Regular Article6-Hydroxydopamine Injections into the Nigrostriatal Pathway Attenuate Striatal Malonate and 3-Nitropropionic Acid Lesions
References (66)
- et al.
Defect in succinate oxidation by isolated mitochondria in a patient with symmetrical lesions in the basal ganglia
J. Neurol. Sci.
(1988) - et al.
Histochemical localization of cytochrome oxidase in the hippocampus: Correlation with specific neuronal types and afferent pathways
Neurosci.
(1982) - et al.
Substantia nigra lesion protects against ischemic damage in the striatum
Neurosci. Lett.
(1987) - et al.
Nigrostriatal pathway modulates striatum vulnerability to quinolinic acid
Neurosci. Lett.
(1991) - et al.
Excitotoxicity of NMDA and kainic acid is modulated by nigrostriatal dopaminergic fibers
Neurosci. Lett.
(1989) - et al.
Circling behavior in rats with partial, unilateral nigro-striatal lesions: Effect of amphetamine, apomorphine and DOPA
Pharmacol. Biochem. Behav.
(1980) - et al.
Dopamine as inhibitory and accelerating effects on ischemia-induced cell damage in the rat striatum
Brain Res. Bull.
(1994) - et al.
Role of presynaptic dopamine receptors in regulation of the glutamatergic neurotransmission in rat neostriatum
Neuroscience
(1984) - et al.
lNd
Neuroscience
(1992) - et al.
Enhanced synthesis of platelet-derived growth factor following injury induced by 6-hydroxydopamine in rat brain
Neuroscience
(1996)
The BDNF content of postnatal and adult rat brains: The effects of 6-hydroxydopamine in adult rat brain
Dev. Brain Res.
Trophic and protective actions of brain-derived neurotrophic factor on striatal DARPP-32-containing neurons in vitro
Dev. Brain Res.
Neuropathological classification of Huntington's disease
J. Neuropathol. Exp. Neurol.
A pure parkinsonian syndrome following acute carbon monoxide intoxication
Arch. Neurol.
Cyanide-induced parkinsonism
Neurology
Mutation of a nuclear succinate dehydrogenase gene results in mitochondrial respiratory chain deficiency
Nature Genet
PET scan investigations of Huntington's disease: Cerebral metabolic correlates of cognitive function
Neurology
Evidence for impairment of energy metabolism in vivo in Huntington's disease using localized1
Neurology
Regional mitochondrial respiratory activity in Huntington's disease brain
J. Neurochem.
Mitochondrial defect in Huntington's disease caudate nucleus
Neurology
Oxidative damage and metabolic dysfunction in HD: Selective vulnerability of the basal ganglia
Ann. Neurol.
Huntingtin and DRPLA proteins selectively interact with the enzyme GAPDH
Nature Med.
Neurochemical and histological characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid
J. Neurosci.
Age-dependent striatal excitotoxic lesions produced by the endogenous mitochondrial inhibitor malonate
J. Neurochem.
Inhibition of succinate dehydrogenase by malonic acid produces an excitotoxic lesion in rat striatum
J. Neurochem.
Selective sparing of a class of striatal neurons in Huntington's disease
Science
Alternative excitotoxic hypotheses
Neurology
Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses
Ann. Neurol.
Excitotoxic cell death
J. Neurobiol.
Histochemical investigations on succinic dehydrogenase in the central nervous system-V
J. Neurochem.
Anatomical correlation of NMDA and TCP receptors in rat brain
J. Neurosci.
Partial inhibition of brain succinate dehydrogenase by 3-nitropropionic acid is sufficient to initiate striatal degeneration in rat
J. Neurochem.
Cited by (58)
Validity of mental and physical stress models
2024, Neuroscience and Biobehavioral ReviewsLicofelone attenuates quinolinic acid induced Huntington like symptoms: Possible behavioral, biochemical and cellular alterations
2011, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :Slices were then subjected in 2% TTC for 5 min at 37 °C in the dark and removed and placed in 4% formaldehyde, pH 7.4 in 0.1 M phosphate buffer. For measurement of lesion volumes, serial, coronal sections (25 mm) were cut throughout the entire striatum using a cryostat as explained by Maragos et al. (1998). Using computer-based image analysis (Image J 1.42q, NIH, USA), lesion volumes of different treatment groups were calculated from each section and multiplying this value by the distance between the sections as described by Kim et al. (2005).
Experimental Models of HD and Reflection on Therapeutic Strategies
2011, International Review of NeurobiologyComparative neuroprotective profile of statins in quinolinic acid induced neurotoxicity in rats
2011, Behavioural Brain ResearchCitation Excerpt :Further present study demonstrates the increased striatal lesion volume (distinct marker for the selective striatal neurodegeneration) suggesting involvement of inflammatory mediators in QA mediated neuronal damage. These findings are in continuation with earlier studies report an increased striatal lesion volume [25,37]. In addition QA induced mitochondrial dysfunction leads to the formation of permeability transition pore that release cytochrome c into cytoplasm, accelerates apoptotic machinery.
Protective effect of montelukast against quinolinic acid/malonic acid induced neurotoxicity: Possible behavioral, biochemical, mitochondrial and tumor necrosis factor-α level alterations in rats
2010, NeuroscienceCitation Excerpt :The slices were then exposed to (2% WV−1) TTC for 5 min at 37 °C in the dark and removed and placed in 4% formaldehyde, pH 7.4 in 0.1 M phosphate buffer. For measurement of lesion volumes, serial, coronal sections (25 mm) were cut throughout the entire striatum using a cryostat as explained by Maragos et al. (1998). Using computer-based image analysis (ImageJ 1.42q, NIH, USA), lesion volumes of different treatment groups were calculated from each section and multiplying this value by the distance between the sections Kim et al. (2005).