderly patients compared to controls. These data suggest a sparing of the accumbens from changes associated with aging. There was relative preservation of the nucleus accumbens in 3 patients with anoxic encephalopathy.

Conclusions

These results show that accumbens was resistant to both aging and anoxia, the mechanism of which is discussed.

Résumé

Résumé<span class='italic'><span class='bold'>Objectif</span></span>

L’étude porte sur les effets du vieillissement et de l’anoxie sur le noyau accumbens.

<span class='italic'><span class='bold'>Méthode</span></span>

Nous avons dénombré les neurones du noyau accumbens (Ace) et du noyau caudé (NC) chez 35 patients de plus de 65 ans et 35 patients de moins de 65 ans, sans maladie neurologique ou psychiatrique.

<span class='italic'><span class='bold'>Résultats</span></span>

Il n’existait pas de différence significative au point de vue statistique entre le nombre de neurones dans l’Ace entre les deux groupes. Cependant, il y avait une diminution du nombre de neurones dans le NC du groupe âgé. Il n’y avait pas de diminution du volume des nucléoles neu-ronaux de l’Ace chez 12 patients âgés comparés à des contrôles. Ces observations suggèrent une épargne sélective de l’Ace par le vieillissement. Chez 3 patients avec encéphalopathie anoxique, l’Ace était relativement préservé.

<span class='italic'><span class='bold'>Conclusions</span></span>

Ces résultats indiquent que l’Ace est résistant au vieillissement et à l’anoxie, et nous discutons des mécanismes en cause.

Type
Original Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1995

References

REFERENCES

1. Ariens-Kappers, CU, Theunissen, WF. Die Phylogenese des Rhhinencephalons, des Corpus Striatum und der Vorderhirn Kommissuren. Folia Neurobiol 1907; 1: 173288.Google Scholar
2. Swanso, LW, Cowan, WM. A note on the connections and development of the nucleus accumbens. Brain Res 1975; 92: 324330.CrossRefGoogle Scholar
3. Totterdell, S, Smith, AD. Cholecystokin in immunoreactive boutons in synaptic contact with hippocampal pyramidal neurons that project to the nucleus accumbens. Neuroscience 1986; 19: 181192.CrossRefGoogle Scholar
4. Jayaraman, A. Organization of thalamic projections in the nucleus accumbens and the caudate nucleus in cats and its relation with hippocampal and other subcortical afferents. J Comp Neurol 1985; 231:396420.Google Scholar
5. Phillipson, OT, Griffiths, AC. The topographic order of inputs to nucleus accumbens in the rat. Neuroscience 1985; 16: 275296.Google Scholar
6. Studler, JM, Reibaud, M, Tramu, G, et al. Pharmacological study on the mixed CCK 8/DA mesonucleus accumbens pathway: evidence for the existence of storage sites containing the two transmitters. Brain Res 1984; 298: 9197.Google Scholar
7. Swerdlow, NR, Koob, GF. The neural substrates of apomorphinestimulated locomotor activity following denervation of the nucleus accumbens. Life Sci 1984; 35: 25372544.Google Scholar
8. Chang, HT, Kitai, ST. Projection neurons of the nucleus accumbens: an intracellular labeling study. Brain Res 1985; 347: 112116.Google Scholar
9. D’ Angio, M, Serrano, A, Rivy, JP, Scatton, B. Tail-pinch stress increases extracellular DORPAC levels (as measured by in vivo voltammetry) in the rat nucleus accumbens but not frontal cortex: antagonism by diazepam and Zolpidem. Brain Res 1987; 409: 169563.Google Scholar
10. Phillips, S, Sangalang, V, Sterns, G. Basal forebrain infarction. A clinicopathologic correlation. Arch Neurol 1987; 44: 11341138.Google Scholar
11. McCaughey, WTE. The pathologic spectrum of Huntington’s chorea. Nerv Ment Dis 1961; 133:91103.Google Scholar
12. Bots, GT, Bruyn, GW. Neuropathological changes of nucleus accumbens in Huntington’s chorea. Acta Neuropathol (Berl) 1981; 55: 2122.Google Scholar
13. Stevens, JR. An anatomy of schizophrenia. Arch Gen Psychiat 1973; 29: 177189.Google Scholar
14. Mattysse, S. Nucleus accumbens and schizophrenia. In: Chronister, RB, de France, JF, eds. The Neurobiology of the Nucleus Accumbens. Brunswick, Maine: Haer Institute, 1981: 351359.Google Scholar
15. Hori, A, Hirose, G, Kataoka, S, et al. Delayed postanoxic encephalopathy after strangulation. Serial neuroradiological and neurochemical studies. Arch Neurol 1991; 48: 871874.Google Scholar
16. Rutherford, MA, Pennock, JM, Murodoch-Eaton, DM, Cowan, FM, Dubowitz, LM. Athetoid cerebral palsy with cysts in the putamen after hypoxic-ischemic encephalopathy. Arch Dis Child 1992; 67: 846850.Google Scholar
17. Mascalchi, M, Dal-Pozzo-Ge, Pinto, F. MRI demonstration of the cerebellar damage in diffuse hypoxic-ischemic encephalopathy. Case report. Ital J Neurol Sci 1992; 13: 517519.Google Scholar
18. Feve, AP, Fenelon, G, Wallays, C, Remy, P, Guillard, A. Axial motor disturbances after hypoxic lesion of the globus pallidus. Mov Disord 1993; 8: 321326.Google Scholar
19. Von Brockhaus, H. Zur feineren Anatomie des Septum und des Striatum. J Psychol Neurol 1942; 51: 155.Google Scholar
20. Walsh, FX, Stevens, TJ, Langlais, PJ, Brid, ED. Dopamine and homovanillic acid concentrations in striatal and limbic regions of human brain. Ann Neurol 1982; 12: 5255.Google Scholar
21.Carpenter, MB, Sutin, J. The corpus striatum. In: Carpenter, MB, Sutin, J, eds. Human Neuroanatomy, 8th Edition. Chapter 17. Baltimore: Waverly Press, 1983; 17: 579611.Google Scholar
22. Herkenham, M, Edley, SM, Stuart, J. Cell clusters in the nucleus accumbens of the rat, and the mosaic relationship of opiate receptors, acetylcholinesterase and subcortical afferent terminations. Neuroscience 1984; 11: 561593.Google Scholar
23. Vonasttel, JP, Myers, RH, Stevens, TJ, et al. Neuropathological classification of Huntington’s disease. J Neuropathol Exp Neurol 1985; 44:559577.Google Scholar
24. Mann, D.M.A. Annotation. Nerve cell protein metabolism and degeneration disease. Neuropathol Appl Neurobiol 1982; 8: 161167.Google Scholar
25. Herzog, AG kang Kemper, TL. Amygdaloid changes in aging and dementia. Arch Neurol 1980; 37: 625629.Google Scholar
26. Mani, RB, Lohr, JB, Jeste, DV. Hippocampal pyramidal cells and aging in the human: a quantitative study of neuronal loss in sectors CA 1 to CA4. Exp Neurol 1986; 94: 2940.Google Scholar
27. Perlmutter, D, Rhoton, AL. Microsurgical anatomy of the anterior cerebral-anterior communicating recurrent artery complex. J Neurosurg 1976; 45: 259272.CrossRefGoogle ScholarPubMed
28. Dunker, RO, Harris, AB. Surgical anatomy of the proximal anterior cerebral artery. J Neurosurg 1976; 44: 359367.CrossRefGoogle ScholarPubMed
29. Myers, RH, Vonsattel, JP, Stevens, TJ, et al. Clinical and neuropathologic assessment of severity in Huntington’s disease. Neurology 1988; 38:341347.Google Scholar
30. Uemura, Y, Kowall, NW, Beal, MF. Selective sparing of NADPHdiaphorase-somatostatin-neuropeptide Y neurons in ischemic gerbil striatum. Ann Neurol 1989; 27: 620625.Google Scholar
31. Beal, MF, Kowall, NW, Ellison, DW, et al. Replication of the neurochemical charcteristics of Huntington’s disease by quinolinic acid. Nature 1986; 321: 168171.CrossRefGoogle Scholar
32. Ferrante, RJ, Kowall, NW, Beal, MF, et al. Selective sparing of a class of striatal neurons in Huntington’s disease. Science 1985; 230: 561563.Google Scholar