Abstract
Epilepsy is one of the most common neurological disorders affecting millions of people. Due to the complicated and unclear mechanisms of epilepsy, still a significant proportion of epilepsy patients remain poorly controlled. Epilepsy is characterized by convulsive seizures that are caused by increased excitability. In this study, by using kainic acid (KA)-induced epilepsy mice, we investigated the neuronal activities and revealed the neuronal compensatory mechanisms after KA-induced toxic hyperexcitability. The results indicate that both phasic inhibition induced by enhanced inhibitory synaptic activity and tonic inhibition mediated by activated astrocytes participate in the compensatory mechanisms. Compensatory mechanisms were already found in various neuronal disorders and were considered important in protecting nervous system from toxic hyperexcitability. This study hopefully will provide valuable clues in understanding the complex neuronal mechanisms of epilepsy, and exploring potential clinical treatment of the disease.
Highlights
Epilepsy is one of the most common neurological disorders affecting 1%–3% of the general population worldwide, and with a tendency to increase annually (Sander, 2003; Duncan et al, 2006)
By adding 100 μM PTX, which is the antagonist of inhibitory GABAA receptors, together with CNQX and AP5, we further examined the effect of inhibitory receptors on kainic acid (KA)-induced excitability change
The Rm values of recorded neurons after KA injection were compared (Table 3), and no significant difference was observed. These results indicate that the neuronal excitability change in KA-induced epilepsy mice is not due to Resting Membrane Potential (RP) change or the differently activated ion channels in recorded neurons
Summary
Epilepsy is one of the most common neurological disorders affecting 1%–3% of the general population worldwide, and with a tendency to increase annually (Sander, 2003; Duncan et al, 2006). It could be caused by multiple reasons including genetic mutations, cerebral trauma, ischemia and high fever. Systemic administration of certain convulsant agents is the most common method to create acute models of seizures, among which kainic acid (KA)-induced model is widely used to study the pathogenesis of epilepsy and antiepileptic drugs (Ben-Ari and Cossart, 2000; Laurén et al, 2010; Obeid et al, 2010). KA is an analog of glutamate and agonist to activate ionotropic glutamate receptor, resulting in cation influx and membrane depolarization, eliciting its excitatory effect (Nadler, 1981; Wang et al, 2005)
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