Abstract
There are no clinical interventions to prevent post-injury epilepsy, a common and devastating outcome after brain insults. Epileptogenic events that run from brain injury to epilepsy are poorly understood. Previous studies in our laboratory suggested Proechimys, an exotic Amazonian rodent, as resistant to acquired epilepsy development in post-status epilepticus models. The present comparative study was conducted to assess (1) stroke-related brain responses 24-h and 30 days after cortical photothrombosis and (2) post-stroke epilepsy between Proechimys rodents and Wistar rats, a traditional animal used for laboratory research. Proechimys group showed smaller volume of ischemic infarction and lesser glial activation than Wistar group. In contrast to Wistar rats, post-stroke decreased levels of pro-inflammatory cytokines and increased levels of anti-inflammatory mediators and growth factors were found in Proechimys. Electrophysiological signaling changes assessed by cortical spreading depression, in vitro and in vivo, showed that Wistar’s brain is most severely affected by stroke. Chronic electrocorticographic recordings showed that injury did not lead to epilepsy in Proechimys whereas 88% of the Wistar rats developed post-stroke epilepsy. Science gains insights from comparative studies on diverse species. Proechimys rodents proved to be a useful animal model to study antiepileptogenic mechanisms after brain insults and complement conventional animal models.
Highlights
Brain injury is a dreadful threat to animals and the capacity for repairing wounded tissue is essential to vertebrate neurobiology
Focal ischemia induced by photothrombosis resulted in macroscopically visible brain injury in both Proechimys and Wistar groups assessed at 24-h after stroke (Fig. 1A1)
These findings suggest that spreading depression (SD) induction suffered resistance to invade the cortical injured region, which is the focus of hyperexcitability in Wistar rats, demonstrated by the spontaneous ictal discharges, or that this response could be influenced by local changes in the inhibitory mechanisms in the perilesional area, such as downregulation of GABAergic markers after stroke as observed in mice 14
Summary
Brain injury is a dreadful threat to animals and the capacity for repairing wounded tissue is essential to vertebrate neurobiology. Solid evidence from numerous clinical and animal studies has suggested that the main hallmarks of the brain dynamic response to ischemic stroke include damage to neurons, glial reactivity, release of inflammatory cytokines and growth factors, and alterations in neural excitability, exposing the brain to an environmental calamity, eventually leading to epileptogenesis 3. Each animal species is adapted to the conditions of the environment in which it evolved; Proechimys are small terrestrial rodents of the Amazon rainforest that play crucial roles in tropical zoonotic diseases and are natural hosts of infectious agents 7. They appear to have an effective immune system as they rarely develop diseases 8. We used comparative approaches between these two animal species to unravel the dynamics of brain responses to stroke, at 24-h and 30 days after injury
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