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Introduction: The resistance of temporal lobe epilepsy to classic drugs is thought to be due to a disruption in the excitation/inhibition gabaergic pathway at least in the hippocampus. Two chloride transporters, NKCC1 and KCC2, are expressed abnormally in the excitatory state of GABA. The present study explored the effect of bumetanide as a selective NKCC1 inhibitor either alone or in combination with the phenobarbital in the pilocarpine model of epilepsy.
Method: An animal model of status epilepticus (SE) was induced with pilocarpine in Wistar male rats, followed by intraperitoneal (IP) injection of phenobarbital and/or bumetanide or saline, at day 45 after the induction of SE. Then rats were monitored and their behavior was recorded  for 20 hours, and 24 later were sacrificed to study the expression of hippocampal  NKCC1 and KCC2 using real time PCR.
Results: The data showed that the antiepileptic effect of combination of bumetanide and phenobarbital on frequency and duration of seizure attacks were more than the effect of phenobarbital alone. Furthermore, in bumetanide and combined treatment groups, NKCC1 expression decreased significantly, compared to untreated epileptic animals. A delayed decrement in NKCC1/KCC2 expression ratio after bumetanide application was also observed.
Conclusion: The combination of bumetanide and phenobarbital increased the inhibition of SE and probably enhanced the inhibitory power of GABA signaling; these finding suggest coadminstartion of bumetanide and phenobarbital in TLE.
نوع مطالعه: Original | موضوع مقاله: Behavioral Neuroscience
دریافت: ۱۳۹۵/۶/۲۱ | پذیرش: ۱۳۹۶/۱۰/۳۰ | انتشار: ۱۳۹۷/۲/۳

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