Hostname: page-component-77c89778f8-9q27g Total loading time: 0 Render date: 2024-07-16T09:48:08.288Z Has data issue: false hasContentIssue false
  • English
  • Français

Modulation of Monoaminergic and Amino Acid Transmission as a Means for Therapeutic Intervention in Ataxia

Published online by Cambridge University Press:  18 September 2015

Plaitakis Andreas
Plaitakis Andreas*
Affiliation:
Mount Sinai School of Medicine, New York
*
Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York, USA 10029
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.

In recent years, substantial progress has been made in understanding the organization and function of the cerebellum at the neuronal, synaptic, and molecular level. More than any other region of the brain, the cerebellum utilizes amino acids as its main excitatory and inhibitory transmitters. Excitatory amino acids, such as glutamate and aspartate, in addition to serving as chemical messengers, may also mediate neurodegenerative processes in human ataxic disorders. Of the monoamines, serotonin has been proposed as a neuromodulator in the cerebellum and is thought to play a role in the pathophysiology of ataxia in animal models, and human cerebellar disorders. These considerations raise the possibility that pharmacologic modification of amino acid and serotonergic transmission may provide a means for therapeutic intervention in ataxia.

Type
Abstract
Information
Canadian Journal of Neurological Sciences , Volume 20 , Issue S3 , May 1993 , pp. S105 - S108
Copyright
Copyright © Canadian Neurological Sciences Federation 1993

References

REFERENCES

1.Tsiotos, P, Plaitakis, A, Mitsakos, A, et al.L-glutamate binding sites of normal and atrophic human cerebellum. Brain Res 1989; 481: 87–96.CrossRefGoogle ScholarPubMed
2.Albin, RL and Gilman, S.Autoradiographic localization of inhibitory and excitatory amino acid transmitter receptors in human normal and olivopontocerebellar atrophy cerebellum. Brain Res 1990; 522: 37–45.CrossRefGoogle Scholar
3.Triarchou, LC, Norton, J, Getti, B.Anterograde transsynaptic degeneration in the deep cerebellar nuclei of Purkinje cell degeneration (ped) mutant mice. Exp Brain Res 1987; 66: 577–588.CrossRefGoogle Scholar
4.Plaitakis, A, Nicklas, WJ, Beri, S.Thiamine deficiency: selective impairment of the cerebellar serotoninergic system. Neurology 1978; 28: 691–698.CrossRefGoogle Scholar
5.Van Woert, MH, Plaitakis, A, Hwang, EC, Beri, S.Effect of thiamine deficiency on brain serotonin turnover. Brain Res 1979; 179: 103–110.CrossRefGoogle ScholarPubMed
6.Chan-Palay, V, Plaitakis, A, Nicklas, WJ, Beri, S.Autoradiographic demonstration of loss of labeled indoleamine axons in the cerebellum in diet-induced thiamine deficiency. Brain Res 1977; 138: 380–384.CrossRefGoogle ScholarPubMed
7.Langlais, PJ, Mair, RG.Protective effects of glutamate antagonist MK-801 on pyrithiamine-induced lesions and amino acid changes in rat brain. J Neurosci 1990; 10: 1664–1674.CrossRefGoogle ScholarPubMed
8.Aldino, C., Mazzari, S, Toffano, G, et al.Effects of intracisternal injections of quinolinic acid on serotonergic neurons in the rat brain. Brain Res 1985; 341: 57–65.CrossRefGoogle Scholar
9.Kish, SJ, Robitaille, Y, El-Awar, M, et al.Striatal monoamine neuro-transmitters and metabolites in dominant inherited olivoponto-cerebellar atrophy. Neurology 1992; 1573–1577.Google Scholar
10.Trouillas, P.Regression of cerebellar syndrome with long-term administration of 5-HTP or the combination of 5-HTP-benzerazide. Ital J Neurol Sci 1984; 5: 253–266.CrossRefGoogle ScholarPubMed
11.Petrouka, SJ, Schmidt, AW, Sleight, AJ, Harrington, MA.Serotonin receptor “families” in the central nervous system: an overview. Ann NY Acad Sci 1990; 600: 104–113.Google Scholar
12.Raiteri, M, Maura, G, Barzizza, A.Activation of presynaptic 5-hydroxytryptamine-like receptors on glutamatergic terminals inhibits N-methyl-D-aspartate-induced cyclic GMP production in rat cerebellar slices. J Pharmacol Exp Ther 1991; 257: 1184–1188.Google Scholar
13.Maroteaux, L, Saudou, F, Amlaiky, N., et al.Mouse 5HT1B serotonin receptor: cloning, functional expression, and localization in motor control centers. Proc Natl Acad Sci USA 1992; 89: 3020–3024.CrossRefGoogle ScholarPubMed
14.Sabra, AF, Hallett, M, Sudansky, L, et al.Treatment of action tremor in multiple sclerosis. Neurology 1982; 32: 912–914.CrossRefGoogle ScholarPubMed
15.Sandy, KR.Successful treatment of cerebellar tremor with clonazepam. Clin Pharmacol 1985; 4: 615–618.Google Scholar
16.Olney, JW.Excitatory amino acids and neuropsychiatrie disorders. Biol Psychiatry 1989; 26: 505–525.CrossRefGoogle Scholar
17.Plaitakis, A, Beri, S, Yahr, M.D.Abnormal glutamate metabolism in adult-onset degenerative neurological disorder. Science 1982; 216: 193–196.Google ScholarPubMed
18.Hussain, MM, Zannis, V, Plaitakis, A.Characterization of glutamate dehydrogenase isoproteins purified from the cerebellum of normal subjects and patients with degenerative neurological disorders, and from human neoplastic cell lines. J Biol Chem 1989; 264: 20730–20735.CrossRefGoogle ScholarPubMed
19.Pearce, IA, Cambray-Deakin, MA, Burgyne, R.D.Glutamate acting on NMDA receptors stimulates neurite outgrowth from cerebellar granule cells. FEBS Lett 1987; 233: 143–147.CrossRefGoogle Scholar
20.Balazs, R, Hack, N, Jorgensen, OS.Stimulation of the N-methyl-D-aspartate receptor has a trophic effect on differentiating cerebellar granule cells. Neurosci Lett 1988; 87: 80–86.CrossRefGoogle Scholar
21.Botez, MI, Young, SN, Botez, T, Pedraza, OL.Treatment of heredodegenerative ataxias with amantadine hydrochloride. Can J Neurol Sci 1991; 18: 307–311.CrossRefGoogle ScholarPubMed
22.Piaitakis, A, Beri, S, Yahr, MD.The treatment of GDH-deficientolivopontocerebellar atrophy with branched chain amino acids. Neurology 1983; 33 (Suppl 2): 78.Google Scholar
23.Plaitakis, A, Shashidharan, P.Branched-chain amino acids in amyotrophic lateral sclerosis. Lancet I 1988: 680–682.CrossRefGoogle Scholar
24.Plaitakis, A.The inherited ataxias. In: Johnson, R., ed. Current Therapies in Neurologic Disease 1985–1986. BC Decker Inc, 1985: 254–262.Google Scholar