Hypoxia protects against the neurotoxicity of kainic acid

Pohle, W. D.; Rauca, Christine

doi:10.1016/0006-8993(94)91693-4

Cited by 44 publications

(34 citation statements)

References 21 publications

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“…Human studies corroborate the occurrence of hypoxia associated with seizures, showing expression of HIF-1a in the epileptogenic focus (Gualtieri et al, 2013) and reduction of oxygen saturation during seizures, especially in seizures whose focus is the temporal lobe and that spread contralaterally (Bateman et al, 2008). Despite the degenerative effects of long hypoxic events, hypoxia preconditioning reduces seizure susceptibility, seizure severity, and acute hippocampal neuron loss (Pohle and Rauca, 1994;Emerson et al, 1999;Rauca et al, 2000;Rubaj et al, 2000;Chang et al, 2005). However, the long-term effects of hypoxic preconditioning on the chronic phase neuron loss and memory are not known.…”

Section: Introductionsupporting

confidence: 48%

“…Hypoxic preconditioning showed a trend towards lower seizure severity during SE. Whereas some studies indicated lower SE severity following hypoxia (Pohle and Rauca, 1994;Rauca et al, 2000), studies with electroshock or amygdala electrical kindling priming showed no effect on SE severity (Andre et al, 2000). One possible mechanism that could explain the effect of hypoxia on SE is the activation of adenosine A3 receptors, depressing postsynaptic sensitivity to glutamate and decreasing glutamatergic cholinergic coupling (Dunwiddie et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

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Decreased neuron loss and memory dysfunction in pilocarpine-treated rats pre-exposed to hypoxia

et al. 2016

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Abstract-Preconditioning can induce a cascade of cellular events leading to neuroprotection against subsequent brain insults. In this study, we investigated the chronic effects of hypoxic preconditioning on spontaneous recurrent seizures (SRS), neuronal death, and spatial memory performance in rats subjected to pilocarpine (Pilo)-induced status epilepticus (SE). Rats underwent a short hypoxic episode (7% O 2 + 93% N 2 ; 30 min on two consecutive days) preceding a 4-h SE (HSE group). Control groups were rats submitted to SE only (SE), rats subjected to hypoxia only (H) or normoxia-saline (C). Animals were monitored for the occurrence of SRS, and spatial memory performance was evaluated in the radial-arm maze. Hippocampal sections were analyzed for cell death and mossy fiber sprouting at 1 or 60 days after SE. Compared to SE group, HSE had increased SE latency, reduced number of rats with SRS, reduced mossy fiber sprouting at 60 days, and reduced cell death in the hilus and the CA3 region 1 and 60 days after SE. Additionally, HSE rats had better spatial memory performance than SE rats. Our findings indicated that short hypoxic preconditioning preceding SE promotes long-lasting protective effects on neuron survival and spatial memory. Ó

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Section: Introductionsupporting

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Decreased neuron loss and memory dysfunction in pilocarpine-treated rats pre-exposed to hypoxia

et al. 2016

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“…In an attempt to understand the molecular mechanisms of this neuroprotection, several groups have been able to mimic the preconditioning in vivo and in vitro with molecules such as ATP-sensitive K + channels agonists or NMDA (Kasischke et al, 1996;Riepe et al, 1997), with agonists and antagonists of the adenosine A1 receptor (Heurteaux et al, 1995), electrically via the application of 2M KCl (Kawahara et al, 1995;Kobayashi et al, 1995) and by anoxia/hypoxia in various models (Pohle and Rauca, 1994;Simon et al, 1993), therefore inducing a cross-tolerance (for review, see Kirino, 2002). However, the hypothesis that a bacterial infection might also lead to cerebral tolerance has not been investigated extensively.…”

Section: Discussionmentioning

confidence: 99%

Transforming Growth Factor-β1-Mediated Neuroprotection against Excitotoxic Injuryin Vivo

Boche

Cunningham

Gauldie

et al. 2003

J Cereb Blood Flow Metab

110

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Summary:Ischemic preconditioning is a phenomenon that describes how a sublethal ischemic insult can induce tolerance to subsequent ischemia. This phenomenon has been observed after focal or global ischemia in different animal models. However, the hypothesis that bacterial infection might lead to neuronal tolerance to injury has not been investigated. To mimic cerebral bacterial infection, we injected bacterial lipopolysaccharide (LPS) in the right dorsal hippocampus, followed 24 hours later by an excitotoxic lesion using kainic acid in the mouse model. Quantification of lesion size after cresyl violet counterstaining revealed that LPS pretreatment afforded neuroprotection to CA3 neurons against KA challenge. To investigate the events underlying this protection, we studied the cytokine profile induced after LPS injection. Interleukin (IL)-1␤ and transforming growth factor beta 1 (TGF-␤1) were the main cytokines expressed at 24 hours after LPS injection. Because IL-1␤ has been described as deleterious in acute injury, we decided to investigate the function of TGF-␤1. An adenovirus expressing a constitutively active form of TGF-␤1 was injected intracerebrally 1 week before the induction of excitotoxic lesion, and neuronal protection was observed. To confirm the neuroprotective role of TGF-␤1, the TGF-␤1 adenovirus was replaced by recombinant human TGF-␤1 protein and total neuroprotection was observed. Furthermore, the antibodymediated blocking of TGF-␤1 action prevented the protective effect of pretreatment with LPS. We have demonstrated in vivo that the cerebral tolerance phenomenon induced by LPS pretreatment is mediated by TGF-␤1 cytokine.

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“…This tolerance is closely related to an increase in the cerebral endogenous antioxidant defense, a mechanism that might contribute to the neuroprotection observed against focal ischemia in our conditions. Because normobaric hypoxia (9% O 2 , 8 hours) has been reported to induce tolerance against kainate-induced seizures (Pohle and Rauca, 1994), one might suppose that the mechanisms of hypoxic preconditioning involve a reduction of the excitotoxic events during focal ischemia. Such a hypothesis has already been suggested for other models of ischemic tolerance (Douen et al, 2000).…”

Section: Bernaudin Et Al 398mentioning

confidence: 99%

Normobaric Hypoxia Induces Tolerance to Focal Permanent Cerebral Ischemia in Association with an Increased Expression of Hypoxia-Inducible Factor-1 and its Target Genes, Erythropoietin and VEGF, in the Adult Mouse Brain

Bernaudin

Nedelec

Divoux

et al. 2002

J Cereb Blood Flow Metab

327

272

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Summary:Tolerance to cerebral ischemia is achieved by preconditioning sublethal stresses, such as ischemia or hypoxia, paradigms in which the decrease of O 2 availability may constitute an early signal inducing tolerance. In accordance with this concept, this study shows that hypoxia induces tolerance against focal permanent ischemia in adult mice. Normobaric hypoxia (8% O 2 of 1-hour, 3-hour, or 6-hour duration), performed 24 hours before ischemia, reduces infarct volume by approximately 30% when compared with controls. To elucidate the mechanisms underlying this neuroprotection, the authors investigated the effects of preconditioning on cerebral expression of hypoxia-inducible factor-1␣ (HIF-1␣) and its target genes, erythropoietin and vascular endothelial growth factor (VEGF). Hypoxia, whatever its duration (1 hour, 3 hours, 6 hours), rapidly increases the nuclear content of HIF-1␣ as well as the mRNA levels of erythropoietin and VEGF. Furthermore, erythropoietin and VEGF are upregulated at the protein level 24 hours after 6 hours of hypoxia. The authors' findings show that (1) hypoxia elicits a delayed, short-lasting (<72 hours) tolerance to focal permanent ischemia in the adult mouse brain; (2) HIF-1 target genes could contribute to the establishment of tolerance; and (3) this model might be a useful paradigm to further study the mechanisms of ischemic tolerance, to identify new therapeutic targets for stroke.

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Hypoxia protects against the neurotoxicity of kainic acid

Cited by 44 publications

References 21 publications

Decreased neuron loss and memory dysfunction in pilocarpine-treated rats pre-exposed to hypoxia

Decreased neuron loss and memory dysfunction in pilocarpine-treated rats pre-exposed to hypoxia

Transforming Growth Factor-β1-Mediated Neuroprotection against Excitotoxic Injuryin Vivo

Normobaric Hypoxia Induces Tolerance to Focal Permanent Cerebral Ischemia in Association with an Increased Expression of Hypoxia-Inducible Factor-1 and its Target Genes, Erythropoietin and VEGF, in the Adult Mouse Brain

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