In mouse brain slices that contain reciprocally connected hippocampus and entorhinal cortex (EC) networks, CA3 outputs control the EC propensity to generate experimentally induced ictal-like discharges resembling electrographic seizures. Neuronal damage in limbic areas, such as CA3 and dentate hilus, occurs in patients with temporal lobe epilepsy and in animal models (e.g., pilocarpine- or kainate-treated rodents) mimicking this epileptic disorder. Hence, hippocampal damage in epileptic mice may lead to decreased CA3 output function that in turn would allow EC networks to generate ictal-like events. Here we tested this hypothesis and found that CA3-driven interictal discharges induced by 4-aminopyridine (4AP, 50 muM) in hippocampus-EC slices from mice injected with pilocarpine 13-22 days earlier have a lower frequency than in age-matched control slices. Moreover, EC-driven ictal-like discharges in pilocarpine- treated slices occur throughout the experiment (less than or equal to6 h) and spread to the CA1/subicular area via the temporoammonic path; in contrast, they disappear in control slices within 2 h of 4AP application and propagate via the trisynaptic hippocampal circuit. Thus, different network interactions within the hippocampus-EC loop characterize control and pilocarpine-treated slices maintained in vitro. We propose that these functional changes, which are presumably caused by seizure-induced cell damage, lead to seizures in vivo. This process is facilitated by a decreased control of EC excitability by hippocampal outputs and possibly sustained by the reverberant activity between EC and CA1/subiculum networks that are excited via the temporoammonic path.

Limbic network interactions leading to hyperexcitability in a model of temporal lobe epilepsy / M., D'Antuono; R., Benini; BIAGINI, Giuseppe; G., D'Arcangelo; M., Barbarosie; V., Tancredi; M., Avoli. - In: JOURNAL OF NEUROPHYSIOLOGY. - ISSN 0022-3077. - STAMPA. - 87(2002), pp. 634-639.

Limbic network interactions leading to hyperexcitability in a model of temporal lobe epilepsy

BIAGINI, Giuseppe;
2002

Abstract

In mouse brain slices that contain reciprocally connected hippocampus and entorhinal cortex (EC) networks, CA3 outputs control the EC propensity to generate experimentally induced ictal-like discharges resembling electrographic seizures. Neuronal damage in limbic areas, such as CA3 and dentate hilus, occurs in patients with temporal lobe epilepsy and in animal models (e.g., pilocarpine- or kainate-treated rodents) mimicking this epileptic disorder. Hence, hippocampal damage in epileptic mice may lead to decreased CA3 output function that in turn would allow EC networks to generate ictal-like events. Here we tested this hypothesis and found that CA3-driven interictal discharges induced by 4-aminopyridine (4AP, 50 muM) in hippocampus-EC slices from mice injected with pilocarpine 13-22 days earlier have a lower frequency than in age-matched control slices. Moreover, EC-driven ictal-like discharges in pilocarpine- treated slices occur throughout the experiment (less than or equal to6 h) and spread to the CA1/subicular area via the temporoammonic path; in contrast, they disappear in control slices within 2 h of 4AP application and propagate via the trisynaptic hippocampal circuit. Thus, different network interactions within the hippocampus-EC loop characterize control and pilocarpine-treated slices maintained in vitro. We propose that these functional changes, which are presumably caused by seizure-induced cell damage, lead to seizures in vivo. This process is facilitated by a decreased control of EC excitability by hippocampal outputs and possibly sustained by the reverberant activity between EC and CA1/subiculum networks that are excited via the temporoammonic path.
87
634
639
Limbic network interactions leading to hyperexcitability in a model of temporal lobe epilepsy / M., D'Antuono; R., Benini; BIAGINI, Giuseppe; G., D'Arcangelo; M., Barbarosie; V., Tancredi; M., Avoli. - In: JOURNAL OF NEUROPHYSIOLOGY. - ISSN 0022-3077. - STAMPA. - 87(2002), pp. 634-639.
M., D'Antuono; R., Benini; BIAGINI, Giuseppe; G., D'Arcangelo; M., Barbarosie; V., Tancredi; M., Avoli
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11380/305749
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