The effect of dizocilpine and enadoline on immediate early gene expression in the gerbil global ischaemia model

Woodburn, V.L.; Hayward, Neil J.; Poat, Judith A.; Woodruff, G.N.; Hughes, J.

doi:10.1016/0028-3908(93)90070-j

Cited by 28 publications

(10 citation statements)

References 20 publications

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“…72,73 Early increased expression of zif268 has been demonstrated after ischemia. 37,69,74 The present study is the first demonstration of altered ischemia-induced early response gene expression in a model of PC. We do not have evidence of cellular or topographical localization of early response genes after focal stroke in the present study.…”

Section: Discussionmentioning

confidence: 99%

Ischemic Preconditioning and Brain Tolerance: Temporal Histological and Functional Outcomes, Protein Synthesis Requirement, and Interleukin-1 Receptor Antagonist and Early Gene Expression

Barone

White

Spera

et al. 1998

Stroke

450

251

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Background and Purpose-A short duration of ischemia (ie, ischemic preconditioning [PC]) can provide significant brain protection to subsequent ischemic events (ie, ischemic tolerance [IT]). The present series of studies was conducted to characterize the temporal pattern of a PC paradigm, to systematically evaluate the importance of protein synthesis in PC-induced IT, and to explore candidate gene expression changes associated with IT. Methods-Temporary middle cerebral artery occlusion (MCAO) (10 minutes) was used for PC. Various periods of reperfusion (ie, 2, 6, and 12 hours and 1, 2, 7, 14, and 21 days) were allowed after PC and before permanent MCAO (PMCAO) (nϭ7 to 9 per group) to establish IT compared with non-PC (sham-operated) rats (nϭ22). Infarct size, forelimb and hindlimb motor function, and cortical perfusion (laser-Doppler flowmetry; nϭ9 per group) were measured after PMCAO. The effects of the protein synthesis inhibitor cycloheximide administered just before PC (nϭ13 to 17) or administered long after PC but just before PMCAO (nϭ7 to 8) on IT were also determined. PC did not produce any significant brain injury, alter cortical blood flow after PMCAO, or produce contralateral cortical neuroprotection. Interleukin-1 receptor antagonist mRNA and protein expression were increased significantly (PϽ0.01) only during the IT period. PC rats also exhibited a significant (PϽ0.01) reduction in c-fos and zif268 mRNA expression after PMCAO. Conclusions-PC is a powerful inducer of ischemic brain tolerance as reflected by preservation of brain tissue and motor function. PC induces IT that is dependent on de novo protein synthesis. New protein(s) that occurs at the PC brain site 1 to 7 days after PC contributes to the neuroprotection. Those proteins that are produced after the more severe PMCAO in PC animals apparently do not contribute to IT. The PC-induced IT is also associated with increased expression of the neuroprotective protein interleukin-1 receptor antagonist and a reduced postischemic expression of the early response genes c-fos and zif268. (Stroke. 1998;29:1937-1951

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Section: Discussionmentioning

confidence: 99%

Ischemic Preconditioning and Brain Tolerance: Temporal Histological and Functional Outcomes, Protein Synthesis Requirement, and Interleukin-1 Receptor Antagonist and Early Gene Expression

Barone

White

Spera

et al. 1998

Stroke

450

251

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“…A number of studies have demonstrated neuroprotection by opioids in models of brain ischemia in whole animals (see Woodburn et al, 1993;Hayward et al, 1993). In many instances ischemia involves glutamate release and Ca 2+ uptake as crucial factors (Murphy and Horrocks, 1993).…”

Section: Discussionmentioning

confidence: 99%

Opioid Effects on ⁴⁵Ca²⁺ Uptake and Glutamate Release in Rat Cerebral Cortex in Primary Culture

Vlaskovska¹,

Schramm

Ingrid³

et al. 1997

Journal of Neurochemistry

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Primary cultures of rat cortex, conveniently prepared from newborn animals, were used to study opioid effects on 45Ca2+ uptake and glutamate release. 45Ca2+ uptake, induced by treatment with glutamate or NMDA, was largely blocked by the NMDA antagonist MK‐801. K+ depolarization‐induced 45Ca2+ uptake was also reduced by MK‐801, indicating that the effect was mediated by glutamate release. Direct analysis verified that glutamate, and aspartate, were indeed released. Opioid peptides of the prodynorphin system were also released and these, or other peptides, were functionally active, because naloxone treatment increased glutamate release, as well as the 45Ca2+ uptake induced by depolarization. Opioid agonists, selective for μ‐, κ‐, and δ‐receptors, inhibited the 45Ca2+ uptake induced by K+ depolarization. The combination of low concentrations of MK‐801 and opioid agonists resulted in additive inhibition of K+‐ induced 45Ca2+ uptake. The results indicate that this system may be useful as an in vitro CNS model for studying modulation by opioids of glutamate release and Ca2+ uptake under acute, and perhaps also chronic, opiate treatment.

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“…Analgesics were not administered post-operatively because of their influence or expected influence on inflammatory process and injury following HS and CA [27]–[33].…”

Section: Methodsmentioning

confidence: 99%

Resistance to Systemic Inflammation and Multi Organ Damage after Global Ischemia/Reperfusion in the Arctic Ground Squirrel

et al. 2014

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IntroductionCardiac arrest (CA) and hemorrhagic shock (HS) are two clinically relevant situations where the body undergoes global ischemia as blood pressure drops below the threshold necessary for adequate organ perfusion. Resistance to ischemia/reperfusion (I/R) injury is a characteristic of hibernating mammals. The present study sought to determine if arctic ground squirrels (AGS) are protected from systemic inflammation and multi organ damage after CA- or HS-induced global I/R and if, for HS, this protection is dependent upon their hibernation season.MethodsFor CA, rats and summer euthermic AGS (AGS-EU) were asphyxiated for 8 min, inducing CA. For HS, rats, AGS-EU, and winter interbout arousal AGS (AGS-IBA) were subject to HS by withdrawing blood to a mean arterial pressure of 35 mmHg and maintaining that pressure for 20 min before reperfusion with Ringers. For both I/R models, body temperature (Tb) was kept at 36.5–37.5°C. After reperfusion, animals were monitored for seven days (CA) or 3 hrs (HS) then tissues and blood were collected for histopathology, clinical chemistries, and cytokine level analysis (HS only). For the HS studies, additional groups of rats and AGS were monitored for three days after HS to access survival and physiological impairment.ResultsRats had increased serum markers of liver damage one hour after CA while AGS did not. For HS, AGS survived 72 hours after I/R whereas rats did not survive overnight. Additionally, only rats displayed an inflammatory response after HS. AGS maintained a positive base excess, whereas the base excess in rats was negative during and after hemorrhage.ConclusionsRegardless of season, AGS are resistant to organ damage, systemic inflammation, and multi organ damage after systemic I/R and this resistance is not dependent on their ability to become decrease Tb during insult but may stem from an altered acid/base and metabolic response during I/R.

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The effect of dizocilpine and enadoline on immediate early gene expression in the gerbil global ischaemia model

Cited by 28 publications

References 20 publications

Ischemic Preconditioning and Brain Tolerance: Temporal Histological and Functional Outcomes, Protein Synthesis Requirement, and Interleukin-1 Receptor Antagonist and Early Gene Expression

Ischemic Preconditioning and Brain Tolerance: Temporal Histological and Functional Outcomes, Protein Synthesis Requirement, and Interleukin-1 Receptor Antagonist and Early Gene Expression

Opioid Effects on ⁴⁵Ca²⁺ Uptake and Glutamate Release in Rat Cerebral Cortex in Primary Culture

Resistance to Systemic Inflammation and Multi Organ Damage after Global Ischemia/Reperfusion in the Arctic Ground Squirrel

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The effect of dizocilpine and enadoline on immediate early gene expression in the gerbil global ischaemia model

Cited by 28 publications

References 20 publications

Ischemic Preconditioning and Brain Tolerance: Temporal Histological and Functional Outcomes, Protein Synthesis Requirement, and Interleukin-1 Receptor Antagonist and Early Gene Expression

Ischemic Preconditioning and Brain Tolerance: Temporal Histological and Functional Outcomes, Protein Synthesis Requirement, and Interleukin-1 Receptor Antagonist and Early Gene Expression

Opioid Effects on 45Ca2+ Uptake and Glutamate Release in Rat Cerebral Cortex in Primary Culture

Resistance to Systemic Inflammation and Multi Organ Damage after Global Ischemia/Reperfusion in the Arctic Ground Squirrel

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Product

Resources

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Opioid Effects on ⁴⁵Ca²⁺ Uptake and Glutamate Release in Rat Cerebral Cortex in Primary Culture