Epilepsy is a severe neurological disorder clinically identified by hyper-excitability and/or hyper-synchrony in the cortex and other subcortical regions of the brain. To regulate such excitability and synchrony, Hodg...Epilepsy is a severe neurological disorder clinically identified by hyper-excitability and/or hyper-synchrony in the cortex and other subcortical regions of the brain. To regulate such excitability and synchrony, Hodgkin and Huxley model has been deployed with either PUFA or calcium buffering coupled with ATP modulate neurotransmitter release. We formulate and analyze a system of differential equations that describe the effects of PUFA, ATP, and calcium buffering in regulating neuronal hyper-excitability and hyper-synchrony in epileptic patients. We observed that PUFA had diverse effects on the gating variables. Specifically, there was a significant reduction in the inhibitory potency of PUFA on the m-gates which may cause a direct inhibition of the voltage-gated Na＋ channels and thus reduce neuronal excitability in epileptic patients. Also, the activation of the potassium channels by PUFA directly limited the neuronal hyper-excitability, while a small change in voltage potential coupled with PUFA restraint activated the voltage dependent ion channels which aided in lowering epileptic excitability in patients. In addition, higher ATP buffer levels in the presence of PUFA caused a significant hyperpolarization which may decrease neuronal excitability while lower ATP level initiated neuron depolarization. These results clearly suggest that PUFA coupled with calcium and ATP buffering could be used to modulate neuronal excitability excessive synchrony in epileptic patients.展开更多
文摘Epilepsy is a severe neurological disorder clinically identified by hyper-excitability and/or hyper-synchrony in the cortex and other subcortical regions of the brain. To regulate such excitability and synchrony, Hodgkin and Huxley model has been deployed with either PUFA or calcium buffering coupled with ATP modulate neurotransmitter release. We formulate and analyze a system of differential equations that describe the effects of PUFA, ATP, and calcium buffering in regulating neuronal hyper-excitability and hyper-synchrony in epileptic patients. We observed that PUFA had diverse effects on the gating variables. Specifically, there was a significant reduction in the inhibitory potency of PUFA on the m-gates which may cause a direct inhibition of the voltage-gated Na＋ channels and thus reduce neuronal excitability in epileptic patients. Also, the activation of the potassium channels by PUFA directly limited the neuronal hyper-excitability, while a small change in voltage potential coupled with PUFA restraint activated the voltage dependent ion channels which aided in lowering epileptic excitability in patients. In addition, higher ATP buffer levels in the presence of PUFA caused a significant hyperpolarization which may decrease neuronal excitability while lower ATP level initiated neuron depolarization. These results clearly suggest that PUFA coupled with calcium and ATP buffering could be used to modulate neuronal excitability excessive synchrony in epileptic patients.
