Opioids modulate post-ischemic progression in a rat model of stroke

Kao, Tsung-Kuei; Ou, Yen‐Chuan; Liao, Su‐Lan; Chen, Wenying; Wang, Chun-Chiang; Chen, Shih‐Yun; Chiang, An-Na; Chen, Chun‐Jung

doi:10.1016/j.neuint.2008.01.007

Cited by 43 publications

(29 citation statements)

References 45 publications

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“…The up-regulation of pDYN mRNA by MDMA not only confirm the contribution of DYN to the effects of drugs of abuse but also the already suggested neuroprotective role for this peptide (Kao et al 2008;Liu et al 2001). Taking into account that MDMA is both a widely abused recreational drug and a neurotoxin, the CREB activation here observed following MDMA appears to be relevant in this context.…”

Section: Discussionsupporting

confidence: 78%

Regulation of opioid gene expression in the rat brainstem by 3,4-methylenedioxymethamphetamine (MDMA): role of serotonin and involvement of CREB and ERK cascade

Benedetto

Candia

D’Addario

et al. 2010

Naunyn-Schmied Arch Pharmacol

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The amphetamine analogue 3,4-methylendioxymetamphetamine (MDMA, Ecstasy) causes complex adaptations at the molecular and cellular levels altering the activity of different brain neurotransmitters. The present study aims to verify the effects of single and repeated injections of MDMA on dynorphin and nociceptin systems gene regulation in the brainstem, an area rich in neurons containing serotonin. Both acute and chronic (twice a day for 7 days) MDMA (8 mg/kg) induced a marked increase in prodynorphin mRNA levels as well as in cAMP response element-binding protein (CREB) and extracellular signal-regulated kinase-1/2 (ERK1/2) phosphorylation, without causing any effect on kappa opioid receptor or nociceptin system (both pronociceptin and its receptor) genes expression, in this brain region. The blockade of 5HT1/5HT2 receptors by methysergide abolished the acute MDMA-induced increase in prodynorphin. Moreover, the concomitant chronic administration of both methysergide and MDMA (7 days) induced a significant increase in all the dynorphin or nociceptin system genes expression and in CREB and ERK phosphorylation. Our data suggest the involvement of dynorphin in the effects evoked by MDMA in the brainstem, possibly via CREB and ERK1/2 cascade activation, since the ERK inhibitor PD98059 prevented the MDMA-induced prodynorphin gene expression, and, acutely, also through the involvement of serotoninergic mechanisms. Chronically, it is also possible to hypothesize a general inhibitor role of serotonin in the effects evoked by MDMA. Moreover, these findings strengthen the hypothesis, already proposed, of a neuroprotective role for both CREB and dynorphin.

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Section: Discussionsupporting

confidence: 78%

Regulation of opioid gene expression in the rat brainstem by 3,4-methylenedioxymethamphetamine (MDMA): role of serotonin and involvement of CREB and ERK cascade

Benedetto

Candia

D’Addario

et al. 2010

Naunyn-Schmied Arch Pharmacol

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“…For example, the reason that μ-ligands had little protective effect on hippocampal neurons (Iwai wt al, 1992) is likely because of low density of DOR in the hippocampus,, while the cause of high-dose μ-ligand induced reduction of neuroexcitotoxicity in cortical neurons (Choi and Viseskul, 1988) might be attributed to activation of DOR that are highly expressed in the cortex. Indeed, recent studies from other independent laboratories demonstrated that DOR is neuroprotective against hypoxic/ischemic stress (Borlongan et al, 2004, 2009; Horiuchi et al, 2004, 2008; Lim et al, 2004; Zhao et al, 2006; Su et al, 2007;Iwato et al, 2007; Xiong et al, 2007; Charron et al, 2008; Kao et al, 2008; Govindaswami et al, 2008; Pamenter and Buck, 2008; Tian et al, 2008a, 2008b; Peng et al, 2009; Zhu et al, 2009) (Table 3). For example, in a rodent model of stroke, up-regulation of DOR expression, and peripherally/centrally administration of DOR agonists (DADLE, DPDPE,TAN-67,Deltorphin-D variant, BW373U86) significantly reduce the infarct volume, attenuate neurological deficits and neuronal loss, and increase neuron survival in post-ischemia in the brain, particularly in the cortex and hippocampus, which can be abolished by DOR antagonist naltrindole (Borlongan et al, 2004, 2009; Su et al, 2007;Iwato et al, 2007; Xiong et al, 2007; Charron et al, 2008; Kao et al, 2008; Govindaswami et al, 2008; Tian et al, 2008a, 2008b).…”

Section: Effect Of Dor Activation On Hypoxic/ischemic Disruption Omentioning

confidence: 99%

“…Opioid receptors belong to classical G protein-coupled receptor superfamily (Raynor et al, 1994; Law et al, 2000;). Recent studies, especially those from our laboratory, have demonstrated that activation of opioid receptors, particularly DOR, is neuroprotective against hypoxic/ischemic insults and DOR activity may be one of the key factors to determine neuronal survival during hypoxic/ischemic as well as excitotoxic stress (Zhang et al, 2000, 2002, 2006; Borlongan et al, 2004, 2009; Horiuchi et al, 2004, 2008; Lim et al, 2004; Ma et al, 2005; Zhao et al, 2006; Su et al, 2007; Xiong et al, 2007; Iwata et al, 2007; Charron et al, 2008; Govindaswami et al, 2008; Kao et al, 2008; Pamenter and Buck, 2008; Tian et al, 2008a, 2008b; Peng et al, 2009; Zhu et al, 2009; Yang et al, 2009). Early evidence suggested that opioids may alter ionic transportation across the membrane in normoxic conditions (North et al, 1987; Fan et al, 1991, 1993; Piros et al, 1996).…”

Section: Introductionmentioning

confidence: 98%

Ionic storm in hypoxic/ischemic stress: Can opioid receptors subside it?

Chao

Xia

2010

Progress in Neurobiology

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Neurons in the mammalian central nervous system are extremely vulnerable to oxygen deprivation and blood supply insufficiency. Indeed, hypoxic/ischemic stress triggers multiple pathophysiological changes in the brain, forming the basis of hypoxic/ischemic encephalopathy. One of the initial and crucial events induced by hypoxia/ischemia is the disruption of ionic homeostasis characterized by enhanced K + efflux and Na + -, Ca 2+ -and Cl − influx, which causes neuronal injury or even death. Recent data from our laboratory and those of others have shown that activation of opioid receptors, particularly δ-opioid receptors (DOR), is neuroprotective against hypoxic/ischemic insult. This protective mechanism may be one of the key factors that determine neuronal survival under hypoxic/ ischemic condition. An important aspect of the DOR-mediated neuroprotection is its action against hypoxic/ischemic disruption of ionic homeostasis. Specially, DOR signal inhibits Na + influx through the membrane and reduces the increase in intracellular Ca 2+ , thus decreasing the excessive leakage of intracellular K + . Such protection is dependent on a PKC-dependent and PKA-independent signaling pathway. Furthermore, our novel exploration shows that DOR attenuates hypoxic/ischemic disruption of ionic homeostasis through the inhibitory regulation of Na + channels. In this review, we will first update current information regarding the process and features of hypoxic/ischemic disruption of ionic homeostasis and then discuss the opioid-mediated regulation of ionic homeostasis, especially in hypoxic/ischemic condition, and the underlying mechanisms.

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“…Moreover, in addition to safety, anesthesia of experimental stroke models has to be free of neuroprotective effect in order to avoid bias in the neuroprotection studies. Finally, for ethical reasons, the ideal anesthetic should provide postoperative analgesia since analgesics cannot be used in stroke model because of their potent neuroprotective action [1, 2]. …”

Section: Introductionmentioning

confidence: 99%

Evidence for the Use of Isoflurane as a Replacement for Chloral Hydrate Anesthesia in Experimental Stroke: An Ethical Issue

Pétrault

Ouk

Lachaud

et al. 2014

BioMed Research International

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Since an ethical issue has been raised regarding the use of the well-known anesthetic agent chloral hydrate, owing to its mutagenic and carcinogenic effects in animals, attention of neuroscientists has turned to finding out an alternative agent able to meet not only potency, safety, and analgesic efficacy, but also reduced neuroprotective effect for stroke research. The aim of this study was to compare the potential of chloral hydrate and isoflurane for both modulating the action of the experimental neuroprotectant MK801 and exerting analgesia. After middle cerebral artery occlusion in rats, no difference was observed in 24 h survival rate, success of ischemia, or infarct volume reduction between both anesthetics. However, isoflurane exerted a more pronounced analgesic effect than chloral hydrate as evidenced by formalin test 3 hours after anesthesia onset, thus encouraging the use of isoflurane in experimental stroke models.

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Opioids modulate post-ischemic progression in a rat model of stroke

Cited by 43 publications

References 45 publications

Regulation of opioid gene expression in the rat brainstem by 3,4-methylenedioxymethamphetamine (MDMA): role of serotonin and involvement of CREB and ERK cascade

Regulation of opioid gene expression in the rat brainstem by 3,4-methylenedioxymethamphetamine (MDMA): role of serotonin and involvement of CREB and ERK cascade

Ionic storm in hypoxic/ischemic stress: Can opioid receptors subside it?

Evidence for the Use of Isoflurane as a Replacement for Chloral Hydrate Anesthesia in Experimental Stroke: An Ethical Issue

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