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Studies have confirmed that iron induces epilepsy onset,and iron ion-induced epilepsy in animal models closely resembles the clinical situation.Models of post-traumatic epilepsy (PTE) were established by intracortical injection of FeCl2 using stereotactic techniques.Electron microscopy revealed neuronal degeneration,with shrinkage of the neuronal soma,hyperplasia of rough endoplasmic reticulum,ribosomal detachment from the endoplasmic reticulum,and vacuolar degeneration of glial cells in the right frontal lobe of FeCl2-induced PTE rats.With prolonged time,injuries became more severe and neuronal apoptosis was observed.Synapses in the hippocampal neuropil significantly increased (primarily type I/excitatory synapses) at day 14 following injury.Type II synapses (inhibitory synapse) were observed in the rat hippocampus at day 30.Cortical neuronal degeneration,apoptosis,glial cell proliferation,and ultrastructural hippocampal changes,in particular changes in type of neuronal synapse,play an important role in PTE onset.
Studies have confirmed that iron induces epilepsy onset, and iron ion-induced epilepsy in animal models closely resembles the clinical situation. Models of post-traumatic epilepsy (PTE) were established by intracortical injection of FeCl2 using stereotactic techniques. Electron microscopy revealed neuronal degeneration, with shrinkage of the neuronal soma, hyperplasia of rough endoplasmic reticulum, ribosomal detachment from the endoplasmic reticulum, and vacuolar degeneration of glial cells in the right frontal lobe of FeCl2-induced PTE rats. Wither prolonged time, injuries became more severe and neuronal apoptosis was observed. Synapses in the hippocampal neuropil significantly increased (to type I / excitatory synapses) at day 14 following injury. Type II synapses (inhibitory synapse) were observed in the rat hippocampus at day 30.Cortical neuronal degeneration, apoptosis, glial cell proliferation, and ultrastructural hippocampal changes, in particular changes in type of neuronal synapse, play a n important role in PTE onset