Status epilepticus-induced neuronal damage in the rat amygdaloid complex: distribution, time-course and mechanisms

Background The time course of cytokine dynamics after seizure remains controversial. Here we evaluated the changes in the levels and sites of interleukin (IL)-1β expression over time in the hippocampus after seizure. Methods Status epilepticus (SE) was induced in adult Wistar rats by means of intraperitoneal injection of kainic acid (KA). Subsequently, the time courses of cellular localization and IL-1β concentration in the hippocampus were evaluated by means of immunohistochemical and quantitative assays. Results On day 1 after SE, CA3 pyramidal cells showed degeneration and increased IL-1β expression. In the chronic phase (>7 days after SE), glial fibrillary acidic protein (GFAP)–-positive reactive astrocytes–-appeared in CA1 and became IL-1β immunoreactive. Their IL-1β immunoreactivity increased in proportion to the progressive hypertrophy of astrocytes that led to gliosis. Quantitative analysis showed that hippocampal IL-1β concentration progressively increased during the acute and chronic phases. Conclusion IL-1β affects the hippocampus after SE. In the acute phase, the main cells expressing IL-1β were CA3 pyramidal cells. In the chronic phase, the main cells expressing IL-1β were reactive astrocytes in CA1.

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Optimal concentration of necrostatin-1 for protecting against hippocampal neuronal damage in mice with status epilepticus

Neural Regeneration Research ◽

10.4103/1673-5374.268903 ◽

2020 ◽

Vol 15 (5) ◽

pp. 936 ◽

Cited By ~ 1

Author(s):

Ri-Sheng Liang ◽

Dong-Qi Lin ◽

Xin-Ying Cai ◽

Chun-Hua Wang ◽

Bin Yang

Keyword(s):

Status Epilepticus ◽

Neuronal Damage ◽

Optimal Concentration

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Histamine 1 receptor knock out mice show age-dependent susceptibility to status epilepticus and consequent neuronal damage

Epilepsy Research ◽

10.1016/j.eplepsyres.2012.01.011 ◽

2012 ◽

Vol 100 (1-2) ◽

pp. 80-92 ◽

Cited By ~ 8

Author(s):

Tiina-Kaisa Kukko-Lukjanov ◽

Maria Grönman ◽

Minnamaija Lintunen ◽

Hanna B. Laurén ◽

Kimmo A. Michelsen ◽

...

Keyword(s):

Status Epilepticus ◽

Neuronal Damage ◽

Knock Out ◽

Age Dependent ◽

Knock Out Mice

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Corrigendum to “Neuronal degeneration and gliosis time-course in the mouse hippocampal formation after pilocarpine-induced status epilepticus” [Brain Res. 1470 (2012) 98–110]

Brain Research ◽

10.1016/j.brainres.2012.08.009 ◽

2012 ◽

Vol 1475 ◽

pp. 116 ◽

Cited By ~ 1

Author(s):

André Luiz do Nascimento ◽

Neide Ferreira dos Santos ◽

Fernanda Campos Pelágio ◽

Simone Aparecida Teixeira ◽

Elenice A. de Moraes Ferrari ◽

...

Keyword(s):

Status Epilepticus ◽

Time Course ◽

Neuronal Degeneration ◽

Hippocampal Formation

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Decreased Cerebrospinal Fluid Orexin-A (Hypocretin-1) Concentrations in Patients after Generalized Convulsive Status Epilepticus

Journal of Clinical Medicine ◽

10.3390/jcm9103354 ◽

2020 ◽

Vol 9 (10) ◽

pp. 3354

Author(s):

Mojdeh Samzadeh ◽

Ewa Papuć ◽

Marzena Furtak-Niczyporuk ◽

Konrad Rejdak

Keyword(s):

Cerebrospinal Fluid ◽

Status Epilepticus ◽

Neuronal Damage ◽

Study Groups ◽

Convulsive Status Epilepticus ◽

Orexin A ◽

Diagnostic Lumbar Puncture ◽

Turn Over ◽

Hypocretin 1

The effects of status epilepticus on the orexin/hypocretin system have yet to be investigated. The present study aimed to assay orexin-A/hypocretin-1 in the cerebrospinal fluid (CSF) of patients after generalized convulsive status epilepticus (GCSE). The study groups included 20 GCSE patients, 24 patients diagnosed with epilepsy but remaining in remission (ER), and 25 normal controls (CTR). Diagnostic lumbar puncture was performed in GCSE patients within 3–10 days of seizure cessation, as well as in the ER and to CTR subjects. Among all GCSE patients, the outcome was graded according to the modified Rankin Scale (mRS) at 1-month follow-up. Orexin-A levels were measured in unextracted CSF samples, using a commercial radioimmunoassay. There was a significant overall difference in median CSF orexin-A concentrations between GCSE, RE, and CTR patients (p < 0.001). The lowest concentrations were noted in the GCSE group compared to ER (p < 0.001) or CTR (p < 0.001). CSF orexin-A levels in GCSE patients inversely correlated with clinical outcome as assessed on the mRS at 1-month follow-up (r = −0.55; p = 0.1). In conclusion, CSF orexin-A levels may serve as a biomarker of increased turn-over of the peptide or post-SE neuronal damage, and implicates the orexin system in the pathogenesis of SE.

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Resveratrol Promotes Mitochondrial Biogenesis and Protects against Seizure-Induced Neuronal Cell Damage in the Hippocampus Following Status Epilepticus by Activation of the PGC-1α Signaling Pathway

International Journal of Molecular Sciences ◽

10.3390/ijms20040998 ◽

2019 ◽

Vol 20 (4) ◽

pp. 998 ◽

Cited By ~ 11

Author(s):

Yao-Chung Chuang ◽

Shang-Der Chen ◽

Chung-Yao Hsu ◽

Shu-Fang Chen ◽

Nai-Ching Chen ◽

...

Keyword(s):

Status Epilepticus ◽

Signaling Pathway ◽

Mitochondrial Biogenesis ◽

Neuronal Damage ◽

Cell Damage ◽

Neuroprotective Effect ◽

Neuronal Cell ◽

Protective Mechanism ◽

Protective Effects ◽

Prolonged Seizure

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is known to regulate mitochondrial biogenesis. Resveratrol is present in a variety of plants, including the skin of grapes, blueberries, raspberries, mulberries, and peanuts. It has been shown to offer protective effects against a number of cardiovascular and neurodegenerative diseases, stroke, and epilepsy. This study examined the neuroprotective effect of resveratrol on mitochondrial biogenesis in the hippocampus following experimental status epilepticus. Kainic acid was microinjected into left hippocampal CA3 in Sprague Dawley rats to induce bilateral prolonged seizure activity. PGC-1α expression and related mitochondrial biogenesis were investigated. Amounts of nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (Tfam), cytochrome c oxidase 1 (COX1), and mitochondrial DNA (mtDNA) were measured to evaluate the extent of mitochondrial biogenesis. Increased PGC-1α and mitochondrial biogenesis machinery after prolonged seizure were found in CA3. Resveratrol increased expression of PGC-1α, NRF1, and Tfam, NRF1 binding activity, COX1 level, and mtDNA amount. In addition, resveratrol reduced activated caspase-3 activity and attenuated neuronal cell damage in the hippocampus following status epilepticus. These results suggest that resveratrol plays a pivotal role in the mitochondrial biogenesis machinery that may provide a protective mechanism counteracting seizure-induced neuronal damage by activation of the PGC-1α signaling pathway.

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