Abstract
BackgroundFollowing brain injury, development of hippocampal sclerosis often led to the temporal lobe epilepsy which is sometimes resistant to common anti-epileptic drugs. Cellular and molecular changes underlying epileptogenesis in animal models were studied, however, the underlying mechanisms of kainic acid (KA) mediated neuronal damage in rat hippocampal neuron cell culture alone has not been elucidated yet.MethodsEmbryonic day 18 (E-18) rat hippocampus neurons were cultured with poly-L-lysine coated glass coverslips. Following optimisation, KA (0.5 μM), a chemoconvulsant agent, was administered at three different time-points (30, 60 and 90 min) to induce seizure in rat hippocampal neuronal cell culture. We examined cell viability, neurite outgrowth density and immunoreactivity of the hippocampus neuron culture by measuring brain derived neurotrophic factor (BDNF), γ-amino butyric acid A (GABAA) subunit α-1 (GABRA1), tyrosine receptor kinase B (TrkB), and inositol trisphosphate receptor (IP3R/IP3) levels.ResultsThe results revealed significantly decreased and increased immunoreactivity changes in TrkB (a BDNF receptor) and IP3R, respectively, at 60 min time point.ConclusionThe current findings suggest that TrkB and IP3 could have a neuroprotective role which could be a potential pharmacological target for anti-epilepsy drugs.
Highlights
Epilepsy is a brain disorder initiated by the perturbation of ionic equilibrium which results in neuronal hyper-excitability that causes unprovoked and recurrent seizure
The results indicated an increment of IP3R, suggesting that downstream brain derived neurotrophic factor (BDNF), tyrosine receptor kinase B (TrkB) and/or GABRA1 were triggered in the kainic acid (KA)-treated neuron culture
Our experiments consistently indicated that TrkB receptors were significantly reduced after KA was introduced into cultured neurons
Summary
Epilepsy is a brain disorder initiated by the perturbation of ionic equilibrium which results in neuronal hyper-excitability that causes unprovoked and recurrent seizure. Seizures in adults and children often affect the hippocampal formation with distinct neuropathological features, including neuronal death, neurogenesis, gliosis, axonal sprouting and reorganisation of neuronal interconnections [3, 4]. These abnormalities typically develop over weeks to years of epileptogenic events, Malays J Med Sci. Nov–Dec 2018; 25(6): 28–45. Cellular and molecular changes underlying epileptogenesis in animal models were studied, the underlying mechanisms of kainic acid (KA) mediated neuronal damage in rat hippocampal neuron cell culture alone has not been elucidated yet
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