Browsing by Subject "Striatum"

Now showing 1 - 3 of 3
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    Astrocyte heterogeneity and gliosis in Huntington’s disease: Histopathological insights into striatal and white matter pathology
    (2026) Taylor Brown; Rocio Gomez-Pastor; Ross Pelzel; Biología Celular e Histología
    Huntington’s disease (HD) is a devastating, autosomal dominant neurodegenerative disorder characterized by progressive motor dysfunction, cognitive decline, and psychiatric disturbances. Among the major pathological hallmarks of HD are mutant huntingtin aggregation, white matter loss and reactive astrogliosis, which together contribute to neuronal dysfunction and death, particularly in the striatum and cortex. Recent studies in HD mouse models have identified a specialized astrocyte subtype that clusters around white matter bundles originating from the secondary cortex and passing through the striatum. While the functional role of these astrocytes remains unclear, they express Glial Fibrillary Acidic Protein (GFAP), a marker typically associated with both fibrous and reactive astrocytes. The discovery of this white matter-associated astrocyte subtype, along with other astrocytic subtypes differing between grey and white matter, underscores the complexity of glial responses in HD. Accurate identification and interpretation of these glial populations are crucial for understanding disease mechanisms and progression. Given the overlapping expression profiles of commonly used astrocyte markers like GFAP, the careful selection and application of both astrocyte and white matter markers in histopathological analyses are essential to advance our understanding of how glial cells contribute to HD pathology. In this review we discuss different histopathological approaches to assess the roles of glia in HD, emphasizing the need for standardized approaches and critical evaluation of marker specificity.
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    Experimental change on dopaminergic neurons in striatum of Parkinson disease rats
    (Murcia : F. Hernández, 2007) Chen, X.Y.; Li, Jiang; Qi, W.Q.; Shen, S.H.
    Background: Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by selective and progressive demise of dopaminecontaining neurons in the midbrain. In this study, we observe the expression of c-Jun in the striatum of rats with 6-hydroxydopamine (6-OHDA)-lesions after apomorphine (APO) intraperitoneal injection (ip) in substantia nigra compacta (SNc), and to study the mechanism of the rotations behavior. Design: The 6- OHDA was unilaterally injected into rat right SNC. The APO- induced abnormal rotations were investigated on the 1st, 4th, 7th, 14th, 21st days after lesion, respectively. Meanwhile dopaminergic degeneration and c-Jun expression were observed with microscope. Nissl’s body staining and immunohistochemical method (ABC) were employed to study the changes of tyrosine hydroxylase (TH) and c-Jun in DA neurons. Results: We found that the number of dopaminergic neurons decreased gradually in the lesioned site and those neurons’ electron-microscopic structure was severe damaged. There were over 75% of dopaminergic neurons lost, contralateral rotations over 7 turns per minute and c-Jun expressing in the ipsilateral striatum. Conclusion: Dopaminergic neurons deletion may be linked to upregulation of c-Jun.
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    Histopathological alterations in the striatum caused by Karwinskia humboldtiana (Buckthorn) fruit in an experimental model of peripheral neuropathy
    (2016) Díaz-Pérez, R.N.; Castillo-González, J.A.; Carcaño-Díaz, K.; García-Juárez, J.; Salazar-Lea, M.E.; Muñoz-Maldonado, G.E.; Montes-de-Oca-Luna, R.; Saucedo-Cárdenas, O.; Soto-Domínguez, A.
    The accidental ingestion of Karwinskia humboldtiana (Kh) fruit in humans and animals causes chronic or acute intoxication. Acute poisoning induces respiratory failure that progresses rapidly to death. Studies in animals intoxicated with Kh describe lesions in cerebral cortex, cerebellum, spinal cord, hippocampus and caudate nucleus. Kh intoxication in Wistar rats models the sub-lethal clinical phase observed in humans. Considering these reports, the present study analyzed the histopathological alterations within the striatum following experimental Kh intoxication. Twenty Wistar rats were divided into three groups (n=5) and were intoxicated with Kh fruit. A control group (n=5) was included. Animals were euthanized at several time points (48, 58 and 170 days post-intoxication). The brain was collected, divided and processed for conventional histology or electron microscopy. Sections were stained with hematoxylin and eosin, cresyl violet, KlüverBarrera, and toluidine blue. Immunolabeling was performed for glial cells in the striatum, and the samples were analyzed with light microscopy. Morphometric and statistical analyses were performed. In control group, neurons, axon bundles and neuropil had a normal appearance. At 48 days, hyperchromic neurons with apparent decreased size were observed interspersed among the normal neurons. At 58 days, we observed an increased number of hyperchromic neurons and disorganization of the myelin sheath and neuropil. At 170 days, these alterations persisted in the paralysis group. In treated groups, we observed signs of gliosis and increased axonal diameters. This study is the first report that describes the histopathological alterations within the striatum caused by chronic intoxication with Kh fruit in the Wistar rat