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Alteration of the cortical spreading depolarization in the mouse defective in translocator protein 18 kDa.

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Τίτλος: Alteration of the cortical spreading depolarization in the mouse defective in translocator protein 18 kDa.
Συγγραφείς: Hattori M; Department of Emergency and Critical Care Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan., Zhang Q; Department of Neurobiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan., Handa T; Department of Neurobiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan., Kikutani K; Department of Emergency and Critical Care Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan., Kasaragod DK; Department of Neurobiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan., Matsumata M; Department of Neurobiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan., Ota K; Department of Emergency and Critical Care Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan., Shime N; Department of Emergency and Critical Care Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan., Aizawa H; Department of Neurobiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan. Electronic address: haizawa@hiroshima-u.ac.jp.
Πηγή: Brain research [Brain Res] 2026 Sep 15; Vol. 1887, pp. 150386. Date of Electronic Publication: 2026 May 15.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Elsevier/North-Holland Biomedical Press Country of Publication: Netherlands NLM ID: 0045503 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-6240 (Electronic) Linking ISSN: 00068993 NLM ISO Abbreviation: Brain Res Subsets: MEDLINE
Imprint Name(s): Original Publication: Amsterdam Elsevier/North-Holland Biomedical Press.
Ιατρικοί όροι (MeSH): Cortical Spreading Depression*/physiology , Receptors, GABA*/genetics , Receptors, GABA*/metabolism , Receptors, GABA*/deficiency , Cerebral Cortex*/metabolism, Blood-Brain Barrier/metabolism ; Neurons/metabolism ; Inflammation/metabolism ; Animals ; Mice, Knockout ; Mice ; Male ; Mice, Inbred C57BL
Περίληψη: Cortical spreading depolarization (CSD) has been implicated in neurological disorders, such as migraine, traumatic brain injury, and stroke. Since neurovascular and inflammatory responses of the cerebral cortex associated with CSD play a critical role in the exaggeration and expansion of the lesions, understanding the molecular mechanisms underlying these phenomena would be indispensable for the development of therapeutic interventions for disorders with CSD. Given that the mitochondrial protein, translocator protein 18 kDa (TSPO), plays a role in cellular metabolism and inflammation, we hypothesized that TSPO can modulate the susceptibility of the brain to CSD. To address this issue, we examined the physiological and molecular changes in cortical tissue under the influence of evoked CSD in TSPO-knockout mice. Histological analysis corroborated that TSPO-knockout mice developed six-layered structures with neuronal and glial cells comparable with those in wild-type mice. In vivo electrophysiology under anesthesia showed that mice with TSPO deletion reduced the number of CSD generation compared with the control group. This change in the CSD was associated with impaired induction of inflammatory genes such as IL-1β, Cox2, and Ccl2. Interestingly, TSPO gene deletion had a protective effect on CSD-induced disruption of the blood-brain barrier function with less extravasation of the Evans blue administered systemically. Collectively, these results highlighted a novel role of TSPO in neurovascular and inflammatory responses as sequelae of CSD.
(Copyright © 2026 Elsevier B.V. All rights reserved.)
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Contributed Indexing: Keywords: Blood–brain barrier; Cytokines; Inflammation; Spreading depolarization; TSPO
Substance Nomenclature: 0 (Receptors, GABA)
0 (Bzrp protein, mouse)
Entry Date(s): Date Created: 20260516 Date Completed: 20260613 Latest Revision: 20260613
Update Code: 20260615
DOI: 10.1016/j.brainres.2026.150386
PMID: 42142864
Βάση Δεδομένων: MEDLINE
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  Data: Alteration of the cortical spreading depolarization in the mouse defective in translocator protein 18 kDa.
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  Data: Cortical spreading depolarization (CSD) has been implicated in neurological disorders, such as migraine, traumatic brain injury, and stroke. Since neurovascular and inflammatory responses of the cerebral cortex associated with CSD play a critical role in the exaggeration and expansion of the lesions, understanding the molecular mechanisms underlying these phenomena would be indispensable for the development of therapeutic interventions for disorders with CSD. Given that the mitochondrial protein, translocator protein 18 kDa (TSPO), plays a role in cellular metabolism and inflammation, we hypothesized that TSPO can modulate the susceptibility of the brain to CSD. To address this issue, we examined the physiological and molecular changes in cortical tissue under the influence of evoked CSD in TSPO-knockout mice. Histological analysis corroborated that TSPO-knockout mice developed six-layered structures with neuronal and glial cells comparable with those in wild-type mice. In vivo electrophysiology under anesthesia showed that mice with TSPO deletion reduced the number of CSD generation compared with the control group. This change in the CSD was associated with impaired induction of inflammatory genes such as IL-1β, Cox2, and Ccl2. Interestingly, TSPO gene deletion had a protective effect on CSD-induced disruption of the blood-brain barrier function with less extravasation of the Evans blue administered systemically. Collectively, these results highlighted a novel role of TSPO in neurovascular and inflammatory responses as sequelae of CSD.<br /> (Copyright © 2026 Elsevier B.V. All rights reserved.)
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        Text: English
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      – SubjectFull: Neurons metabolism
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