Abstract
The hippocampus plays an important role in the genesis of mesial temporal lobe epilepsy, and the entorhinal cortex (EC) may affect the hippocampal network activity because of the heavy interconnection between them. However, the mechanism by which the EC affects the discharge patterns and the transmission mode of epileptiform discharges within the hippocampus needs further study. Here, multielectrode recording techniques were used to study the spatiotemporal characteristics of epileptiform discharges in adult mouse hippocampal slices and combined EC-hippocampal slices and determine whether and how the EC affects the hippocampal neuron discharge patterns. The results showed that low-Mg2+ artificial cerebrospinal fluid induced interictal discharges in hippocampal slices, whereas, in combined EC-hippocampal slices the discharge pattern was alternated between interictal and ictal discharges, and ictal discharges initiated in the EC and propagated to the hippocampus. The pharmacological effect of the antiepileptic drug valproate (VPA) was tested. VPA reversibly suppressed the frequency of interictal discharges but did not change the initiation site and propagation speed, and it completely blocked ictal discharges. Our results suggested that EC was necessary for the hippocampal ictal discharges, and ictal discharges were more sensitive than interictal discharges in response to VPA.
Highlights
Mesial temporal lobe epilepsy is the most common type of intractable epilepsy
The results suggested that entorhinal cortex (EC) was necessary for ictal discharges in the low-Mg2+ -induced epileptic hippocampal slice models, and ictal discharges were more sensitive than interictal discharges in response to VPA
The interictal discharges initiated in CA3a and propagated bidirectionally to CA1 and CA3c, whereas the ictal discharge was first observed in the dentate gyrus (DG) and propagated from the CA3c to CA1 along the stratum pyramidale
Summary
Mesial temporal lobe epilepsy (mTLE) is the most common type of intractable epilepsy. It is closely associated with malfunctions of the mesial temporal lobe structures, such as the hippocampus and the entorhinal cortex (EC), which are heavily interconnected [1, 2]. Several studies have investigated the cellular and network mechanisms of epileptiform discharges in the hippocampus [4,5,6]. De Curtis and Avanzini [7] and McCormick and Contreras [8] reported that the mechanisms of epileptiform discharges mainly depend on intrinsic neuronal properties, recurrent synaptic interconnections, and nonsynaptic interactions among closely located neurons, which lead to excessive neuronal synchronization. Observations in animal models indicated that the epileptogenic zone was broad, and the substrate for seizure generation was distributed over several limbic structures [11], including the hippocampus, EC, and amygdala
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