ArticleMolecular brain2009
Maternal epileptic seizure induced by pentylenetetrazol: apoptotic neurodegeneration and decreased GABAB1 receptor expression in prenatal rat brain.
Article in Molecular brain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 71 citations in OpenAlex.
- Mouse offspring exposed to preeclampsia/eclampsia-like symptoms exhibit cerebral hypoperfusion and mild cognitive impairment at 2 mo of age.American journal of physiology. Heart and circulatory physiology · 2026Article
- Investigating the Effect of Low Molecular Weight Heparin, Enoxaparin, on Pentylenetetrazole (PTZ)-Induced Neuronal Damage in C6 and HT-22 Cell Lines.Cell biochemistry and biophysics · 2026Article
- Considering Litter Effects in Preclinical Research: Evidence from E17.5 Acid-Sensing Ion Channel 2a Knockout Mice Exposed to Acute Seizures.Brain sciences · 2025Article
- The impact of early-life environment on absence epilepsy and neuropsychiatric comorbidities.IBRO neuroscience reports · 2022Review
- Revealing the Antiepileptic Effect of α-Asaronol on Pentylenetetrazole-Induced Seizure Rats Using NMR-Based Metabolomics.ACS omega · 2022Article
- ZOMEC via the p-Akt/Nrf2 Pathway Restored PTZ-Induced Oxidative Stress-Mediated Memory Dysfunction in Mouse Model.BioMed research international · 2022Article
- Downregulated GPR30 expression in the epileptogenic foci of female patients with focal cortical dysplasia type IIb and tuberous sclerosis complex is correlated withBrain pathology (Zurich, Switzerland) · 2021Article
- Neuronal injury and death following focal mild brain injury: The role of network excitability and seizure.Iranian journal of basic medical sciences · 2020Article
- Beta Lactams Antibiotic Ceftriaxone Modulates Seizures, Oxidative Stress and Connexin 43 Expression in Hippocampus of Pentylenetetrazole Kindled Rats.Journal of epilepsy research · 2016Article
- Protective Effects of Otophylloside N on Pentylenetetrazol-Induced Neuronal Injury In vitro and In vivo.Frontiers in pharmacology · 2016Article
- Osmotin attenuates amyloid beta-induced memory impairment, tau phosphorylation and neurodegeneration in the mouse hippocampus.Scientific reports · 2015Article
- Downregulation of dopamine D₁ receptors and increased neuronal apoptosis upon ethanol and PTZ exposure in prenatal rat cortical and hippocampal neurons.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014Article
- Anthocyanins protect against kainic acid-induced excitotoxicity and apoptosis via ROS-activated AMPK pathway in hippocampal neurons.CNS neuroscience & therapeutics · 2014Article
- Neuroprotective effect of osmotin against ethanol-induced apoptotic neurodegeneration in the developing rat brain.Cell death & disease · 2014Article
- Oxidative stress associated with neuronal apoptosis in experimental models of epilepsy.Oxidative medicine and cellular longevity · 2014Review
- Effects of Hydro-alcoholic Extract of Anethum Graveolens Seed on Pentylenetetrazol-induced Seizure in Adult Male Mice.Basic and clinical neuroscience · 2014Article
- Decreased GABABR expression and increased neuronal cell death in developing rat brain after PTZ-induced seizure.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2013Article
- Calpastatin overexpression limits calpain-mediated proteolysis and behavioral deficits following traumatic brain injury.Experimental neurology · 2012Article
- The effect of PTZ-induced epileptic seizures on hippocampal expression of PSA-NCAM in offspring born to kindled rats.Journal of biomedical science · 2012Article
- Neuroprotection with metformin and thymoquinone against ethanol-induced apoptotic neurodegeneration in prenatal rat cortical neurons.BMC neuroscience · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epilepsy is a prominent sign of neurological dysfunction in children with various fetal and maternal deficiencies. However, the detailed mechanism and influences underlying epileptic disorders are still unrevealed. The hippocampal neurons are vulnerable to epilepsy-induced pathologic changes and often manifests as neuronal death. The present study was designed to investigate the effect of maternal epileptic seizure on apoptotic neuronal death, modulation of GABAB1 receptor (R), and protein kinase A-alpha (PKA) in prenatal rat hippocampal neurons at gestational days (GD) 17.5. Seizure was induced in pregnant rat using intraperitoneal injection of pentylenetetrazol (PTZ) (40 mg/kg for 15 days). To confirm the seizure electroencephalography (EEG) data was obtained by the Laxtha EEG-monitoring device in the EEG recording room and EEG were monitored 5 min and 15 min after PTZ injection. The RT-PCR and Western blot results showed significant increased expression of cytochrome-c and caspases-3, while decreased levels of GABAB1R, and PKA protein expression upon ethanol, PTZ and ethanol plus PTZ exposure in primary neuronal cells cultured from PTZ-induced seizure model as compare to non-PTZ treated maternal group. Apoptotic neurodegeneration was further confirmed with Fluoro-Jade B and propidium iodide staining, where neurons were scattered and shrunken, with markedly condensed nuclei in PTZ treated group compared with control. This study for the first time indicate that PTZ-induced seizures triggered activation of caspases-3 to induce widespread apoptotic neuronal death and decreased GABAB1R expression in hippocampal neurons, providing a possible mechanistic link between maternal epilepsy induced neurodegeneration alteration of GABAB1R and PKA expression level during prenatal brain development. This revealed new aspects of PTZ and ethanol's modulation on GABAB1R, learning and memory. Further, explain the possibility that children delivered by epileptic mothers may have higher risk of developmental disturbances and malformations.
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