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Tytuł pozycji:

Spreading depression as an innate antiseizure mechanism.

Tytuł:
Spreading depression as an innate antiseizure mechanism.
Autorzy:
Tamim I; Neurovascular Research Unit, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.; Charité-Universitätsmedizin Berlin, Klinik und Hochschulambulanz für Neurologie und Centrum für Schlaganfallforschung Berlin (CSB), Berlin, Germany.
Chung DY; Neurovascular Research Unit, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
de Morais AL; Neurovascular Research Unit, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Loonen ICM; Neurovascular Research Unit, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Qin T; Neurovascular Research Unit, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Misra A; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Schlunk F; Charité-Universitätsmedizin Berlin, Klinik und Hochschulambulanz für Neurologie und Centrum für Schlaganfallforschung Berlin (CSB), Berlin, Germany.
Endres M; Charité-Universitätsmedizin Berlin, Klinik und Hochschulambulanz für Neurologie und Centrum für Schlaganfallforschung Berlin (CSB), Berlin, Germany.
Schiff SJ; Center for Neural Engineering, Departments of Engineering Science and Mechanics and Physics, The Pennsylvania State University, State College, PA, USA.
Ayata C; Neurovascular Research Unit, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. .; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. .
Źródło:
Nature communications [Nat Commun] 2021 Apr 13; Vol. 12 (1), pp. 2206. Date of Electronic Publication: 2021 Apr 13.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
Język:
English
Imprint Name(s):
Original Publication: [London] : Nature Pub. Group
MeSH Terms:
Depression*
Seizures/*chemically induced
Seizures/*drug therapy
Seizures/*metabolism
4-Aminopyridine ; Animals ; Bicuculline/pharmacology ; Brain Stem ; Cortical Spreading Depression ; Female ; Gene Knock-In Techniques ; Kainic Acid/pharmacology ; Male ; Mice ; Nervous System ; Optogenetics ; Penicillins/pharmacology ; Potassium Channel Blockers/adverse effects ; Seizures/pathology ; Tetrodotoxin/pharmacology
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Grant Information:
K08 NS112601 United States NS NINDS NIH HHS; KL2 TR002542 United States TR NCATS NIH HHS; R01 EB014641 United States EB NIBIB NIH HHS; R01 NS102969 United States NS NINDS NIH HHS
Substance Nomenclature:
0 (Penicillins)
0 (Potassium Channel Blockers)
4368-28-9 (Tetrodotoxin)
BH3B64OKL9 (4-Aminopyridine)
SIV03811UC (Kainic Acid)
Y37615DVKC (Bicuculline)
Entry Date(s):
Date Created: 20210414 Date Completed: 20210428 Latest Revision: 20220120
Update Code:
20240104
PubMed Central ID:
PMC8044138
DOI:
10.1038/s41467-021-22464-x
PMID:
33850125
Czasopismo naukowe
Spreading depression (SD) is an intense and prolonged depolarization in the central nervous systems from insect to man. It is implicated in neurological disorders such as migraine and brain injury. Here, using an in vivo mouse model of focal neocortical seizures, we show that SD may be a fundamental defense against seizures. Seizures induced by topical 4-aminopyridine, penicillin or bicuculline, or systemic kainic acid, culminated in SDs at a variable rate. Greater seizure power and area of recruitment predicted SD. Once triggered, SD immediately suppressed the seizure. Optogenetic or KCl-induced SDs had similar antiseizure effect sustained for more than 30 min. Conversely, pharmacologically inhibiting SD occurrence during a focal seizure facilitated seizure generalization. Altogether, our data indicate that seizures trigger SD, which then terminates the seizure and prevents its generalization.

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