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Lesion mesencephalic

Muscle-derived differentiation factor (MDF) induces tyrosine hydroxylase expression in a variety of central nervous system neurons, including those of striatum, cerebellum, and cortex. Normally, i.e., without MDF, these neurons do not express this enzyme of catecholamine synthesis. Further in vitro studies revealed that MDF enhances TH-mRNA 40-fold in fetal mesencephalic neurons. In vivo studies, employing infusion of partially isolated MDF, reported this molecule to enhance tyrosine hydroxylase activity in dopamine-depleted striata of 6-OHDA-lesioned animals. Furthermore, an increase of striatal dopamine concentrations and a partial compensation of rotational asymmetry were observed. In contrast, dopaminergic parameters were not affected by administration of MDF in control animals, suggesting that adult dopaminergic neurons may regain sensitivity toward differentiation factors after lesion. [Pg.181]

Hansen JT, Sakai K, Greenamyre JT, Moran S (1995) Sprouting of dopaminergic fibers from spared mesencephalic dopamine neurons in the unilateral partial lesioned rat. Brain Res 670 197-204. [Pg.189]

Dunnett SB, Hernandez TD, Summerfield A, Jones GH, Arbuthnott GW (1988) Graft-derived recovery from 6-OHDA lesions specificity of ventral mesencephalic graft tissues. Exp Brain Res 77 411-424. [Pg.285]

Wictorin, K., Brundin, P., Sauer, H., Lindvall, O., and Bjorklund, A., Long distance directed axonal growth from human dopaminergic mesencephalic neuroblasts implanted along the nigrostriatal pathway in 6-hydroxydopamine lesioned adult rats, J. Comp. Neurol., 323, 475, 1992. [Pg.17]

Graham WC, Crossman AR. Woodruff GN. Autoradiographic studies in animal models of hemi-parkisonism reveal dopamine D2 but not DI receptor supersensitivity. I. 6-OHDA lesions of ascending mesencephalic dopaminergic pathways in the rat. Brain Res 1990 514 93-102. [Pg.141]

Eghbali M, Santoro C, Paredes W, Gardner EL, Zukin RS (1987) Visualization of multiple opioid-receptor types in rat striatum after specific mesencephalic lesions. Proc. Nat. Acad. Sci. USA, 84, 6582-6586. [Pg.460]

A 16-year-old boy developed unsteadiness and double vision 5 minutes after intranasal inhalation of a small amount of amfetamine cut with cocaine. Cranial MRI (magnetic resonance imaging) revealed a mesencephalic lesion that was seen to have decreased 12 days later, and he became symptom-free after 3 weeks. The ischaemic lesion was thought to be due to vasospasm caused by synergistic stimulation of the sympathetic nervous system amfetamine causes the release of adrenaline (epinephrine) and noradrenaline (norepinephrine), while cocaine prevents their reuptake. ... [Pg.200]

Colonnier, M., Steriade, M., and Landry, P., 1979, Selective resistance of sensory cells of the mesencephalic trigeminal nucleus to kainic acid-induced lesions. Brain Res. 172 522-556. [Pg.264]

Wernicke-Korsakoff syndrome results from alcohol-induced thiamin deficiency. It affects the central nervous system. The patients suffer from irreversible memory loss as a result of severe mesencephalic lesions. [Pg.120]

Moukhles etaL (1994) transplanted dopamine-rich ventral mesencephalic suspension in a partially dopamine-depleted striatum of rats performing a reaction-time motor task. In the lesion group premature responses and delayed responses were seen. In the grafted animals the premature responses improved totally, the number of delayed responses remained high. [Pg.336]


See other pages where Lesion mesencephalic is mentioned: [Pg.214]    [Pg.215]    [Pg.216]    [Pg.3]    [Pg.177]    [Pg.239]    [Pg.68]    [Pg.2702]    [Pg.176]    [Pg.279]    [Pg.110]    [Pg.157]    [Pg.127]   
See also in sourсe #XX -- [ Pg.213 ]




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