Objectives: The present study is aimed at investigating the possible protective effects of H. sabdariffa on ethanol-elicited deficits of motor coordination and estimated total number of the Purkinje cells of the cerebellums of adolescent male Wistar rats.
Methods: Forty male Wistar rats aged 21 days were divided into five groups. Na/wtr group was given water orally and injected with normal saline intra peritoneally (ip). Eth/wtr group was given water orally and ethanol (ip). Another three experimental groups (Eth/Hsab) were given different dosages of H. sabdariffa and ethanol (ip). All groups were treated intermittently for the total period of treatment of two weeks. The motor coordination of rats was tested prior and subsequent to the treatments. The rats were euthanized, and their cerebellums were examined. The total number of Purkinje cells was estimated using physical fractionator method.
Results: Upon revolving drum test, the number of falls of rats increased following ethanol treatment. There was no significant difference between the total number of falls prior and subsequent to treatment in all Eth/Hsab groups. The estimated total number of Purkinje cells in Eth/Hsab groups was higher than in Eth/wtr group.
Conclusion: H. sabdariffa may prevent the ethanol-induced deficits of motor coordination and estimated total number of Purkinje cells of the cerebellums in adolescent rats (Tab. 3, Fig. 1, Ref. 42).
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http://dx.doi.org/10.4149/bll_2015_021 | DOI Listing |
Mol Biol Cell
January 2025
Department of Cell Biology, Emory University, 615 Michael St, Atlanta, GA, USA, 30322.
Rare inherited diseases caused by mutations in the copper transporters (CTR1) or induce copper deficiency in the brain, causing seizures and neurodegeneration in infancy through poorly understood mechanisms. Here, we used multiple model systems to characterize the molecular mechanisms by which neuronal cells respond to copper deficiency. Targeted deletion of CTR1 in neuroblastoma cells produced copper deficiency that produced a metabolic shift favoring glycolysis over oxidative phosphorylation.
View Article and Find Full Text PDFSTAR Protoc
January 2025
Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA; Initiative for Columbia Ataxia and Tremor, Columbia University, New York, NY 10032, USA. Electronic address:
As Purkinje cells of the cerebellum have a very fast firing rate, techniques with high temporal resolution are required to capture cerebellar physiology. Here, we present a protocol to record physiological signals in humans using cerebellar electroencephalography (cEEG). We describe steps for electrode placement and recording.
View Article and Find Full Text PDFBackground: Christianson syndrome (CS) is an x-linked recessive neurodevelopmental and neurodegenerative condition characterized by severe intellectual disability, cerebellar degeneration, ataxia, and epilepsy. Mutations to the gene encoding NHE6 are responsible for CS, and we recently demonstrated that a mutation to the rat gene causes a similar phenotype in the spontaneous rat model, which exhibits cerebellar degeneration with motor dysfunction. In previous work, we used the PhP.
View Article and Find Full Text PDFJ Clin Med
January 2025
Department of Clinical Therapeutics, Alexandra General Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece.
Paraneoplastic cerebellar degeneration (PCD) is an inflammatory autoimmune process caused by onconeural antibodies directed against cerebellar Purkinje cells. In most cases, prognosis is poor as disease progression leads to pancerebellar dysfunction and permanent neurological damage. Through this case report, we aim to highlight the clinical presentation, diagnostic process, and therapeutic implications associated with PCD secondary to SCLC.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Neuroregeneration, Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA Amsterdam, The Netherlands.
Semaphorin 3A (Sema3A) is an axon guidance molecule, which is also abundant in the adult central nervous system (CNS), particularly in perineuronal nets (PNNs). PNNs are extracellular matrix structures that restrict plasticity. The cellular sources of Sema3A in PNNs are unknown.
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