Hyperthermic preconditioning severely accelerates neuronal damage in the gerbil ischemic hippocampal dentate gyrus via decreasing SODs expressions

Kim, Dong Won; Cho, Jeong‐Hwi; Cho, Geum-Sil; Kim, In Hye; Park, Joon Ha; Ahn, Ji Hyeon; Chen, Bai Hui; Shin, Bich-Na; Tae, Hyun‐Jin; Hong, Seongkweon; Cho, Jun Hwi; Kim, Young‐Myeong; Won, Moo‐Ho; Lee, Jae Chul

doi:10.1016/j.jns.2015.09.008

Cited by 7 publications

(4 citation statements)

References 37 publications

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“…In our present study, hyperthermia for 30 min before TFI (HT/ischemia group) resulted in the earlier death of pyramidal cells in CA1 on day 2 after TFI and induced death in CA2/3 pyramidal cells on day 2 after TFI, which was not observed in the NT/ischemia group. These results are similar to the findings of previous studies showing that, in rats and gerbils, ischemia-reperfusion under hyperthermic conditions induces more accelerated neuronal cell death in the hippocampal CA1 from approximately 1 day after transient ischemia ( 4 - 6 ), and disruption of ischemic resistance of pyramidal neurons in the hippocampal CA2/3 ( 4 , 6 ) and granular cells in the hippocampal dentate gyrus ( 19 ). Furthermore, in a rat model of focal ischemic stroke, hyperthermia was found to increase infarct size and worsen behavioral outcomes when ischemic duration was maintained for more than 2 h ( 7 ).…”

Section: Discussionsupporting

confidence: 91%

“…To examine changes in neurons and HIF-1α expression, immunohistochemistry was performed according to previously published methods ( 9 , 19 , 20 ). In short, the brain sections were immersed in 0.3% hydrogen peroxide (H 2 O 2 ) and soaked in 5% normal goat serum.…”

Section: Methodsmentioning

confidence: 99%

“…Analyses of the numbers of NeuN immunoreactive neurons and HIF-1α immunoreactivity in CA1 and CA2/3 were conducted according to previously published methods ( 9 , 19 - 21 ). In short, images of NeuN immunoreactive structures and HIF-1α immunoreactive structures were captured using an AxioM1 light microscope at ×20 magnification.…”

Section: Methodsmentioning

confidence: 99%

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Hyperthermia accelerates neuronal loss differently between the hippocampal CA1 and CA2/3 through different HIF‑1α expression after transient ischemia in gerbils

et al. 2022

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The hippocampus has a different vulnerability to ischemia according to the subfields CA1 to CA3 (initials of cornu ammonis). It has been reported that body temperature changes during ischemia affect the degree of neuronal death following transient ischemia. Hypoxia-inducible factor 1α (HIF-1α) plays a key role in regulating cellular adaptation to low oxygen conditions. In the present study, we investigated the pattern of neuronal death (loss) in CA1 and CA2/3 following 5 min transient forebrain ischemia (TFI) under hyperthermia (39.5±0.2˚C) and the relationship between neuronal death and changes in HIF-1α expression using western blot analysis and immunohistochemistry in gerbils. Normothermia or hyperthermia was induced for 30 min before and during the TFI, and neuronal death and HIF-1α expression were observed at 0, 3, 6 and 12 h, 1, 2 and 5 days after TFI. Under normothermia, TFI-induced neuronal death of CA1 pyramidal neurons occurred on day 5 after TFI, but CA2/3 pyramidal neurons did not die. In contrast, under hyperthermia, the death of CA1 and CA2/3 pyramidal neurons was observed on day 2 after TFI. Under normothermia, HIF-1α expression was significantly elevated in both CA1 and CA2/3 pyramidal neurons at 12 h and 1 day after TFI, and the increased HIF-1α immunoreactivity in CA1 was dramatically reduced from 2 days after TFI, but not in CA2/3 pyramidal neurons. Under hyperthermia, the basal expression of HIF-1α in the sham group was significantly higher in both CA1 and CA2/3 pyramidal neurons at 0 h after TFI than in the normothermia group. HIF-1 expression was continuously higher, peaked at 12 h after TFI, and then significantly decreased from 1 day after TFI. Overall, the present results indicate that resistance to ischemia in CA2/3 pyramidal neurons is closely associated with the persistence of increased expression of HIF-1α after ischemic insults and that hyperthermia-induced exacerbation of death of pyramidal neurons is closely related to decreased HIF-1α expression after ischemic insults.

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Section: Discussionsupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

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Hyperthermia accelerates neuronal loss differently between the hippocampal CA1 and CA2/3 through different HIF‑1α expression after transient ischemia in gerbils

et al. 2022

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“…Clinical reports have confirmed that hyperthermia can accelerate infarction and worsen outcomes of ischemic stroke patients (20,21). Recently, we have reported that hyperthermia can accelerate and worsen neuronal damage or death in the gerbil hippocampus after tFI (13,22,23).…”

Section: Transient Forebrain Ischemia Under Hyperthermic Condition Acmentioning

confidence: 79%

Transient forebrain ischemia under hyperthermic condition accelerates memory impairment and neuronal death in the gerbil hippocampus by increasing NMDAR1 expression

et al. 2021

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Altered expression levels of N-methyl-D-aspartate receptor (NMDAR), a ligand-gated ion channel, have a harmful effect on cellular survival. Hyperthermia is a proven risk factor of transient forebrain ischemia (tFI) and can cause extensive and severe brain damage associated with mortality. The objective of the present study was to investigate whether hyperthermic preconditioning affected NMDAR1 immunoreactivity associated with deterioration of neuronal function in the gerbil hippocampal CA1 region following tFI via histological and western blot analyses. Hyperthermic preconditioning was performed for 1 h before tFI, which was developed by ligating common carotid arteries for 5 min. tFI-induced cognitive impairment under hyperthermia was worse compared with that under normothermia. Loss (death) of pyramidal neurons in the CA1 region occurred fast and was more severe under hyperthermia compared with that under normothermia. NMDAR1 immunoreactivity was not observed in the somata of pyramidal neurons of sham gerbils with normothermia. However, its immunoreactivity was strong in the somata and processes at 12 h post-tFI. Thereafter, NMDAR1 immunoreactivity decreased with time after tFI. On the other hand, NMDAR1 immunoreactivity under hyperthermia was significantly increased in the somata and processes at 6 h post-tFI. The change pattern of NMDAR1 immunoreactivity under hyperthermia was different from that under normothermia. Overall, accelerated tFI-induced neuronal death under hyperthermia may be closely associated with altered NMDAR1 expression compared with that under normothermia.

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The Impact of Cerebral Ischemia on Antioxidant Enzymes Activity and Neuronal Damage in the Hippocampus

Sadeghzadeh,

Hosseini,

Mobed

et al. 2023

Cell Mol Neurobiol

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Hyperthermic preconditioning severely accelerates neuronal damage in the gerbil ischemic hippocampal dentate gyrus via decreasing SODs expressions

Cited by 7 publications

References 37 publications

Hyperthermia accelerates neuronal loss differently between the hippocampal CA1 and CA2/3 through different HIF‑1α expression after transient ischemia in gerbils

Hyperthermia accelerates neuronal loss differently between the hippocampal CA1 and CA2/3 through different HIF‑1α expression after transient ischemia in gerbils

Transient forebrain ischemia under hyperthermic condition accelerates memory impairment and neuronal death in the gerbil hippocampus by increasing NMDAR1 expression

The Impact of Cerebral Ischemia on Antioxidant Enzymes Activity and Neuronal Damage in the Hippocampus

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