Publication:
Burst firing of single neurons in the human medial temporal lobe changes before epileptic seizures.

cris.virtualsource.author-orcida2d50a78-8e65-4968-a668-0ca96c36bc83
cris.virtualsource.author-orcid204a564e-aea2-47ef-b62f-df7e037321cb
datacite.rightsrestricted
dc.contributor.authorGast, Heidemarie
dc.contributor.authorNiediek, Johannes
dc.contributor.authorSchindler, Kaspar
dc.contributor.authorBoström, Jan
dc.contributor.authorCoenen, Volker A
dc.contributor.authorBeck, Heinz
dc.contributor.authorElger, Christian E
dc.contributor.authorMormann, Florian
dc.date.accessioned2024-10-24T18:17:15Z
dc.date.available2024-10-24T18:17:15Z
dc.date.issued2016-10
dc.description.abstractOBJECTIVE To better understand the mechanisms that lead to the sudden and unexpected occurrence of seizures, with the neuronal correlate being abnormally synchronous discharges that disrupt neuronal function. METHODS To address this problem, we recorded single neuron activity in epilepsy patients during the transition to seizures to uncover specific changes of neuronal firing patterns. We focused particularly on neurons repeatedly firing discrete groups of high-frequency action potentials (so called bursters) that have been associated with ictogenesis. We analyzed a total of 459 single neurons and used the mean autocorrelation time as a quantitative measure of burstiness. To unravel the intricate roles of excitation and inhibition, we also examined differential contributions from putative principal cells and interneurons. RESULTS During interictal recordings, burstiness was significantly higher in the seizure onset hemisphere, an effect found only for principal cells, but not for interneurons, and which disappeared before seizures. CONCLUSION These findings deviate from conventional views of ictogenesis that propose slowly-increasing aggregates of bursting neurons which give rise to seizures once they reach a critical mass. SIGNIFICANCE Instead our results are in line with recent hypotheses that bursting may represent a protective mechanism by preventing direct transmission of postsynaptic high-frequency oscillations.
dc.description.numberOfPages6
dc.description.sponsorshipDepartement Klinische Forschung, Forschungsgruppe Neurologie
dc.description.sponsorshipUniversitätsklinik für Neurologie
dc.identifier.doi10.7892/boris.89050
dc.identifier.pmid27592159
dc.identifier.publisherDOI10.1016/j.clinph.2016.08.010
dc.identifier.urihttps://boris-portal.unibe.ch/handle/20.500.12422/145570
dc.language.isoen
dc.publisherElsevier
dc.relation.ispartofClinical neurophysiology
dc.relation.issn1388-2457
dc.relation.organizationDCD5A442C22EE17DE0405C82790C4DE2
dc.relation.organizationDCD5A442BAE0E17DE0405C82790C4DE2
dc.subjectBurstiness
dc.subjectInterictal
dc.subjectInterneurons
dc.subjectPre-ictal
dc.subjectPrincipal cells
dc.subject.ddc600 - Technology::610 - Medicine & health
dc.titleBurst firing of single neurons in the human medial temporal lobe changes before epileptic seizures.
dc.typearticle
dspace.entity.typePublication
dspace.file.typetext
oaire.citation.endPage3334
oaire.citation.issue10
oaire.citation.startPage3329
oaire.citation.volume127
oairecerif.author.affiliationDepartement Klinische Forschung, Forschungsgruppe Neurologie
oairecerif.author.affiliationUniversitätsklinik für Neurologie
oairecerif.author.affiliation2Universitätsklinik für Neurologie
oairecerif.author.affiliation2Departement Klinische Forschung, Forschungsgruppe Neurologie
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unibe.description.ispublishedpub
unibe.eprints.legacyId89050
unibe.journal.abbrevTitleCLIN NEUROPHYSIOL
unibe.refereedtrue
unibe.subtype.articlejournal

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