Viral-like brain inflammation during development causes increased seizure susceptibility in adult rats

Galic, Michael A.; Riazi, Kiarash; Henderson, Amy; Tsutsui, Shigeki; Pittman, Quentin J.

doi:10.1016/j.nbd.2009.07.025

Cited by 101 publications

(82 citation statements)

References 101 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Epidemiological analyses have also demonstrated that these viral infections often lead to development of persistent epilepsy after infection is resolved (61)(62)(63)(64). Galic and colleagues (2009) showed that neonatal exposure to poli(I:C) increased susceptibility to seizures and memory deficits in adult rats, and that these behavioral changes were associated to neuroinflammation and an increased hippocampal expression of NMDA receptors (65). The results reported in our study indicate that even normocephalic ZIKV-exposed infants might be at increased risk .…”

Section: Cc-by-nc-ndsupporting

confidence: 62%

Neonatal Zika virus infection causes epileptic seizures, viral persistence and long-term behavioral impairment

Frost

Franca

Barbosa

et al. 2017

Preprint

View full text Add to dashboard Cite

Section: Cc-by-nc-ndsupporting

confidence: 62%

Neonatal Zika virus infection causes epileptic seizures, viral persistence and long-term behavioral impairment

Frost

Franca

Barbosa

et al. 2017

Preprint

View full text Add to dashboard Cite

“…In this context, experiments in animal models show that epileptogenic brain injuries (e.g., trauma, hypoxia/ischemia), mimicking bacterial or viral infections (Galic et al 2008(Galic et al , 2009Riazi et al 2010;Stewart et al 2010), or recurrent seizure activity per se (Vezzani et al 2011c) can induce a prominent innate immunity response in glia, which activates rapid and self-perpetuating inflammatory processes in brain tissue (Aronica et al 2012b;Vezzani et al 2013a,b). Notably, this innate immunity response has a significant role in experimental seizure generation, cell loss, and comorbidities developing in the animals.…”

Section: Resultsmentioning

confidence: 99%

Immunity and Inflammation in Epilepsy

Vezzani

Lang

Aronica

2015

Cold Spring Harb Perspect Med

191

145

View full text Add to dashboard Cite

This review reports the available evidence on the activation of the innate and adaptive branches of the immune system and the related inflammatory processes in epileptic disorders and the putative pathogenic role of inflammatory processes developing in the brain, as indicated by evidence from experimental and clinical research. Indeed, there is increasing knowledge supporting a role of specific inflammatory mediators and immune cells in the generation and recurrence of epileptic seizures, as well as in the associated neuropathology and comorbidities. Major challenges in this field remain: a better understanding of the key inflammatory pathogenic pathways activated in chronic epilepsy and during epileptogenesis, and how to counteract them efficiently without altering the homeostatic tissue repair function of inflammation. The relevance of this information for developing novel therapies will be highlighted.

show abstract

“…Furthermore, neuronal degeneration is observed likely due to increases of PICs [24,25]. For example, IL-1β can increase seizure susceptibility in rat brains [26]. Intracerebral injection of a high dosage of IL-1β results in limbic seizures in wild type mice, but not in transgenic mice with deficient IL-1β receptors [27].…”

Section: Discussionmentioning

confidence: 99%

Inhibiting HIF-1α Decreases Expression of TNF-α and Caspase-3 in Specific Brain Regions Exposed Kainic Acid-Induced Status Epilepticus

Yang

He²,

Meng³

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: A recent study demonstrates that pro-inflammatory cytokines (PICs, i.e., IL-1β, IL-6 and TNF-α) in specific brain regions of rats play a role in regulating kainic acid (KA)-induced status epilepticus (SE) via a GABAergic mechanism. The purposes of this report were to examine contributions of hypoxia inducible factor subtype 1α (HIF-1α) to expression of PICs in these specific brain regions in epileptic rats. Particularly, we investigated the parietal cortex, hippocampus and amygdala. In addition, we further examined expression of Caspase-3 indicating cell apoptosis in those brain regions of epileptic rats after infusing 2-methoxyestradiol (2-MET, inhibitor of HIF-1α) and etanercept (TNF-α receptor antagonist). Methods: ELISA was used to determine the levels of HIF-1α and PICs and western blot analysis was used to examine Caspase-3 expression. Results: Our data show that HIF-1α was significantly increased in the parietal cortex, hippocampus and amygdala 1, 3 and 7 days after induction of SE (P<0.05 vs. control rats). Our results also show that inhibiting HIF-1α by central infusion of 2-MET significantly decreased the amplified TNF-α expression in these brain regions evoked by SE (P<0.05 vs. vehicle control), but did not modify IL-1β and IL-6. Our results demonstrate that 2-MET and etanercept attenuated an increase in Caspase-3 evoked by SE. Conclusion: Overall, we suggest that HIF-1α activated by SE is likely to contribute to epileptic activity via a TNF-α pathway, which has pharmacological implications to target specific HIF-1α and TNF-α pathways for neuronal dysfunction and vulnerability related to epilepsy.

show abstract

Viral-like brain inflammation during development causes increased seizure susceptibility in adult rats

Cited by 101 publications

References 101 publications

Neonatal Zika virus infection causes epileptic seizures, viral persistence and long-term behavioral impairment

Neonatal Zika virus infection causes epileptic seizures, viral persistence and long-term behavioral impairment

Immunity and Inflammation in Epilepsy

Inhibiting HIF-1α Decreases Expression of TNF-α and Caspase-3 in Specific Brain Regions Exposed Kainic Acid-Induced Status Epilepticus

Contact Info

Product

Resources

About