Ceftriaxone and selenium mitigate seizures and neuronal injury in pentylenetetrazole-kindled rats: Oxidative stress and inflammatory pathway

Mohamed, Asmaa H.; Ali, Dina; Kolieb, Eman; Abdelaziz, Eman Z.

doi:10.1016/j.intimp.2023.110304

Cited by 2 publications

(1 citation statement)

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“…Excessive production of free radicals can disrupt intracellular calcium homeostasis, thus affecting neuronal excitability. Therefore, antioxidant therapy may be an important technique for reversing neurodegenerative processes associated with epilepsy ( 69 ).…”

Section: Mechanisms Underlying Imbalances In Neurotransmitter Regulationmentioning

confidence: 99%

Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review

et al. 2023

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Severe head trauma can lead to seizures. Persistent epileptic seizures and their progression are associated with the severity of trauma. Although case reports have revealed that early use of anti-seizure drugs after trauma can prevent epilepsy, clinical case–control studies have failed to confirm this phenomenon. To date, many brain trauma models have been used to study the correlation between post-traumatic seizures and related changes in neural circuit function. According to these studies, neuronal and glial responses are activated immediately after brain trauma, usually leading to significant cell loss in injured brain regions. Over time, long-term changes in neural circuit tissues, especially in the neocortex and hippocampus, lead to an imbalance between excitatory and inhibitory neurotransmission and an increased risk of spontaneous seizures. These changes include alterations in inhibitory interneurons and the formation of new, over-recurrent excitatory synaptic connections. In this study, we review the progress of research related to post-traumatic epilepsy to better understand the mechanisms underlying the initiation and development of post-traumatic seizures and to provide theoretical references for the clinical treatment of post-traumatic seizures.

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Section: Mechanisms Underlying Imbalances In Neurotransmitter Regulationmentioning

confidence: 99%

Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review

et al. 2023

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Ciliary neurotrophic factor activation of astrocytes mediates neuronal damage via the IL‑6/IL‑6R pathway

Wang,

Lu,

Xia

et al. 2024

Mol Med Rep

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The occurrence of epilepsy is a spontaneous and recurring process due to abnormal neuronal firing in the brain. epilepsy is understood to be caused by an imbalance between excitatory and inhibitory neurotransmitters in the neural network. The close association between astrocytes and synapses can regulate the excitability of neurons through the clearance of neurotransmitters. Therefore, the abnormal function of astrocytes can lead to the onset and development of epilepsy. The onset of epilepsy can produce a large number of inflammatory mediators, which can aggravate epileptic seizures, leading to a vicious cycle. neurons and glial cells interact to promote the onset and maintenance of epilepsy, but the specific underlying molecular mechanisms need to be further studied. ciliary neurotrophic factor (cnTF) belongs to the il-6 cytokine family and is mainly secreted by astrocytes and Schwann cells. in the normal physiological state, cnTF levels are low, but in an epileptic state, cnTF levels in the serum and tears of patients are elevated. astrocyte activation plays an important role in epileptic seizures. cnTF activates astrocytes to produce a variety of secreted proteins, which are secreted into the astrocyte culture medium (acM), thus forming a distinct culture medium (cnTF-acM) that can be used to study the effect of astrocytes on neurons in vitro. cnTF-activated astrocytes increase the secretion of the pro-inflammatory factor il-6. in the present study, cnTF-acM was applied to primary cerebral cortical neurons to observe the specific effects of il-6 in cnTF-acM on neuronal activity and excitability. The results suggested that cnTF-acM can reduce neuronal activity via the il-6/il-6r pathway, promote neuronal apoptosis, increase ca 2+ inflow, activate the large conductance calcium-activated potassium channel and enhance neuronal excitability. The results of the present study further revealed the functional changes of astrocytes after cnTF activated astrocytes and the effects on neuronal activity and excitability, thereby providing new experimental evidence for the role of communication between astrocytes and neurons in the mechanism of epileptic seizures.

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Ceftriaxone and selenium mitigate seizures and neuronal injury in pentylenetetrazole-kindled rats: Oxidative stress and inflammatory pathway

Cited by 2 publications

References 68 publications

Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review

Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review

Ciliary neurotrophic factor activation of astrocytes mediates neuronal damage via the IL‑6/IL‑6R pathway

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