The Experts below are selected from a list of 72 Experts worldwide ranked by ideXlab platform

Raymond C. Koehler - One of the best experts on this subject based on the ideXlab platform.

  • neuroprotective effect of acid sensing ion channel inhibitor psalmotoxin 1 after Hypoxia ischemia in Newborn piglet striatum
    Neurobiology of Disease, 2011
    Co-Authors: Zeng Jin Yang, Erin L. Carter, Kathleen K. Kibler, Lee J. Martin, Raymond C. Koehler
    Abstract:

    Abstract Na+,Ca2+-permeable acid-sensing ion channel 1a (ASIC1a) is involved in the pathophysiologic process of adult focal brain ischemia. However, little is known about its role in the pathogenesis of global cerebral ischemia or Newborn Hypoxia–ischemia (H–I). Here, using a Newborn piglet model of asphyxia-induced cardiac arrest, we investigated the effect of ASIC1a-specific blocker psalmotoxin-1 on neuronal injury. During asphyxia and the first 30 min of recovery, brain tissue pH fell below 7.0, the approximate activation pH of ASIC1a. Psalmotoxin-1 injection at 20 min before Hypoxia, but not at 20 min of recovery, partially protected the striatonigral and striatopallidal neurons in putamen. Psalmotoxin-1 pretreatment largely attenuated the increased protein kinase A-dependent phosphorylation of DARPP-32 and N-methyl- d -aspartate (NMDA) receptor NR1 subunit and decreased nitrative and oxidative damage to proteins at 3 h of recovery. Pretreatment with NMDA receptor antagonist MK-801 also provided partial neuroprotection in putamen, and combined pretreatment with psalmotoxin-1 and MK-801 yielded additive neuroprotection. These results indicate that ASIC1a activation contributes to neuronal death in Newborn putamen after H–I through mechanisms that may involve protein kinase A-dependent phosphorylation of NMDA receptor and nitrative and oxidative stress.

  • Neuroprotective effect of acid-sensing ion channel inhibitor psalmotoxin-1 after Hypoxia–ischemia in Newborn piglet striatum
    Neurobiology of disease, 2011
    Co-Authors: Zeng Jin Yang, Erin L. Carter, Kathleen K. Kibler, Lee J. Martin, Raymond C. Koehler
    Abstract:

    Abstract Na+,Ca2+-permeable acid-sensing ion channel 1a (ASIC1a) is involved in the pathophysiologic process of adult focal brain ischemia. However, little is known about its role in the pathogenesis of global cerebral ischemia or Newborn Hypoxia–ischemia (H–I). Here, using a Newborn piglet model of asphyxia-induced cardiac arrest, we investigated the effect of ASIC1a-specific blocker psalmotoxin-1 on neuronal injury. During asphyxia and the first 30 min of recovery, brain tissue pH fell below 7.0, the approximate activation pH of ASIC1a. Psalmotoxin-1 injection at 20 min before Hypoxia, but not at 20 min of recovery, partially protected the striatonigral and striatopallidal neurons in putamen. Psalmotoxin-1 pretreatment largely attenuated the increased protein kinase A-dependent phosphorylation of DARPP-32 and N-methyl- d -aspartate (NMDA) receptor NR1 subunit and decreased nitrative and oxidative damage to proteins at 3 h of recovery. Pretreatment with NMDA receptor antagonist MK-801 also provided partial neuroprotection in putamen, and combined pretreatment with psalmotoxin-1 and MK-801 yielded additive neuroprotection. These results indicate that ASIC1a activation contributes to neuronal death in Newborn putamen after H–I through mechanisms that may involve protein kinase A-dependent phosphorylation of NMDA receptor and nitrative and oxidative stress.

Ertugrul Kilic - One of the best experts on this subject based on the ideXlab platform.

  • Normobaric oxygen treatment improves neuronal survival functional recovery and axonal plasticity after Newborn Hypoxia-ischemia.
    Behavioural brain research, 2019
    Co-Authors: Taha Kelestemur, Mustafa Caglar Beker, Ahmet B. Caglayan, Berrak Caglayan, Serdar Altunay, Selim Kutlu, Ertugrul Kilic
    Abstract:

    Abstract Background Newborn Hypoxia ischemia (HI) is one of the most prevalent cases in the emergency and can result from fetal Hypoxia during delivery. In HI, restricted blood supply to the fetal brain may cause epilepsy or mental disorders. Methods In the present study, seven-day-old pups were subjected HI and treated with different normobaric oxygen (NBO) concentrations (21%, 70% or 100%). In the acute phase, we analyzed infarct area, disseminate neuronal injury and surviving neurons. In addition, we studied the regulation of PTEN and MMP-9 proteins which were suggested to be activated by HI in the ischemic tissue. Moreover, long-term effects of NBO treatments were evaluated with open field, rotarod and Barnes maze tests. We also examined axonal plasticity with EGFP-AAV injection. Results Here, we demonstrate that hyperoxic NBO concentration causes an increase in cellular survival and a decrease in the number of apoptotic cells, meanwhile inhibiting the proteins involved in cellular death mechanisms. Moreover, we found that hyperoxia decreases anxiety, promotes motor coordination and improve spatial learning and memory. Notably that axonal sprouting was promoted by hyperoxia. Conclusion Our data suggest that NBO is a promising approach for the treatment of Newborn HI, which encourage proof-of-concept studies in Newborn.

Zeng Jin Yang - One of the best experts on this subject based on the ideXlab platform.

  • neuroprotective effect of acid sensing ion channel inhibitor psalmotoxin 1 after Hypoxia ischemia in Newborn piglet striatum
    Neurobiology of Disease, 2011
    Co-Authors: Zeng Jin Yang, Erin L. Carter, Kathleen K. Kibler, Lee J. Martin, Raymond C. Koehler
    Abstract:

    Abstract Na+,Ca2+-permeable acid-sensing ion channel 1a (ASIC1a) is involved in the pathophysiologic process of adult focal brain ischemia. However, little is known about its role in the pathogenesis of global cerebral ischemia or Newborn Hypoxia–ischemia (H–I). Here, using a Newborn piglet model of asphyxia-induced cardiac arrest, we investigated the effect of ASIC1a-specific blocker psalmotoxin-1 on neuronal injury. During asphyxia and the first 30 min of recovery, brain tissue pH fell below 7.0, the approximate activation pH of ASIC1a. Psalmotoxin-1 injection at 20 min before Hypoxia, but not at 20 min of recovery, partially protected the striatonigral and striatopallidal neurons in putamen. Psalmotoxin-1 pretreatment largely attenuated the increased protein kinase A-dependent phosphorylation of DARPP-32 and N-methyl- d -aspartate (NMDA) receptor NR1 subunit and decreased nitrative and oxidative damage to proteins at 3 h of recovery. Pretreatment with NMDA receptor antagonist MK-801 also provided partial neuroprotection in putamen, and combined pretreatment with psalmotoxin-1 and MK-801 yielded additive neuroprotection. These results indicate that ASIC1a activation contributes to neuronal death in Newborn putamen after H–I through mechanisms that may involve protein kinase A-dependent phosphorylation of NMDA receptor and nitrative and oxidative stress.

  • Neuroprotective effect of acid-sensing ion channel inhibitor psalmotoxin-1 after Hypoxia–ischemia in Newborn piglet striatum
    Neurobiology of disease, 2011
    Co-Authors: Zeng Jin Yang, Erin L. Carter, Kathleen K. Kibler, Lee J. Martin, Raymond C. Koehler
    Abstract:

    Abstract Na+,Ca2+-permeable acid-sensing ion channel 1a (ASIC1a) is involved in the pathophysiologic process of adult focal brain ischemia. However, little is known about its role in the pathogenesis of global cerebral ischemia or Newborn Hypoxia–ischemia (H–I). Here, using a Newborn piglet model of asphyxia-induced cardiac arrest, we investigated the effect of ASIC1a-specific blocker psalmotoxin-1 on neuronal injury. During asphyxia and the first 30 min of recovery, brain tissue pH fell below 7.0, the approximate activation pH of ASIC1a. Psalmotoxin-1 injection at 20 min before Hypoxia, but not at 20 min of recovery, partially protected the striatonigral and striatopallidal neurons in putamen. Psalmotoxin-1 pretreatment largely attenuated the increased protein kinase A-dependent phosphorylation of DARPP-32 and N-methyl- d -aspartate (NMDA) receptor NR1 subunit and decreased nitrative and oxidative damage to proteins at 3 h of recovery. Pretreatment with NMDA receptor antagonist MK-801 also provided partial neuroprotection in putamen, and combined pretreatment with psalmotoxin-1 and MK-801 yielded additive neuroprotection. These results indicate that ASIC1a activation contributes to neuronal death in Newborn putamen after H–I through mechanisms that may involve protein kinase A-dependent phosphorylation of NMDA receptor and nitrative and oxidative stress.

Taha Kelestemur - One of the best experts on this subject based on the ideXlab platform.

  • Normobaric oxygen treatment improves neuronal survival functional recovery and axonal plasticity after Newborn Hypoxia-ischemia.
    Behavioural brain research, 2019
    Co-Authors: Taha Kelestemur, Mustafa Caglar Beker, Ahmet B. Caglayan, Berrak Caglayan, Serdar Altunay, Selim Kutlu, Ertugrul Kilic
    Abstract:

    Abstract Background Newborn Hypoxia ischemia (HI) is one of the most prevalent cases in the emergency and can result from fetal Hypoxia during delivery. In HI, restricted blood supply to the fetal brain may cause epilepsy or mental disorders. Methods In the present study, seven-day-old pups were subjected HI and treated with different normobaric oxygen (NBO) concentrations (21%, 70% or 100%). In the acute phase, we analyzed infarct area, disseminate neuronal injury and surviving neurons. In addition, we studied the regulation of PTEN and MMP-9 proteins which were suggested to be activated by HI in the ischemic tissue. Moreover, long-term effects of NBO treatments were evaluated with open field, rotarod and Barnes maze tests. We also examined axonal plasticity with EGFP-AAV injection. Results Here, we demonstrate that hyperoxic NBO concentration causes an increase in cellular survival and a decrease in the number of apoptotic cells, meanwhile inhibiting the proteins involved in cellular death mechanisms. Moreover, we found that hyperoxia decreases anxiety, promotes motor coordination and improve spatial learning and memory. Notably that axonal sprouting was promoted by hyperoxia. Conclusion Our data suggest that NBO is a promising approach for the treatment of Newborn HI, which encourage proof-of-concept studies in Newborn.

Erin L. Carter - One of the best experts on this subject based on the ideXlab platform.

  • neuroprotective effect of acid sensing ion channel inhibitor psalmotoxin 1 after Hypoxia ischemia in Newborn piglet striatum
    Neurobiology of Disease, 2011
    Co-Authors: Zeng Jin Yang, Erin L. Carter, Kathleen K. Kibler, Lee J. Martin, Raymond C. Koehler
    Abstract:

    Abstract Na+,Ca2+-permeable acid-sensing ion channel 1a (ASIC1a) is involved in the pathophysiologic process of adult focal brain ischemia. However, little is known about its role in the pathogenesis of global cerebral ischemia or Newborn Hypoxia–ischemia (H–I). Here, using a Newborn piglet model of asphyxia-induced cardiac arrest, we investigated the effect of ASIC1a-specific blocker psalmotoxin-1 on neuronal injury. During asphyxia and the first 30 min of recovery, brain tissue pH fell below 7.0, the approximate activation pH of ASIC1a. Psalmotoxin-1 injection at 20 min before Hypoxia, but not at 20 min of recovery, partially protected the striatonigral and striatopallidal neurons in putamen. Psalmotoxin-1 pretreatment largely attenuated the increased protein kinase A-dependent phosphorylation of DARPP-32 and N-methyl- d -aspartate (NMDA) receptor NR1 subunit and decreased nitrative and oxidative damage to proteins at 3 h of recovery. Pretreatment with NMDA receptor antagonist MK-801 also provided partial neuroprotection in putamen, and combined pretreatment with psalmotoxin-1 and MK-801 yielded additive neuroprotection. These results indicate that ASIC1a activation contributes to neuronal death in Newborn putamen after H–I through mechanisms that may involve protein kinase A-dependent phosphorylation of NMDA receptor and nitrative and oxidative stress.

  • Neuroprotective effect of acid-sensing ion channel inhibitor psalmotoxin-1 after Hypoxia–ischemia in Newborn piglet striatum
    Neurobiology of disease, 2011
    Co-Authors: Zeng Jin Yang, Erin L. Carter, Kathleen K. Kibler, Lee J. Martin, Raymond C. Koehler
    Abstract:

    Abstract Na+,Ca2+-permeable acid-sensing ion channel 1a (ASIC1a) is involved in the pathophysiologic process of adult focal brain ischemia. However, little is known about its role in the pathogenesis of global cerebral ischemia or Newborn Hypoxia–ischemia (H–I). Here, using a Newborn piglet model of asphyxia-induced cardiac arrest, we investigated the effect of ASIC1a-specific blocker psalmotoxin-1 on neuronal injury. During asphyxia and the first 30 min of recovery, brain tissue pH fell below 7.0, the approximate activation pH of ASIC1a. Psalmotoxin-1 injection at 20 min before Hypoxia, but not at 20 min of recovery, partially protected the striatonigral and striatopallidal neurons in putamen. Psalmotoxin-1 pretreatment largely attenuated the increased protein kinase A-dependent phosphorylation of DARPP-32 and N-methyl- d -aspartate (NMDA) receptor NR1 subunit and decreased nitrative and oxidative damage to proteins at 3 h of recovery. Pretreatment with NMDA receptor antagonist MK-801 also provided partial neuroprotection in putamen, and combined pretreatment with psalmotoxin-1 and MK-801 yielded additive neuroprotection. These results indicate that ASIC1a activation contributes to neuronal death in Newborn putamen after H–I through mechanisms that may involve protein kinase A-dependent phosphorylation of NMDA receptor and nitrative and oxidative stress.