The role of opioid receptors in hypoxic preconditioning against seizures in brain

Rubaj, Andrzej; Gustaw, Katarzyna; Zgodziński, Witold; Kleinrok, Z; Sieklucka-Dziuba, M

doi:10.1016/s0091-3057(00)00294-x

Cited by 25 publications

(14 citation statements)

References 30 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: Introductionmentioning

confidence: 74%

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: Introductionmentioning

confidence: 74%

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

et al. 2016

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“…24 h before pentylenetetrazolinduced seizure could attenuate the seizure, but the protection was not present with morphine at 5 and 75 mg/kg in the mice [19] . Therefore, in this study we used fentanyl 200 g/kg because this dose is equipotent to morphine 20 mg/kg that was in the middle of the effective doses of preconditioning in the above morphine preconditioning study [20] .…”

Section: Discussionmentioning

confidence: 89%

Effects of Fentanyl Pretreatment on Regional Cerebral Blood Flow in Focal Cerebral Ischemia in Rats

Z.¹,

Hunter

Liu

et al. 2010

Pharmacology

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Background:There are reports that opioid preconditioning induces opioid-receptor-dependent neuroprotection against cerebral ischemia. This experiment was performed to test whether pretreatment with fentanyl, a synthetic primary µ-opioid receptor agonist, would affect the regional cerebral blood flow (rCBF) in focal cerebral ischemia in rats. Methods: Twenty-four hours before permanent and unilateral middle cerebral artery (MCA) occlusion, rats were pretreated with normal saline, 200 µg/kg of fentanyl i.p. or 500 µg/kg of fentanyl i.p. The rats were anesthetized with isoflurane and were mechanically ventilated to cannulate the vessels and to occlude MCA. One hour after MCA occlusion, the rCBF was measured using ¹⁴C-iodoantipyrine. Results: The cortical rCBF decreased 1 h after MCA occlusion in all the experimental groups. In the ischemic cortex, the rCBF of the rats treated with 500 µg/kg of fentanyl was significantly greater (+80%, p < 0.05) than that of the control animals. The rCBF of the ischemic cortex of the rats treated with fentanyl 200 µg/kg seemed higher than in the control animals, but the difference was not statistically significant. The rCBF was similar in the nonischemic brain regions such as the contralateral cortex or pons among the experimental groups. Conclusion: Our data demonstrated that pretreatment with fentanyl improved the rCBF in the focal ischemic area without change in rCBF in the nonischemic cortex. Our data suggest that fentanyl could be effective in improving the rCBF in the focal ischemic area when used as a preconditioning agent and that improvement of rCBF could be one of the contributing factors of neuroprotection by opioid preconditioning.

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“…The dose of naloxone was based on those in published studies. 16 In other animals, the IPC event was replaced by the administration of the opioid receptor agonist morphine (0.01-10 mg/kg IP). In the morphinetreated animals, ischemic retinal injury was created in one eye by again raising the IOP above systolic blood pressure for 45 minutes, 24 hours after morphine administration.…”

Section: Methodsmentioning

confidence: 99%

“…13,14 There is a growing body of evidence from studies of the heart and brain supporting the idea that activation of the opioid system plays a central role in IPC and that the nonselective opioid antagonist naloxone can prevent the development of preconditioning in these tissues. [15][16][17][18] In other organs, activation of opioid receptors by an exogenous agonist (opioid preconditioning) has been shown to elicit a protective effect during situations of stress produced by hypoxia, ischemia, cold, or an acidic environment. 8,[17][18][19][20][21] Activation of opioid receptors reduced infarct size in stroke and myocardial ischemia models.…”

mentioning

confidence: 99%

Opioid Receptor-Activation: Retina Protected from Ischemic Injury

Husain

Potter

Crosson

2009

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.In nonocular systems, activation of opioid receptors has been shown to ameliorate tissue damage induced by ischemic stress. The current study was an investigation of whether opioid receptors activated by endogenous or exogenous agonists can ameliorate ischemic retinal injury. METHODS. In an investigation of whether endogenous opioid receptor-activation reduces ischemic injury, the effects of the opioid antagonist naloxone (3 mg/kg; IP) on retinal neuroprotection induced by ischemic preconditioning (IPC) were evaluated. Whether exogenous opioid administration can reduce ischemic retinal injury was determined by pretreating rats with morphine (0.01-10 mg/kg) before injury. Morphometric and electroretinogram (ERG) analyses were used to assess the differences in retinal structure and function. The expression of opioid receptor subtypes was evaluated by Western blot and immunohistochemical analyses. RESULTS. In control animals, 7 days after ischemic retinal injury, ERG a-and b-wave amplitudes were significantly reduced (23% and 41%, respectively). In addition, degeneration of the inner retina resulted in a 34% reduction in overall retina thickness. In animals receiving IPC before ischemic injury, ERG wave forms and retinal morphology were preserved. Pretreatment with naloxone reversed both the functional and structural retinal protection induced by IPC. In animals treated with morphine 24-hours before ischemic injury, ERG waveforms were preserved in a dose-dependent fashion (ED 50 ϭ 0.18 mg/kg), and this protective response was reversed by naloxone pretreatment. Immunohistochemical and Western blot data demonstrated that the ␦-, -, and -opioid receptor subtypes are expressed in the retina. CONCLUSIONS. These data provide evidence that activation of one (or more) opioid receptor(s) facilitates the development of IPC within the retina and can reduce ischemic retina injury.

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The role of opioid receptors in hypoxic preconditioning against seizures in brain

Cited by 25 publications

References 30 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

Effects of Fentanyl Pretreatment on Regional Cerebral Blood Flow in Focal Cerebral Ischemia in Rats

Opioid Receptor-Activation: Retina Protected from Ischemic Injury

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