KATP channel openers, adenosine agonists and epileptic preconditioning are stress signals inducing hippocampal neuroprotection

Blondeau, Nicolas; Plamondon, Hélène; Richelme, Christian; Heurteaux, Catherine; Lazdunski, Michel

doi:10.1016/s0306-4522(00)00304-3

Cited by 108 publications

(69 citation statements)

References 58 publications

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“…Involvement of K ATP channels in development of tolerance to forebrain ischemia has been reported, and the neuroprotective effect was abolished or mimicked by a nonselective K ATP channel blocker (glibenclamide) (Heurteaux et al, 1995) or opener (cromakalim) (Blondeau et al, 2000). To our knowledge, the present study is the first to suggest the crucial role of mitochondrial K ATP channel activation during focal cerebral ischemia in acquisition of tolerance.…”

Section: Fig 2 Effects Of Ischemic Preconditioning (30-minute Middlsupporting

confidence: 59%

Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Yoshida

Nakakimura

Cui

et al. 2004

J Cereb Blood Flow Metab

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Summary:Involvement of adenosine and adenosine triphosphate-sensitive potassium (K ATP ) channels in the development of ischemic tolerance has been suggested in global ischemia, but has not been studied extensively in focal cerebral ischemia. This study evaluated modulating effects of adenosine A 1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) and mitochondrial K ATP channel blocker 5HD (5-hydroxydecanoate) on the development of tolerance to focal cerebral ischemia in rats. Preconditioning with 30-minute middle cerebral artery occlusion (MCAO) reduced cortical and subcortical infarct volume following 120-minute MCAO (test ischemia) given 72 hours later. The neuroprotective effect of preconditioning was attenuated by 0.1 mg/kg DPCPX given before conditioning ischemia (30-minute MCAO), but no influence was provoked when it was administered before test ischemia. DPCPX had no effect on infarct volume after conditioning or test ischemia when given alone. The preconditioning-induced neuroprotection disappeared when 30 mg/kg 5HD was administered before test ischemia. These results suggest a possible involvement of adenosine A 1 receptors during conditioning ischemia and of mitochondrial K ATP channels during subsequent severe ischemia in the development of tolerance to focal cerebral ischemia.

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Section: Fig 2 Effects Of Ischemic Preconditioning (30-minute Middlsupporting

confidence: 59%

Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Yoshida

Nakakimura

Cui

et al. 2004

J Cereb Blood Flow Metab

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“…Activation of the plasmalemmal K ATP channels hyperpolarizes neurons (Figure 3) and may stabilize the resting membrane potential during ischemic insults and stress [125] , which, in turn, can protect neurons against neuronal damage and neurodegeneration that is caused by anoxic membrane depolarization and excitotoxicity [115,126] . Expression of K ATP channel Figure 3.…”

Section: K Atp Channels and Their Neuroprotective Role In Cerebral Ismentioning

confidence: 99%

Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia

Sun

Feng

2012

Acta Pharmacol Sin

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ATP-sensitive potassium (K ATP ) channels are weak, inward rectifiers that couple metabolic status to cell membrane electrical activity, thus modulating many cellular functions. An increase in the ADP/ATP ratio opens K ATP channels, leading to membrane hyperpolarization. K ATP channels are ubiquitously expressed in neurons located in different regions of the brain, including the hippocampus and cortex. Brief hypoxia triggers membrane hyperpolarization in these central neurons. In vivo animal studies confirmed that knocking out the Kir6.2 subunit of the K ATP channels increases ischemic infarction, and overexpression of the Kir6.2 subunit reduces neuronal injury from ischemic insults. These findings provide the basis for a practical strategy whereby activation of endogenous K ATP channels reduces cellular damage resulting from cerebral ischemic stroke. K ATP channel modulators may prove to be clinically useful as part of a combination therapy for stroke management in the future.

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“…The exact mechanism underlying ischemic preconditioning (IPC)-induced tolerance remains unclear, although a number of possible induction pathways have been investigated, including, among others, neuroactive cytokines (Nawashiro et al, 1996;Ohtsuki et al, 1996), activation of glutamate receptors (Best et al, 1996;Pringle et al, 1996), adenosine receptors, the ATP-sensitive potassium channel (K ϩ ATP ) (Heurteaux et al, 1995;Perez-Pinzon et al, 1996Riepe et al, 1997;Blondeau et al, 2000), nitric oxide (Caggiano and Kraig, 1998;Centeno et al, 1999;GonzalezZulueta et al, 2000), oxidative stress (Ohtsuki et al, 1992), hypothermia (Nishio et al, 2000), and hyperthermia (Chopp et al, 1989;Rordorff et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

εPKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice

et al. 2003

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Glutamate receptors and calcium have been implicated as triggering factors in the induction of tolerance by ischemic preconditioning (IPC) in the brain. However, little is known about the signal transduction pathway that ensues after the IPC induction pathway. The main goals of the present study were to determine whether NMDA induces preconditioning via a calcium pathway and promotes translocation of the protein kinase C ⑀ (⑀PKC) isozyme and whether this PKC isozyme is key in the IPC signal transduction pathway. We corroborate here that IPC and a sublethal dose of NMDA were neuroprotective, whereas blockade of NMDA receptors during IPC diminished IPC-induced neuroprotection. Calcium chelation blocked the protection afforded by both NMDA and ischemic preconditioning significantly, suggesting a significant role of calcium. Pharmacological preconditioning with the nonselective PKC isozyme activator phorbol myristate acetate could not emulate IPC, but blockade of PKC activation with chelerythrine during IPC blocked its neuroprotection. These results suggested that there might be a dual involvement of PKC isozymes during IPC. This was corroborated when neuroprotection was blocked when we inhibited ⑀PKC during IPC and NMDA preconditioning, and IPC neuroprotection was emulated with the activator of ⑀PKC. The possible correlation between NMDA, Ca 2ϩ , and ⑀PKC was found when we emulated IPC with the diacylglycerol analog oleoylacetyl glycerol, suggesting an indirect pathway by which Ca 2ϩ could activate the calcium-insensitive ⑀PKC isozyme. These results demonstrated that the ⑀PKC isozyme played a key role in both IPC-and NMDA-induced tolerance.

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KATP channel openers, adenosine agonists and epileptic preconditioning are stress signals inducing hippocampal neuroprotection

Cited by 108 publications

References 58 publications

Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia

εPKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice

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KATP channel openers, adenosine agonists and epileptic preconditioning are stress signals inducing hippocampal neuroprotection

Cited by 108 publications

References 58 publications

Adenosine A1 Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Adenosine A1 Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia

εPKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice

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Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats

Adenosine A₁ Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats