Home > Publications Database > Hippocampal spreading depolarization as a driver of postictal ambulation. > print

001     283024
005     20260217131342.0
024 7 _ |2 doi
|a 10.1126/scitranslmed.adv3260
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|a pmid:40961224
024 7 _ |2 ISSN
|a 1946-6234
024 7 _ |2 ISSN
|a 1946-6242
037 _ _ |a DZNE-2025-01436
041 _ _ |a English
082 _ _ |a 500
100 1 _ |0 0009-0003-8113-7200
|a Mitlasóczki, Bence
|b 0
245 _ _ |a Hippocampal spreading depolarization as a driver of postictal ambulation.
260 _ _ |a Washington, DC
|b AAAS
|c 2025
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|a Journal Article
520 _ _ |a Postseizure (postictal) symptoms are regularly encountered in epilepsy and can be life threatening, yet their neurobiological underpinnings remain understudied. Using two-photon or widefield imaging, field potential and unit recordings, optogenetics, and basic behavioral assessment under healthy conditions or viral encephalitis, we studied seizures and postictal symptoms in mice. We show a propensity of the hippocampus for seizure-associated spreading depolarization (sSD). Through optogenetic stimulation, we provide evidence that induced isolated hippocampal SD is sufficient to elicit postictal ambulation (PIA), whereas induced isolated seizure-like episodes are not. Furthermore, PIA occurred in the absence of SD progression to the neocortex. In addition, we analyzed Behnke-Fried depth-electrode recordings in four patients with focal epilepsy. Of 13 recorded seizures, we observed five slow shifts at seizure termination in the regionwise analysis that could reflect putative sSD. In support of our experiments in mice, we also found an increased vulnerability of the human temporomesial system (hippocampus and amygdala) for this phenomenon and longer recovery times of affected as compared with nonaffected brain regions. This work suggests sSD as a previously underrecognized pathoclinical entity underlying distinct postictal symptoms in epilepsy.
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650 _ 2 |2 MeSH
|a Animals
650 _ 2 |2 MeSH
|a Hippocampus: physiopathology
650 _ 2 |2 MeSH
|a Humans
650 _ 2 |2 MeSH
|a Seizures: physiopathology
650 _ 2 |2 MeSH
|a Male
650 _ 2 |2 MeSH
|a Female
650 _ 2 |2 MeSH
|a Walking: physiology
650 _ 2 |2 MeSH
|a Mice
650 _ 2 |2 MeSH
|a Mice, Inbred C57BL
650 _ 2 |2 MeSH
|a Optogenetics
650 _ 2 |2 MeSH
|a Electroencephalography
650 _ 2 |2 MeSH
|a Adult
700 1 _ |a Gutiérrez Gómez, Adrián
|b 1
700 1 _ |a Kamali, Midia
|b 2
700 1 _ |a Babushkina, Natalia
|b 3
700 1 _ |a Baues, Mayan
|b 4
700 1 _ |a Kück, Laura
|b 5
700 1 _ |a Haubrich, André Nathan
|b 6
700 1 _ |a Tamiolakis, Theodoros
|b 7
700 1 _ |0 P:(DE-2719)9000501
|a Breuer, Annika
|b 8
700 1 _ |0 0000-0002-1037-5506
|a Granak, Simon
|b 9
700 1 _ |a Schwering-Sohnrey, Merlin
|b 10
700 1 _ |0 0000-0002-7973-7405
|a Gerhauser, Ingo
|b 11
700 1 _ |0 0000-0001-8151-5644
|a Baumgärtner, Wolfgang
|b 12
700 1 _ |a Schwarz, Martin Karl
|b 13
700 1 _ |0 0000-0002-1638-426X
|a Ewell, Laura
|b 14
700 1 _ |0 P:(DE-2719)9000241
|a Opitz, Thoralf
|b 15
700 1 _ |0 0000-0002-6688-4916
|a Pitsch, Julika
|b 16
700 1 _ |0 0000-0002-9461-1042
|a Musall, Simon
|b 17
700 1 _ |0 0000-0002-3177-8582
|a Surges, Rainer
|b 18
700 1 _ |0 P:(DE-2719)9000221
|a Mormann, Florian
|b 19
700 1 _ |0 P:(DE-2719)2000044
|a Beck, Heinz
|b 20
700 1 _ |0 0000-0002-6065-1660
|a Wenzel, Michael
|b 21
773 _ _ |0 PERI:(DE-600)2518839-2
|a 10.1126/scitranslmed.adv3260
|g Vol. 17, no. 816, p. eadv3260
|n 816
|p eadv3260
|t Science translational medicine
|v 17
|x 1946-6234
|y 2025
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