Neurobehavioural changes and morphological study of cerebellar purkinje cells in kaolin induced hydrocephalus

Olopade, Funmilayo; Femi-Akinlosotu, Omowumi; Adekanmbi, Adejoke Joan; Ajani, Seun; Shokunbi, Temitayo

doi:10.1007/s12565-020-00561-z

Cited by 5 publications

(4 citation statements)

References 36 publications

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“…Multiple shrunken Purkinje cells and neuropil vacuolations were present in the cerebellar cortex of untreated hydrocephalic mice, just as reported in our earlier studies (Olopade et al., 2020), but vanadium‐treated mice had more healthy Purkinje cells. The motor deficits observed in the untreated hydrocephalic mice could be associated with the numerous pyknotic cells seen in the motor cortex and the degenerating Purkinje cells present in the cerebellar cortex.…”

Section: Discussionsupporting

confidence: 85%

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Vanadium administration ameliorates cortical structural and functional changes in juvenile hydrocephalic mice

Olopade,

Femi‐Akinlosotu,

Dauda

et al. 2024

J of Comparative Neurology

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Vanadium is a prevalent neurotoxic transition metal with therapeutic potentials in some neurological conditions. Hydrocephalus poses a major clinical burden in neurological practice in Africa. Its primary treatment (shunting) has complications, including infection and blockage; alternative drug‐based therapies are therefore necessary. This study investigates the function and cytoarchitecture of motor and cerebellar cortices in juvenile hydrocephalic mice following treatment with varying doses of vanadium. Fifty juvenile mice were allocated into five groups (n = 10 each): controls, hydrocephalus‐only, low‐ (0.15 mg/kg), moderate‐ (0.3 mg/kg), and high‐ (3.0 mg/kg) dose vanadium groups. Hydrocephalus was induced by the intracisternal injection of kaolin and sodium metavanadate administered by intraperitoneal injection 72hourly for 28 days. Neurobehavioral tests: open field, hanging wire, and pole tests, were carried out to assess locomotion, muscular strength, and motor coordination, respectively. The cerebral motor and the cerebellar cortices were processed for cresyl violet staining and immunohistochemistry for neurons (NeuN) and astrocytes (glial fibrillary acidic protein). Hydrocephalic mice exhibited body weight loss and behavioral deficits. Horizontal and vertical movements and latency to fall from hanging wire were significantly reduced, while latency to turn and descend the pole were prolonged in hydrocephalic mice, suggesting impaired motor ability; this was improved in vanadium‐treated mice. Increased neuronal count, pyknotic cells, neurodegeneration and reactive astrogliosis were observed in the hydrocephalic mice. These were mostly mitigated in the vanadium‐treated mice, except in the high‐dose group where astrogliosis persisted. These results demonstrate a neuroprotective potential of vanadium administration in hydrocephalus. The molecular basis of these effects needs further exploration.

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Section: Discussionsupporting

confidence: 85%

“…Vanadium‐treated mice did not show this effect. We have previously reported degeneration and loss of Purkinje cells in the cerebellar cortex, with diminished dendritic arborization in hydrocephalic mice (Olopade et al., 2020). These changes were ameliorated in the vanadium‐treated groups.…”

Section: Discussionmentioning

confidence: 92%

Vanadium administration ameliorates cortical structural and functional changes in juvenile hydrocephalic mice

Olopade,

Femi‐Akinlosotu,

Dauda

et al. 2024

J of Comparative Neurology

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“…The hanging wire test mainly evaluates the grasping power of rats [ 21 ]. The experimental rats were placed on the cage cover; when they grasped the cage cover tightly, we turned the cage over quickly and recorded the time when the hind limbs released the cage.…”

Section: Methodsmentioning

confidence: 99%

Treadmill Training Reduces Cerebral Ischemia-Reperfusion Injury by Inhibiting Ferroptosis through Activation of SLC7A11/GPX4

Liu

Cui

Dong

et al. 2022

Oxidative Medicine and Cellular Longevity

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The mechanism by which exercise training attenuates cerebral ischemia/reperfusion (I/R) injury, especially in the regulation of iron level in neuronal damage, has not been systematically studied. Here, we showed that treadmill training inhibited ferroptosis after I/R injury in rats. Modified neurologic severity score (mNSS) test showed that the motor function, reflex, and balance abilities in the I/R injury rats after treadmill intervention were significantly improved. Treadmill training decreased the level of lipid peroxides in the cerebral cortex of ischemic rats. We found that the protein levels of ferroptosis-related proteins including nuclear transcription factor E2-related factor 2 (Nrf2), cystine/glutamate reverse transporter (SLC7A11), and glutathione peroxidase 4 (GPx4) were decreased in rats after cerebral I/R injury, while treadmill training prevented the reduction of these proteins. Furthermore, we demonstrated that erastin- (a ferroptosis activator-) induced downregulation of SLC7A11 reversed the neuroprotective effect of treadmill training. This study provides the first evidence suggesting that treadmill training suppresses ferroptosis by activating the SLC7A11/GPx4 pathway, thereby protecting against cerebral I/R injury.

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“…This organ of the central nervous system is a multifunctional component of the brain, which is responsible not only for motor control, but participates in cognitive functions, afferent and behavioral reactions, the dynamics of emotional and mental state, their changes [3,19]. It is in the neurocytes of the cerebellar cortex that structural and functional changes occur that cause organ dysfunction [8,11]. As a result of the stress response, there is heterogeneity of central neurocytes -Purkinje cells, which form the ganglion layer, in the cytoplasm of which the amount of Nissl chromatophilic substance decreases, its enlightenment and vacuolation occur [12,16].…”

Section: Introductionmentioning

confidence: 99%

Reorganization of cerebellar cortex structural components one day after experimental thermal injury

Ohinska

2021

Biomed. and Biosoc. Anthrop.

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Thermal injury is a lesion caused by thermal agents. With deep and large burns, the course of this type of injury becomes a general disease of the whole organism with the involvement of vital organs. The skin is the first to perceive the action of this exogenous factor, and secondarily there are changes in all body systems, in particular in the cerebellum. The aim of our study was to establish micro- and submicroscopic changes in the structural components of the cerebellar cortex one day after the experimental thermal injury. Simulation of experimental thermal injury was performed on white laboratory male rats. Grade III burns were applied under thiopental-sodium anesthesia with copper plates heated in boiled water to a temperature of 97-100°C. The size of the affected area was 18-20 % of the epilated body surface of rats. The cerebellum was collected after one day, further processing of the material for micro- and submicroscopic examination was performed according to accepted methods. Histological specimens were stained with methylene blue, and for electron microscopy the obtained ultrathin sections were contrasted with uranyl acetate and lead citrate according to the Reynolds method. At the micro- and submicroscopic levels, it was found that 1 day after the experimental thermal injury, reactive changes are observed in neurons, microcirculatory tract and glial cells. Thus, one day after the thermal trauma of the skin, the experimental animals showed the initial violations of the blood-brain barrier of the cerebellar cortex, which are adaptive-compensatory in nature. Initial, destructive, changes in neuro-glial-capillary relations, which occur primarily on their damage to the walls of hemocapillaries and are manifested by a violation of the micro- and ultrastructure of the main cells of the cerebellum – Purkinje, neurocytes of molecular and granular layers, neuroglyocytes, with peri-gliocyocytes were found.

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Neurobehavioural changes and morphological study of cerebellar purkinje cells in kaolin induced hydrocephalus

Cited by 5 publications

References 36 publications

Vanadium administration ameliorates cortical structural and functional changes in juvenile hydrocephalic mice

Vanadium administration ameliorates cortical structural and functional changes in juvenile hydrocephalic mice

Treadmill Training Reduces Cerebral Ischemia-Reperfusion Injury by Inhibiting Ferroptosis through Activation of SLC7A11/GPX4

Reorganization of cerebellar cortex structural components one day after experimental thermal injury

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