Suppression of interictal bursting in hippocampus unleashes seizures in entorhinal cortex: a proepileptic effect of lowering [K+]0 and raising [Ca2+]0

Bragdon, Andrew; Kojima, Hisashi; Wilson, Wilkie A.

doi:10.1016/0006-8993(92)91088-v

Cited by 62 publications

(66 citation statements)

References 24 publications

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“…Moreover, we have reported in a previous study performed in combined EC-hippocampus slices (D'Arcangelo et al, 2001) that stimulus-induced IOSs observed during 4AP treatment appear first in the EC (and sometimes simultaneously in subiculum), and only later they become evident in the DG, CA3, and CA1. This evidence supports the view that limbic seizures in patients presenting with temporal lobe epilepsy (Rutecki et al, 1989;Spencer and Spencer, 1994;Bartolomei et al, 2001) and in animal models (Bragdon et al, 1992;Dreier and Heinemann, 1991;Nagao et al, 1996;Avoli et al, 1996) originate in EC and then propagate to the hippocampus proper. Similar temporal patterns of IOS activation were obtained in this study following brief train of stimuli at 10 Hz or recurring single-shock stimulation at 0.05 Hz.…”

Section: Discussionsupporting

confidence: 85%

“…Moreover, Benini et al (2003) have reported a similar inhibitory action on 4AP-induced parahippocampal ictogenesis during repetitive stimulation of the lateral-basolateral nuclei of the amygdala at 0.5-1 Hz in a rat combined hippocampus-EC-amygdala slice preparation. It has also been shown that CA3-driven interictal activity, whenever capable of reaching the EC, can exert similar inhibitory effects on the generation of spontaneous ictal discharges (Barbarosie and Avoli, 1997;Benini et al, 2003;Bragdon et al, 1992;cf., for review, de Curtis and Avanzini, 2001). However, this condition was not met in our study since the main CA3 outputs, which run through the Schaffer collateral system, were always cut at the beginning of the experiment.…”

Section: Discussionmentioning

confidence: 99%

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Repetitive low-frequency stimulation reduces epileptiform synchronization in limbic neuronal networks

D’Arcangelo

Panuccio

Tancredi

et al. 2005

Neurobiology of Disease

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Deep-brain electrical or transcranial magnetic stimulation may represent a therapeutic tool for controlling seizures in patients presenting with epileptic disorders resistant to antiepileptic drugs. In keeping with this clinical evidence, we have reported that repetitive electrical stimuli delivered at approximately 1 Hz in mouse hippocampus-entorhinal cortex (EC) slices depress the EC ability to generate ictal activity induced by the application of 4-aminopyridine (4AP) or Mg 2+ -free medium (Barbarosie, M., Avoli, M., 1997. CA3-driven hippocampalentorhinal loop controls rather than sustains in vitro limbic seizures. J. Neurosci. 17,[9308][9309][9310][9311][9312][9313][9314]. Here, we confirmed a similar control mechanism in rat brain slices analyzed with field potential recordings during 4AP (50 MM) treatment. In addition, we used intrinsic optical signal (IOS) recordings to quantify the intensity and spatial characteristics of this inhibitory influence. IOSs reflect the changes in light transmittance throughout the entire extent of the slice, and are thus reliable markers of limbic network epileptiform synchronization. First, we found that in the presence of 4AP, the IOS increases, induced by a train of electrical stimuli (10 Hz for 1 s) or by recurrent, single-shock stimulation delivered at 0.05 Hz in the deep EC layers, are reduced in intensity and area size by low-frequency (1 Hz), repetitive stimulation of the subiculum; these effects were observed in all limbic areas contained in the slice. Second, by testing the effects induced by repetitive subicular stimulation at 0.2-10 Hz, we identified maximal efficacy when repetitive stimuli are delivered at 1 Hz. Finally, we discovered that similar, but slightly less pronounced, inhibitory effects occur when repetitive stimuli at 1 Hz are delivered in the EC, suggesting that the reduction of IOSs seen during repetitive stimulation is pathway dependent as well as activity dependent. Thus, the activation of limbic networks at low frequency reduces the intensity and spatial extent of the IOS changes that accompany ictal synchronization in an in vitro slice preparation. This conclusion supports the view that repetitive stimulation may represent a potential therapeutic tool for controlling seizures in patients with pharmacoresistant epileptic disorders. D 2004 Elsevier Inc. All rights reserved.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Repetitive low-frequency stimulation reduces epileptiform synchronization in limbic neuronal networks

D’Arcangelo

Panuccio

Tancredi

et al. 2005

Neurobiology of Disease

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“…Some reports have proposed that interictal activity contributes to the transition from interictal to ictal discharge (Prince et al, 1983;Jensen and Yaari, 1988), yet other studies have showed that interictal activity interferes with ictal discharge generation (Swartzwelder et al, 1987;Bragdon et al, 1992). As demonstrated in an earlier report (Avoli et al, 1992), here we confirm that when ictal discharges are abolished in the hippocampus through perforant path cut, interictal activity is unaffected.…”

Section: Interictal-ictal Interactionsupporting

confidence: 88%

CA3-Driven Hippocampal-Entorhinal Loop Controls Rather than SustainsIn VitroLimbic Seizures

1997

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Continuous application of 4-aminopyridine (4-AP, 50 M) to combined slices of hippocampus-entorhinal cortex obtained from adult mice induces (1) interictal discharges that initiate in the CA3 area and propagate via the hippocampal regions CA1 and subiculum to the entorhinal cortex and return to the hippocampus through the dentate gyrus; and (2) ictal discharges that originate in the entorhinal cortex and propagate via the dentate gyrus to the hippocampus proper. Ictal discharges disappear over time, whereas synchronous interictal discharges continue to occur throughout the experiment. Lesioning the Schaffer collaterals abolishes interictal discharges in CA1, entorhinal cortex, and dentate gyrus and discloses entorhinal ictal discharges that propagate, via the dentate gyrus, to the CA3 subfield. Interictal discharges originating in CA3 also prevent the occurrence of ictal events generated in the entorhinal cortex during application of Mg 2ϩ -free medium. In both models, ictal discharge generation recorded in the entorhinal cortex after Schaffer collateral cut is prevented by mimicking CA3 neuronal activity through rhythmic electrical stimulation (0.25-1.5 Hz) of the CA1 hippocampal output region. Our findings demonstrate that interictal discharges of hippocampal origin control the expression of ictal epileptiform activity in the entorhinal cortex. Sectioning the Schaffer collaterals may model the chronic epileptic condition in which cell damage in the CA3 subfield results in loss of CA3 control over the entorhinal cortex. Hence, we propose that the functional integrity of hippocampal output neurons may represent a critical control point in temporal lobe epileptogenesis.

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“…These findings therefore suggest that changes in interictal activity may lead to ictogenesis. Interestingly, in a simplified system of epilepti-form synchronization such as the in vitro brain slice preparation, blocking the propagation of fast, CA3-driven interictal-like events to the EC causes the appearance of ictal-like discharges in the latter limbic area (Bragdon et al, 1992;Barbarosie and Avoli, 1997;Barbarosie et al, 2000;Benini et al, 2003). In addition, it has been shown in these studies these ictal-like events appear to be initiated by slow interictal events that are locally generated.…”

Section: Interictal Activitymentioning

confidence: 79%

Convulsive status epilepticus duration as determinant for epileptogenesis and interictal discharge generation in the rat limbic system

Bortel

Lévesque

Biagini

et al. 2010

Neurobiology of Disease

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We analyzed with EEG-video monitoring the epileptic activity recorded during the latent and chronic periods in rats undergoing 30 or 120 min pilocarpine-induced convulsive status epilepticus (SE). Interictal discharges frequency in the entorhinal cortex (EC) of animals exposed to 120 min SE was significantly higher in the chronic than in the latent period. Following seizure appearance, interictal spikes diminished in duration in the CA3 of the 120 min SE group, and occurred at higher rates in the amygdala in all animals. Rats exposed to 120 min SE generated shorter seizures but presented twice as many non-convulsive seizures per day as the 30 min group. Finally, seizures most frequently initiated in CA3 in the 120 min SE group but had similar onset in CA3 and EC in the 30 min group. These findings indicate that convulsive SE duration influences the development of interictal and ictal activity, and that interictal discharges undergo structure-specific changes after seizure appearance.

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Suppression of interictal bursting in hippocampus unleashes seizures in entorhinal cortex: a proepileptic effect of lowering [K+]0 and raising [Ca2+]0

Cited by 62 publications

References 24 publications

Repetitive low-frequency stimulation reduces epileptiform synchronization in limbic neuronal networks

Repetitive low-frequency stimulation reduces epileptiform synchronization in limbic neuronal networks

CA3-Driven Hippocampal-Entorhinal Loop Controls Rather than SustainsIn VitroLimbic Seizures

Convulsive status epilepticus duration as determinant for epileptogenesis and interictal discharge generation in the rat limbic system

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