Hostname: page-component-848d4c4894-2xdlg Total loading time: 0 Render date: 2024-06-16T10:06:00.512Z Has data issue: false hasContentIssue false

Effects of Glutamate and Aspartate on Ataxic Gait Induced by 3-Acetyl Pyridine in Rats

Published online by Cambridge University Press:  18 September 2015

G. De Michele
Affiliation:
Department of Neurobiology, Clinical Research Institute of Montreal
F.B. Jolicoeur
Affiliation:
Department of Neurobiology, Clinical Research Institute of Montreal
D.B. Rondeau
Affiliation:
Department of Neurobiology, Clinical Research Institute of Montreal
R.F. Butterworth
Affiliation:
Department of Neurobiology, Clinical Research Institute of Montreal
A. Barbeau*
Affiliation:
Department of Neurobiology, Clinical Research Institute of Montreal
*
Clinical Research Institute of Montreal, 110 Pine Ave. West, Montreal, Québec, Canada H2W 1R7
Rights & Permissions [Opens in a new window]

Summary:

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.

The main purpose of this study was to examine the effects of intraventricular injections of glutamate and aspartate on the walking gait of rendered ataxic by the administration of 3-acetyl pyridine. Both amino acids significantly improved the walking gait of these animals. The effects of other substances known to have a stimulatory influence on locomotor activity in rats were also investigated. Amphetamine, apomorphine and thyrotropin releasing hormone (TRH) had no effect on the ataxic gait of 3-AP treated animals. Substance P significantly improved the gait of ataxic animals, but to a lesser extent than that seen with glutamate and aspartate.

Type
Quebec Cooperative Study of Friedreich's Ataxia
Copyright
Copyright © Canadian Neurological Sciences Federation 1980

References

REFERENCES

Butterworth, R.F., Hamel, E., Landreville, F. and Barbeau, A. (1978). Cerebellar ataxia produced by 3-acetyl pyridine in rat. Can. J. Neurol. Sci. 5: 13311333.CrossRefGoogle ScholarPubMed
Desclin, J.C. (1971). Histological evidence supporting the inferior olive as the major source of cerebellar climbing fibers. Brain Res. 77: 365384.CrossRefGoogle Scholar
Desclin, J.C. and Escubi, J. (1974). Effects of 3-acetyl pyridine on the central nervous system of the rat. as demonstrated by silver methods. Brain Res. 77: 349363.CrossRefGoogle Scholar
Guidotti, A., Biggio, G. and Costa, E. (1975). 3-Acetyl pyridine: a tool to inhibit the tremor and the increase of cGMPcontent in cerebellar cortex elicited by harmaline. Brain Res. 96: 201205.CrossRefGoogle Scholar
Hicks, S.P. (1955). Pathologic effects of antimetabolites. Amer. J. Path. 31: 189197.Google ScholarPubMed
Holmes, G. (1907). A form of familial degeneration of cerebellum. Brain 30: 466471.CrossRefGoogle Scholar
Huxtable, R., Azari, H.I., Reisine, T., Johnson, P., Yamamura, H.I. and Barbeau, A. (1979). Regional distribution of amino acids in Friedreich’s ataxia patients. Can. J. Neurol. Sci. 6: 255258.CrossRefGoogle Scholar
Jolicoeur, F.B., Rondeau, D.B., Hamel, E., Butterworth, R.F. and Barbeau, A. (1979). Measurement of ataxia and related neurological signs in the laboratory rat. Can. J. Neurol. Sci. 6: 209215.CrossRefGoogle ScholarPubMed
Mcbride, W.J., Rea, M.A. and Nadi, N.S. (1978). Effects of 3-acetyl pyridine on the levels of several amino acids in different CNS regions of the rat. Ncurochcm. Res. 3: 793801.Google Scholar
Nadi, N.S., Kantf, R.D., Mcbride, W.J. and Aprison, M.H. (1977). Effects of 3-acetyl pyridine on several putative neuro-transmitter amino acids in the cerebellum and medulla of the rat. J. Ncurochcm. 28: 661662.CrossRefGoogle Scholar
Rea, M.A., Mcbride, W.J. and Rohde, B.H. (1980). Regional and synaptosomal levels of amino acid neurotransmitters in the 3-acetyl pyridine deafferentated rat cerebellum. J. Neurochem. 34: 11041106.CrossRefGoogle Scholar
Robinson, N. (1968). Chemical changes in spinal cord in Friedreich’s ataxia and motor neurone disease. J. Neurol. Neurosurg. Psychiat. 31: 330333.CrossRefGoogle ScholarPubMed