Efficacy of dexamethasone on penicillin-induced epileptiform activity in rats: An electrophysiological study

Yılmaz, Tevfik; Akça, Metehan; Turan, Yahya; Ocak, Hakan; Kamaşak, Kağan; Yıldırım, Mehmet

doi:10.1016/j.brainres.2014.01.040

Cited by 8 publications

(2 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Numerous studies have focused on the effects of glucocorticoids in epilepsy and convulsions, but the conclusions are controversial so far [11,12,[28][29][30][31][32][33]. Different dosages, courses, and time points of glucocorticoid administration might be responsible for these discrepancies.…”

Section: Discussionmentioning

confidence: 99%

“…In a lithium-pilocarpine-induced model, three doses of DEX (5, 10, and 20 mg/kg) were checked, and only DEX at a dose of 10 mg/kg demonstrated an effect of seizure reduction [29]. In a penicillin-induced model, DEX at dosages of 1, 3, and 10 mg/kg were assessed on epileptiform activity, and spike frequencies were significantly suppressed by DEX administration at both 3 mg/kg and 10 mg/kg [30]. Consistently, our previous study also showed a protective effect on the epileptic brain with 3 doses of 10 mg/kg DEX during quiescence in the pilocarpine-induced epileptic model [20].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus

et al. 2020

View full text Add to dashboard Cite

The filamentous actin (F-actin) cytoskeleton is progressively damaged after status epilepticus (SE), which is related to delayed neuronal death, aberrant recurrent circuits and epileptogenesis. Glucocorticoids regulate dendritic spine remodeling by acting on glucocorticoid receptors and the dynamics of the F-actin cytoskeleton. Our previous study showed that administration of dexamethasone (DEX) in the latent period of the pilocarpine epileptic model reduces damage to the hippocampal filamentous actin cytoskeleton and the loss of hippocampal neurons and aids in maintaining the synaptic structures, but it is not sufficient to stop epileptogenesis. In this work, we focused on the role of glucocorticoids in regulating the hippocampal F-actin cytoskeleton during SE. We examined the abundance of synaptic F-actin, analyzed the hippocampal F-actin/G-actin (F/G) ratio and pCofilin, and evaluated the number of hippocampal neurons and pre/postsynaptic markers in pilocarpine-induced status epilepticus mice with or without administration of dexamethasone (DEX). We found that the latency of Stage 3 seizures increased, the mortality decreased, the damage to the synaptic F-actin cytoskeleton in the hippocampal subfields was significantly attenuated, and a greater number of postsynaptic structures were retained in the hippocampal subfields after treatment with DEX. These results indicate that treatment with dexamethasone stabilizes the synaptic F-actin cytoskeleton and reduces the damage to the brain due to SE. This approach is expected to be beneficial in alleviating delayed neuron damage and the process of epileptogenesis.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus

et al. 2020

View full text Add to dashboard Cite

show abstract

The Use of Anti-inflammatory Drugs in Epilepsy

Valle-Dorado

Córdova-Dávalos

Pérez-Pérez

et al. 2016

Methods in Pharmacology and Toxicology

View full text Add to dashboard Cite

Neonatal dexamethasone accelerates spreading depression in the rat, and antioxidant vitamins counteract this effect

et al. 2014

View full text Add to dashboard Cite

The use of dexamethasone (Dex) to treat chronic lung disease in preterm infants may produce adverse effects in the developing brain. Here, we evaluated the effects of neonatal Dex on the propagation of cortical spreading depression (CSD), and tested the action of vitamins C and E against the effect of Dex. Five groups of Wistar rats received, respectively: [1] no treatment (Naïve); [2] Vehicle (V); [3] tapering doses of Dex (Dex; 0.5mg/kg, 0.3mg/kg, and 0.1mg/kg) on postnatal day (PND) 1-3; [4] Dex plus 200mg/kg vitamin C and 100mg/kg vitamin E (DexCE); [5] only vitamins C and E (CE). Vehicle and vitamins were administered on PND 1-6. CSD was recorded after the pups reached maturity (PND 60-70). The Dex-treated group presented with higher CSD velocities (mean values ± SD, in mm/min: 4.14 ± 0.22, n=10) compared with the control groups (Naïve: 3.52 ± 0.13, n=8; V: 3.57 ± 0.18, n=10; CE: 3.51 ± 0.24, n=10; p<0.05 for all). Vitamins C and E antagonized this effect (DexCE group; CSD velocity: 3.43 ± 0.12, n=9). No intergroup difference was observed concerning P-wave amplitude and duration. In all groups, after the cortex underwent CSD, the electrocorticogram (ECoG) amplitude increased approximately 50% compared with the baseline amplitude for the same animal (CSD-induced ECoG potentiation); however, no intergroup difference was observed. Data suggest that coadministration of antioxidant vitamins with Dex may be a helpful therapeutic strategy to reduce brain adverse effects of dexamethasone.

show abstract

Efficacy of dexamethasone on penicillin-induced epileptiform activity in rats: An electrophysiological study

Cited by 8 publications

References 23 publications

Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus

Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus

The Use of Anti-inflammatory Drugs in Epilepsy

Neonatal dexamethasone accelerates spreading depression in the rat, and antioxidant vitamins counteract this effect

Contact Info

Product

Resources

About