Hostname: page-component-cd9895bd7-p9bg8 Total loading time: 0 Render date: 2024-12-26T06:58:58.942Z Has data issue: false hasContentIssue false
  • English
  • Français

Huntingtin Localization In Rat Cortex And Striatum

Published online by Cambridge University Press:  02 July 2020

William L'Amoreaux  and
Sandra Nevins
William L'Amoreaux
Affiliation:
Department of Biology, The College of Staten Island, Staten Island, NY10314
Sandra Nevins
Affiliation:
Department of Biology, The College of Staten Island, Staten Island, NY10314
Get access

Extract

Huntington’s Disease (HD) is a progressive neurodegenerative disease that is characterized by loss 19 of motor function and a decline in cognitive functions. HD is characterized morphologically by loss of neurons in the basal ganglia. During the progression of HD, striatal projection neurons die but cholinergic and somatostatin-containing intemeurons survive. The mutated gene for HD has been described and the protein transcribed by the disease (huntingtin or HT) described. Within the striatum, there is a lack of correlation between presence of HT and neuronal vulnerability. HT has been shown to be associated with intracellular vesicles in human tissues.

Female rats were transcardially perfused with 4% paraformaldehyde, 0.1 M lysine, 10 mM sodium periodate (PLP) in 0.1 M phosphate buffer. Following fixation, the brain was removed and the cortex and striatum removed from the brain as 5 mm3 pieces and transferred to fresh PLP containing 0.25% glutaraldehyde.

Type
Neurobiology
Information
Microscopy and Microanalysis , Volume 5 , Issue S2: Proceedings: Microscopy & Microanalysis '99, Microscopy Society of America 57th Annual Meeting, Microbeam Analysis Society 33rd Annual Meeting, Portland, Oregon August 1-5, 1999 , August 1999 , pp. 1298 - 1299
Copyright
Copyright © Microscopy Society of America

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Bruyn, G W Neurological Manifestations of Systemic Diseases Amsterdam North Holland Publ.(1979)Google Scholar

2. Wilson, R. S. et al., J. Clin. Exp. Neuropsychol.9(l987)l47.Google Scholar

3. De La Monte, S. M. et al., J. Neuropathol. Exp. Neurol.47(l988)5l6.CrossRefGoogle Scholar

4. Hedreen, J. C. et al., Neurosci. Lett. 133(1991)257.CrossRefGoogle Scholar

5. Reiner, A. et al., Proc. Natl. Acad. Sci 85(1988)5733.CrossRefGoogle Scholar

6. Albin, R. L. et al., N. Engl. J. Med. 322(1990)1293.CrossRefGoogle Scholar

7. Ferrante, R. J. et al., Science 230(1985)561.CrossRefGoogle Scholar

8. Ferrante, R. J. et al., J. Neuropathol. Exp. Neurol. 46(1987)12.CrossRefGoogle Scholar

9. Huntington's, Disease Collaborative Research Group, Cell 72(1993)971.Google Scholar

10. DiFiglia, M. et al., Neuron 14(1995)1075CrossRefGoogle Scholar

11. Fusco, F. et al., J. Neurosci. (1999)in press.Google Scholar

12. DiFiglia, M. et al., Science 277(1997)1990.CrossRefGoogle Scholar