کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6264190 | 1613965 | 2012 | 8 صفحه PDF | دانلود رایگان |

Status epilepticus (SE) when occurred during brain development can cause short- and long-term consequences, which are frequently associated with NMDA-mediated glutamatergic excitotoxicity. In the present work, we investigated the putative neuroprotective role of ketamine, an NMDA receptor antagonist, on early life SE-induced acute neuronal death and long-term behavioral abnormalities. Male Wistar rats (16 postnatal days) were induced to SE by LiCl-pilocarpine i.p. administration (3Â mEq/kg; 60Â mg/kg, respectively). Fifteen or 60Â min after pilocarpine injection, animals received a ketamine administration (22.5Â mg/kg i.p.). Neuronal degeneration was assessed 24Â h after SE induction. Another subset of animals was destined to behavioral tasks in adulthood (75-80 postnatal days). Fluoro-Jade C labeling revealed a marked neuronal death on CA1 hippocampal subfield, habenula, thalamus and amygdala in SE animals. Ketamine post-SE onset treatment prevented neuronal death in all regions assessed. In the elevated plus maze, SE induced an increase in anxiety-like behaviors whereas ketamine administration during seizures was able to prevent this alteration. Ketamine administration in non-SE animals resulted in high anxiety levels. There were no observed differences among groups in the open field task in all parameters analyzed. Our results suggest that ketamine post-SE onset treatment was effective in preventing acute and long-standing alterations caused by SE early in life, which indicates a putative role of glutamatergic system on SE-induced brain damage as well as long-lasting behavioral consequences.
⺠Early-life induced status epilepticus can cause short- and long-term damage in brain. ⺠Post-SE onset ketamine treatment avoided neuronal loss in several brain regions. ⺠Ketamine treatment 15 min after SE onset was more effective than a 60 min treatment. ⺠Ketamine treatment reduced the anxiogenic effects of SE observed in adult animals.
Journal: Brain Research - Volume 1474, 20 September 2012, Pages 110-117