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Striatal lesions

Coenzyme Q10 and vitamin E are found in wheat germ. Furthermore, studies in mice have shown that administration of coenzyme Q10 elevate the level of mitochondrial a-tocopherol (Lass et al., 1999). Beal and his colleagues (2002) investigated the potential usefulness of coenzyme Q10 in animal models of PD, amyotrophic lateral sclerosis (ALS), and HD. It has been demonstrated that coenzyme Q10 can protect against striatal lesions produced by the mitochondrial toxins malonate and 3-nitropropionic acid. These toxins have been utilized to model the striatal pathology, which... [Pg.645]

Hefti F, Melamed E, Sahakian BJ, Wurtman RJ (1980) Circling behavior in rats with partial, unilateral nigro-striatal lesions effects of amphetamine, apomorphine, and DOPA. Pharmacol Biochem Behav 72 185-188. [Pg.287]

Beal ME, Kowall NW, Ferrante RJ, Ben Cipolloni P (1989) Quinolinic acid striatal lesions in primates as a model of Huntington s disease. AnnNeur ol 26 137. [Pg.398]

PanH S., Frey K. A, Young A B., and Penney ] B, Jr (1983) Changes in [ H] muscimol binding in substantia nigra, entopeduncular nucleus, globus pallidus, and thalamus after striatal lesions as demon-... [Pg.198]

KorfJ and Venema K (1983) Ammo acids in the substantia nigra in rats with striatal lesions produced by kainic acid. / Neurochem 40, 1171-1173... [Pg.231]

Meibach, R. C., Brown, L., and Brooks, F. H., 1978, Histofluorescence of kainic acid-induced striatal lesions, Brain Res. 148 219-223. [Pg.267]

ScHWARCz, R., and Coyle, J. T., 1977a, Striatal lesions with kainic acid neurochemical characteristics. Brain Res. 127235-249. [Pg.268]

Kelly, P. A. T., Graham, D. I., and McCulloch, J., 1982, Specific alterations in local cerebral glucose utilization following striatal lesions. Brain Res. 233 157-172. [Pg.403]

In vitro, the presence of 800 mM iron increased (> 100 %) the production of HO by 5 pM 6-hydroxydopamine while Mn caused a significant reduction (72%) (Mendez-Alvarez etal. 2001). The presence of ascorbate (100 pM) induced a continuous generation of HO while the presence of hydroxyl reductants (100 pM) limited this production to the first minutes of the reaction. In vivo, tyrosine hydroxylase immunohistochemistry revealed that intrastriatal injections of rats with 6-hydroxydop-amine (30 nmol) + (600 nmol), 6-hydroxydopamine -I- ascorbate -i- Fe (5 nmol), and 6-hydroxydop-amine -i- ascorbate -t Mn (5 nmol) caused large striatal lesions, which were markedly reduced (60%) by the substitution of ascorbate by l-cysteine. Injections of Fe or Mn alone showed no significant difference to those of saline. [Pg.517]

New small animal methods, supplementing oxotremorine tremor, etc., have made possible study of adrenergic actions based mainly upon the changes in locomotor activity and stereotypy exerted by amphetamine and apomorphine and by drug effects upon turning behavior after striatal lesions caused by 6-hydroxydopamine, electrolysis and suction. [Pg.24]


See other pages where Striatal lesions is mentioned: [Pg.352]    [Pg.879]    [Pg.880]    [Pg.46]    [Pg.55]    [Pg.645]    [Pg.3]    [Pg.265]    [Pg.74]    [Pg.83]    [Pg.204]    [Pg.495]    [Pg.238]    [Pg.233]    [Pg.250]    [Pg.349]    [Pg.387]    [Pg.387]    [Pg.672]    [Pg.21]   
See also in sourсe #XX -- [ Pg.3 , Pg.240 , Pg.262 ]




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Lesion

Striatal kainic acid lesion

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