Pathophysiology of Epilepsy

Jenrow, Kenneth A.; Elisevich, Kost

doi:10.1017/9781108754200.002

Cited by 3 publications

(2 citation statements)

References 105 publications

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“…Epilepsy manifested by seizures originates from an uncontrolled over-excitation of motor brain areas. 325 At the cellular level this overexcitation stems from a slow synchronous depolarisation of neurones, known as paroxysmal depolarisation shift (PDS) within the epileptic foci. The PDS develops from large and relatively slow excitatory postsynaptic potentials mediated by AMPA and NMDA glutamate receptors activated by aberrant and large glutamate release within the foci.…”

Section: Epilepsy and Migraine Epilepsymentioning

confidence: 99%

Astrocytes in human central nervous system diseases: a frontier for new therapies

Verkhratsky,

Butt,

et al. 2023

Sig Transduct Target Ther

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Astroglia are a broad class of neural parenchymal cells primarily dedicated to homoeostasis and defence of the central nervous system (CNS). Astroglia contribute to the pathophysiology of all neurological and neuropsychiatric disorders in ways that can be either beneficial or detrimental to disorder outcome. Pathophysiological changes in astroglia can be primary or secondary and can result in gain or loss of functions. Astroglia respond to external, non-cell autonomous signals associated with any form of CNS pathology by undergoing complex and variable changes in their structure, molecular expression, and function. In addition, internally driven, cell autonomous changes of astroglial innate properties can lead to CNS pathologies. Astroglial pathophysiology is complex, with different pathophysiological cell states and cell phenotypes that are context-specific and vary with disorder, disorder-stage, comorbidities, age, and sex. Here, we classify astroglial pathophysiology into (i) reactive astrogliosis, (ii) astroglial atrophy with loss of function, (iii) astroglial degeneration and death, and (iv) astrocytopathies characterised by aberrant forms that drive disease. We review astroglial pathophysiology across the spectrum of human CNS diseases and disorders, including neurotrauma, stroke, neuroinfection, autoimmune attack and epilepsy, as well as neurodevelopmental, neurodegenerative, metabolic and neuropsychiatric disorders. Characterising cellular and molecular mechanisms of astroglial pathophysiology represents a new frontier to identify novel therapeutic strategies.

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Section: Epilepsy and Migraine Epilepsymentioning

confidence: 99%

Astrocytes in human central nervous system diseases: a frontier for new therapies

Verkhratsky,

Butt,

et al. 2023

Sig Transduct Target Ther

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“…A seizure is a transient brain malfunction caused by an abnormal release of cortical neurons, resulting in a discrepancy of excitation and inhibition in cortical neuronal networks. 18 Seizures in epilepsy patients are complicated by excitatory glutamatergic pathways, inflammation, and oxidative stress. Seizures can be attributed in part to immune-inflammatory dysregulation and neuronal hyperexcitation driven by brain inflammation.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Ruscogenin against Cognitive Impairment on Pentylenetetrazole-induced Epileptic Seizures in Rats

Ma,

Almoallim,

Alharbi

et al. 2023

Ind. J. Pharm. Edu. Res

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Background: Epilepsy, which affects about 1% of the world's population, is the third most common neurological disease after stroke and Alzheimer's disease. It is characterized by recurrent spontaneous seizures due to abnormal neuronal excitability and hypersynchrony. Objectives: The current work was aimed at discovering the neuroprotective properties of ruscogenin against Pentylenetetrazole (PTZ)-induced epilepsy in rats. Materials and Methods: The epileptic episode was induced in the rats by injecting 45 mg/kg of PTZ. Rats were pretreated with 10 mg/ kg of ruscogenin 30 min before the PTZ challenge. The seizure severity and latency were assessed in the control and experimental rats. The status of oxidative markers, inflammatory cytokines, and neurotransmitters was examined using the corresponding assay kits. The histopathological analysis was done on the brain tissues of the experimental rats. The viability of control and treated neural SHSY-5Y cells was assessed with the MTT assay. Results: The ruscogenin treatment effectively reduced the seizure severity and augmented the latency in the epilepsy rats. The levels of Nitric Oxide (NO) and NO syntheses were effectively reduced in the brain tissues of epilepsy rats by the ruscogenin treatment. Ruscogenin decreased the oxidative index and increased the antioxidant index in the brain tissues of epilepsy rats. The levels of neurotransmitters were increased, and inflammatory cytokines were decreased in the epileptic rats by the ruscogenin. The results of histopathological analysis demonstrated the neuroprotective effects of ruscogenin. The viability of PTZ-challenged neural SHSY-5Y cells was increased by the ruscogenin treatment. Conclusion:In conclusion, the current results revealed that pretreatment with ruscogenin decreased the PTZ-induced epilepsy in rats by exerting its antioxidant and anti-inflammatory effects. Therefore, it may be concluded that ruscogenin may be a possible therapeutic option to treat epilepsy.

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The modulator action of thiamine against pentylenetetrazole-induced seizures, apoptosis, nitric oxide, and oxidative stress in rats and SH-SY5Y neuronal cell line

Taşkıran

Ergül

2021

Chemico-Biological Interactions

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Pathophysiology of Epilepsy

Cited by 3 publications

References 105 publications

Astrocytes in human central nervous system diseases: a frontier for new therapies

Astrocytes in human central nervous system diseases: a frontier for new therapies

Neuroprotective Effect of Ruscogenin against Cognitive Impairment on Pentylenetetrazole-induced Epileptic Seizures in Rats

The modulator action of thiamine against pentylenetetrazole-induced seizures, apoptosis, nitric oxide, and oxidative stress in rats and SH-SY5Y neuronal cell line

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