Neuroprotective effect of lithium in cold- induced traumatic brain injury in mice

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dc.contributor.authorÇiftçi, Elvan
dc.contributor.authorKaraçay, Reyda
dc.contributor.authorÇağlayan, Aysun
dc.contributor.authorAltunay, Serdar
dc.contributor.authorAteş, Nilay
dc.contributor.authorAltıntaş, Mehmet O.
dc.contributor.authorKılıç, Ertuğrul
dc.date.accessioned2021-02-19T21:16:22Z
dc.date.available2021-02-19T21:16:22Z
dc.date.issued2020
dc.departmentALKÜ
dc.description.abstractApart from its well-established therapeutic activity on bipolar disorder and depression, lithium exerts neuroprotective activity upon neurodegenerative disorders, such as traumatic brain injury (TBI). However, the cellular signaling mechanisms mediating lithium's neuroprotective activity and long-term dose- and time-dependent effects on close and remote proximity are largely unknown. Herein, we tested prophylactic and acute effects of lithium (2 mmol/kg) after cold- induced TBI. In both conditions, treatments with lithium resulted in reduced infarct volume and apoptosis. Its acute treatment resulted in the increase of Akt, ERK-1/2 and GSK-3 alpha/beta phosphoylations. Interestingly, its prophylactic treatment instead resulted in decreased phosphorylations of Akt, ERK-1/2, p38, JNK-1 moderately and GSK-3 alpha/beta significantly. Then, we tested subacute (35-day follow-up) role of low (0.2 mmol/kg) and high dose (2 mmol/kg) lithium and revealed that high dose lithium group was the most mobile so the least depressed in the tail suspension test. Anxiety level was assessed by light-dark test, all groups' anxiety levels were decreased with time, but lithium had no effect on anxiety like behavior. When subacute effects of injury and drug treatment were evaluated on the defined brain regions, infarct volume was decreased in the high dose lithium group significantly. In contrast to other brain regions, hippocampal atrophies were observed in both lithium treatment groups, which were significant in the low dose lithium group in both hemispheres, which was associated with the reduced cell proliferation and neurogenesis. Our data demonstrate that lithium treatment protects neurons from TBI. However, long term particularly low-dose lithium causes hippocampal atrophy and decreased neurogenesis.
dc.description.sponsorshipTurkish Academy of Sciences (TUBA)Turkish Academy of Sciences
dc.description.sponsorshipThis study was supported by The Turkish Academy of Sciences (TUBA).
dc.identifier.doi10.1016/j.bbr.2020.112719
dc.identifier.issn0166-4328
dc.identifier.issn1872-7549
dc.identifier.pmid32479849
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.bbr.2020.112719
dc.identifier.urihttps://hdl.handle.net/20.500.12868/401
dc.identifier.volume392en_US
dc.identifier.wosWOS:000552654000017
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthor0-belirlenecek
dc.language.isoen
dc.publisherElsevier
dc.relation.ispartofBehavioural Brain Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectTraumatic brain injury
dc.subjectHippocampal volume
dc.subjectLithium
dc.subjectCell signaling
dc.titleNeuroprotective effect of lithium in cold- induced traumatic brain injury in mice
dc.typeArticle

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