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Ataxia (and Dysmetria)
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Generally, ataxia results from damage in the cerebellum or to the pathways leading into or out of the cerebellum. This is a part of the brain that contributes greatly to fine motor control, which is a way of saying “small movements that work together with other small movements.” Essentially, the cerebellum receives input from your muscles via your spine and mixes that with input from your brain using a combination of highly interconnected “Purkinje cells” and an incredibly high number of small “granule cells” (Marsden & Harris, 2011). When I say an incredibly high number, I mean it: roughly 80% of the neurons in your brain are located in your cerebellum, and this number is even higher for mammals such as the African elephant, which has about 98% of its neurons located in the cerebellum (Kaas & Herculano-Houzel, 2017). Those extremely numerous cells seem to be essential for maneuvering large bodies in complex ways.
Principles of neuromotor development
Published in Mijna Hadders-Algra, Kirsten R. Heineman, The Infant Motor Profile, 2021
Mijna Hadders-Algra, Kirsten R. Heineman
The development of the cerebellum has its own timing. Cells in the cerebellum originate from two proliferative zones: (1) the ventricular zone which brings forth the deep cerebellar nuclei and the Purkinje cells, and (2) the external granular layer originating from the rhombic lip (Volpe 2009b). Cell proliferation in the cerebellum starts at 11 weeks PMA in the ventricular zone and at 15 weeks in the external granular layer. The external granular layer is a transient structure reaching its peak thickness between 28 and 34 weeks PMA. It produces the most numerous cells of the cerebellum, the granule cells. These cells migrate from the external granular layer inward to their final destination in the internal granular layer. The latter grows most prominently between mid-gestation and three months post-term. The external granular layer shrinks, in particular between two and three months post-term. However, it takes until the second half of the first postnatal year for the external granular layer to dissolve entirely (Hadders-Algra 2018a).
Brain Motor Centers and Pathways
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The cell bodies of granule cells, 5–8 µm across, are located in the granular layer. They number more than 50 billion in humans, or more than all the other neurons in the brain combined. Granule cells have 5 or 6 relatively short dendrites, less than 30 µm long, with claw-like terminations that synapse with mossy fiber rosettes, the bulbous terminals of MFs, and with the axon terminals of Golgi cells. All these neuronal elements are enclosed in a tight, glia-encapsulated structure referred to as a cerebellar glomerulus. As it approaches the cerebellar cortex, an MF branches into a number of folia, the branches being in sagittal, or transverse planes. In each folium, an MF divides into 2 or 3 preterminal branches, with each preterminal branch bearing about 10 mossy rosettes. Each MF rosette makes excitatory synapses with the dendrites of about 20 granule cells.
Investigation of the mechanism of tanshinone IIA to improve cognitive function via synaptic plasticity in epileptic rats
Published in Pharmaceutical Biology, 2023
Chen Jia, Rui Zhang, Liming Wei, Jiao Xie, Suqin Zhou, Wen Yin, Xi Hua, Nan Xiao, Meile Ma, Haisheng Jiao
Synaptic plasticity refers to neurons’ ability to alter synaptic connectivity over time (Shefa et al. 2018; Yepes 2020). The loss of synaptic connections in the hippocampus has been linked to the cognitive disorder in epilepsy, suggesting a vital role in its pathogenesis (Jiang et al. 2015; Tang et al. 2017). The dentate gyrus exhibits aberrant synaptic plasticity associated with MFS in chronic human epilepsy and epileptic animal model (Scharfman et al. 2003; Mello and Longo 2009; Twible et al. 2021). Epilepsy may cause an extensive neuronal loss in the hippocampus (Schoene-Bake et al. 2014; Zhao et al. 2020), followed by neuronal network remodelling characterized by severe MFS and granular cell neurogenesis (Lynch and Sutula 2000; Williams et al. 2002; Sloviter et al. 2006). Numerous researchers believe that the death of hippocampal neurons is a crucial factor in the onset of MFS (Sutula and Dudek 2007). This research demonstrated no apparent structural damage in the hippocampal CA3 regions in any tanshinone IIA treatment group, especially in the TS IIA-M and TS IIA-H groups. In contrast, the VPA and model groups showed obvious abnormal MFS, ultrastructural disorder and vacuolar degeneration. The disorganized ultrastructure and blurred tissue morphology of the CA3 area were improved after tanshinone IIA treatment. Tanshinone IIA administration may assist preserve the normal synaptic connection between neurons and alleviate the ultrastructural abnormality and vacuolar degeneration of the hippocampus CA3 region induced by epilepsy.
Effects of pyrethroids on the cerebellum and related mechanisms: a narrative review
Published in Critical Reviews in Toxicology, 2023
Fei Hao, Ye Bu, Shasha Huang, Wanqi Li, Huiwen Feng, Yuan Wang
Recently, it has been suggested that DM may exert its neurotoxic effects through intracellular accumulation and low release of the reelin protein (Kumar et al. 2013). Reelin is an extracellular matrix molecule that supports the normal development of the CNS, including hippocampus, cerebellum and cortex. In the cerebellum, reelin participates in arranging Purkinje cell monolayers, Bergman glial fibers and facilitating granule cell migration. Reelin protein deficiency in DM-treated animals may lead to certain structural abnormalities that could directly impact the functional performance of the cerebellum. It included impaired migration of granule cells and Purkinje cells, inhibition of neuronal outgrowth, reduced density of dendritic spines and decreased rotational movements (Zhao et al. 1995). Reelin signaling involves several factors, including the lipoprotein receptor lipoprotein E receptor 2 (ApoER2), the very low-density lipoprotein receptor (VLDLR) and adaptor protein Dab1 (Dab1). Reelin can bind to the ApoER2 and VLDLR, leading to phosphorylation of Dab1. Therefore, it is hypothesized that DM may cause cerebellar dysfunction through the reelin signaling pathway.
Mechanisms of COVID-19-induced cerebellitis
Published in Current Medical Research and Opinion, 2022
Mohammad Banazadeh, Sepehr Olangian-Tehrani, Melika Sharifi, Mohammadreza Malek-Ahmadi, Farhad Nikzad, Nooria Doozandeh-Nargesi, Alireza Mohammadi, Gary J. Stephens, Mohammad Shabani
The cerebellum is an evenly formed structure with a distinct neural arrangement based on stereotypes. The geometry of the cerebellum resembles a hemispherical ellipse with a central vermis and two adjacent hemispheres. The cerebellum’s rostro-caudal contour is undulating due to the existence of transverse fissures. The pattern of fissures on the cortical surface of the cerebellum permits the identification of 10 distinct lobules. Each of these lobules is associated with specialized brain–cerebellar functional loops. From a dorsal–ventral perspective, the cerebellar cortical array reveals three different layers. Purkinje cell dendritic arborization and inhibitory interneurons are seen in the molecular layer (basket and stellate cells). The Purkinje cell layer is generated ventrally by Purkinje cell somas and Bergman glia. The granular layer at the deeper cortical level comprises many granule cells controlled by Golgi, unipolar brush cells, and Lugaro neurons, as well as several types of glia. The axons of ascending granule cells divide into parallel excitatory fibers that connect the somas and dendrites of Purkinje cells9,10.