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      Effect of the Entorhinal Cortex on Ictal Discharges in Low-Mg 2+ -Induced Epileptic Hippocampal Slice Models

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          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-Mg 2+ 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.

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          On the cellular and network bases of epileptic seizures.

          D A McCormick, D Contreras (2001)
          The highly interconnected networks of the mammalian forebrain can generate a wide variety of synchronized activities, including those underlying epileptic seizures, which often appear as a transformation of otherwise normal brain rhythms. The cerebral cortex and hippocampus are particularly prone to the generation of the large, synchronized bursts of activity underlying many forms of seizures owing to strong recurrent excitatory connections, the presence of intrinsically burst-generating neurons, ephaptic interactions among closely spaced neurons, and synaptic plasticity. The simplest form of epileptiform activity in these structures is the interictal spike, a synchronized burst of action potentials generated by recurrent excitation, followed by a period of hyperpolarization, in a localized pool of pyramidal neurons. Seizures can also be generated in response to a loss of balance between excitatory and inhibitory influences and can take the form of either tonic depolarizations or repetitive, rhythmic burst discharges, either as clonic or spike-wave activity, again mediated both by intrinsic membrane properties and synaptic interactions. The interaction of the cerebral cortex and the thalamus, in conjunction with intrathalamic communication, can also generate spike waves similar to those occurring during human absence seizure discharges. Although epileptic syndromes and their causes are diverse, the cellular mechanisms of seizure generation appear to fall into only two categories: rhythmic or tonic "runaway" excitation or the synchronized and rhythmic interplay between excitatory and inhibitory neurons and membrane conductances.
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            The hippocampal CA3 network: an in vivo intracellular labeling study.

            X. G. Li, P Somogyi, A Ylinen … (1994)
            The intrahippocampal distribution of axon collaterals of individual CA3 pyramidal cells was investigated in the rat. Pyramidal cells in the CA3 region of the hippocampus were physiologically characterized and filled with biocytin in anesthetized animals. Their axonal trees were reconstructed with the aid of a drawing tube. Single CA3 pyramidal cells arborized most extensively in the CA1 region, covering approximately two-thirds of the longitudinal axis of the hippocampus. The total length of axon collaterals in the CA3 region was less than in CA1 and the axon branches tended to cluster in narrow bands (200-800 microns), usually several hundred microns anterior or posterior to the cell body. The majority of the recurrent collaterals of a given neuron remained in the same subfield (CA3a, b, or c) as the parent cell. CA3a neurons innervated predominantly the basal dendrites, whereas neurons located proximal to the hilus (CA3c) terminated predominantly on the apical dendrites of both CA1 and CA3 cells. Two cells, with horizontal dendrites and numerous thorny excrescences at the CA3c-hilus transitional zone, were also labeled and projected to both CA3 and CA1 regions. All CA3 neurons projected some collaterals to the hilar region. Proximal (CA3c) neurons had numerous collaterals in the hilus proper. One CA3c pyramidal cell in the dorsal hippocampus sent an axon collaterals to the inner third of the molecular layer. CA3c pyramidal cells in the ventral hippocampus had extensive projections to the inner third of the dentate molecular layer, as well as numerous collaterals in the hilus, CA3, and CA1 areas, and several axon collaterals penetrated the subiculum. The total projected axon length of a single neuron ranged from 150 to 300 mm. On the basis of the projected axon length and bouton density (mean interbouton distance: 4.7 microns), we estimate that a single CA3 pyramidal cell can make synapses with 30,000-60,000 neurons in the ipsilateral hippocampus. The concentrated distribution of the axon collaterals ("patches") indicates that subpopulations of neurons may receive disproportionately denser innervation, whereas innervation in the rest of the target zones is rather sparse. These observations offer new insights into the physiological organization of the CA3 pyramidal cell network.
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              Interictal spikes in focal epileptogenesis.

              Marco de Curtis, Giuliano Avanzini (2001)
              Interictal electroencephalography (EEG) potentials in focal epilepsies are sustained by synchronous paroxysmal membrane depolarization generated by assemblies of hyperexcitable neurons. It is currently believed that interictal spiking sets a condition that preludes to the onset of an ictal discharge. Such an assumption is based on little experimental evidence. Human pre-surgical studies and recordings in chronic and acute models of focal epilepsy showed that: (i) interictal spikes (IS) and ictal discharges are generated by different populations of neuron through different cellular and network mechanisms; (ii) the cortical region that generates IS (irritative area) does not coincide with the ictal-onset area; (iii) IS frequency does not increase before a seizure and is enhanced just after an ictal event; (iv) spike suppression is found to herald ictal discharges; and (v) enhancement of interictal spiking suppresses ictal events. Several experimental evidences indicate that the highly synchronous cellular discharge associated with an IS is generated by a multitude of mechanisms involving synaptic and non-synaptic communication between neurons. The synchronized neuronal discharge associated with a single IS induces and is followed by a profound and prolonged refractory period sustained by inhibitory potentials and by activity-dependent changes in the ionic composition of the extracellular space. Post-spike depression may be responsible for pacing interictal spiking periodicity commonly observed in both animal models and human focal epilepsies. It is proposed that the strong after-inhibition produced by IS protects against the occurrence of ictal discharges by maintaining a low level of excitation in a general condition of hyperexcitability determined by the primary epileptogenic dysfunction.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neural Plast
                Journal ID (iso-abbrev): Neural Plast
                Journal ID (publisher-id): NP
                Title: Neural Plasticity
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-5904
                ISSN (Electronic): 1687-5443
                Publication date (Print): 2014
                Publication date (Electronic): 3 March 2014
                Volume: 2014
                Electronic Location Identifier: 205912
                Affiliations
                1Department of Neurology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, 1630 Dong-Fang Road, Shanghai 200127, China
                2School of Biomedical Engineering, Shanghai Jiao Tong University, 800 Dong-Chuan Road, Shanghai 200240, China
                Author notes
                *Pu-Ming Zhang: pmzhang@ 123456sjtu.edu.cn and

                Academic Editor: Masayuki Matsushita

                Article
                DOI: 10.1155/2014/205912
                PMC ID: 3960561
                PubMed ID: 24729906
                SO-VID: f85e379b-ccf4-48e8-a5f6-c8caeca8610d
                Copyright © Copyright © 2014 Ye-Jun Shi et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 September 2013
                Date accepted : 30 January 2014
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Neurosciences
                Data availability:
                ScienceOpen disciplines: Neurosciences

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