Increased Expression of K < sub > Na < /sub > 1.2 Channel by MAPK Pathway Regulates Neuronal Activity Following Traumatic Brain Injury
Neurochem Res. 2023 Oct 25. doi: 10.1007/s11064-023-04044-1. Online ahead of print.ABSTRACTRecent studies have indicated that functional abnormalities in the KNa1.2 channel are linked to epileptic encephalopathies. However, the role of KNa1.2 channel in traumatic brain injury (TBI) remains limited. We collected brain tissue from the TBI mice and patients with post-traumatic epilepsy (PTE) to determine changes in KNa1.2 channel following TBI. We also investigated whether the MAPK pathway, which was activated by the released cytokines after injury, regulated KNa1.2 channel in in vitro. Finally, to elucidate the physiological...
Source: Neurochemical Research - October 24, 2023 Category: Neuroscience Authors: Ru Liu Lei Sun Xiaorui Shi Ci Li Xi Guo Yingting Wang Xiu Wang Kai Zhang Yongjun Wang Qun Wang Jianping Wu Source Type: research
Increased Expression of K < sub > Na < /sub > 1.2 Channel by MAPK Pathway Regulates Neuronal Activity Following Traumatic Brain Injury
Neurochem Res. 2023 Oct 25. doi: 10.1007/s11064-023-04044-1. Online ahead of print.ABSTRACTRecent studies have indicated that functional abnormalities in the KNa1.2 channel are linked to epileptic encephalopathies. However, the role of KNa1.2 channel in traumatic brain injury (TBI) remains limited. We collected brain tissue from the TBI mice and patients with post-traumatic epilepsy (PTE) to determine changes in KNa1.2 channel following TBI. We also investigated whether the MAPK pathway, which was activated by the released cytokines after injury, regulated KNa1.2 channel in in vitro. Finally, to elucidate the physiological...
Source: Neurochemical Research - October 24, 2023 Category: Neuroscience Authors: Ru Liu Lei Sun Xiaorui Shi Ci Li Xi Guo Yingting Wang Xiu Wang Kai Zhang Yongjun Wang Qun Wang Jianping Wu Source Type: research
Increased Expression of K < sub > Na < /sub > 1.2 Channel by MAPK Pathway Regulates Neuronal Activity Following Traumatic Brain Injury
Neurochem Res. 2023 Oct 25. doi: 10.1007/s11064-023-04044-1. Online ahead of print.ABSTRACTRecent studies have indicated that functional abnormalities in the KNa1.2 channel are linked to epileptic encephalopathies. However, the role of KNa1.2 channel in traumatic brain injury (TBI) remains limited. We collected brain tissue from the TBI mice and patients with post-traumatic epilepsy (PTE) to determine changes in KNa1.2 channel following TBI. We also investigated whether the MAPK pathway, which was activated by the released cytokines after injury, regulated KNa1.2 channel in in vitro. Finally, to elucidate the physiological...
Source: Neurochemical Research - October 24, 2023 Category: Neuroscience Authors: Ru Liu Lei Sun Xiaorui Shi Ci Li Xi Guo Yingting Wang Xiu Wang Kai Zhang Yongjun Wang Qun Wang Jianping Wu Source Type: research
Increased Expression of K < sub > Na < /sub > 1.2 Channel by MAPK Pathway Regulates Neuronal Activity Following Traumatic Brain Injury
Neurochem Res. 2023 Oct 25. doi: 10.1007/s11064-023-04044-1. Online ahead of print.ABSTRACTRecent studies have indicated that functional abnormalities in the KNa1.2 channel are linked to epileptic encephalopathies. However, the role of KNa1.2 channel in traumatic brain injury (TBI) remains limited. We collected brain tissue from the TBI mice and patients with post-traumatic epilepsy (PTE) to determine changes in KNa1.2 channel following TBI. We also investigated whether the MAPK pathway, which was activated by the released cytokines after injury, regulated KNa1.2 channel in in vitro. Finally, to elucidate the physiological...
Source: Neurochemical Research - October 24, 2023 Category: Neuroscience Authors: Ru Liu Lei Sun Xiaorui Shi Ci Li Xi Guo Yingting Wang Xiu Wang Kai Zhang Yongjun Wang Qun Wang Jianping Wu Source Type: research
Zingerone Alleviates Morphine Tolerance and Dependence in Mice by Reducing Oxidative Stress-Mediated NLRP3 Inflammasome Activation
This study provides a novel therapeutic approach to reduce the side effects of MPH.PMID:37864024 | DOI:10.1007/s11064-023-04043-2 (Source: Neurochemical Research)
Source: Neurochemical Research - October 20, 2023 Category: Neuroscience Authors: Shahrzad Molavinia Mehrad Nikravesh Marzieh Pashmforoosh Hossein Rajabi Vardanjani Mohammad Javad Khodayar Source Type: research
Zingerone Alleviates Morphine Tolerance and Dependence in Mice by Reducing Oxidative Stress-Mediated NLRP3 Inflammasome Activation
This study provides a novel therapeutic approach to reduce the side effects of MPH.PMID:37864024 | DOI:10.1007/s11064-023-04043-2 (Source: Neurochemical Research)
Source: Neurochemical Research - October 20, 2023 Category: Neuroscience Authors: Shahrzad Molavinia Mehrad Nikravesh Marzieh Pashmforoosh Hossein Rajabi Vardanjani Mohammad Javad Khodayar Source Type: research
Zingerone Alleviates Morphine Tolerance and Dependence in Mice by Reducing Oxidative Stress-Mediated NLRP3 Inflammasome Activation
This study provides a novel therapeutic approach to reduce the side effects of MPH.PMID:37864024 | DOI:10.1007/s11064-023-04043-2 (Source: Neurochemical Research)
Source: Neurochemical Research - October 20, 2023 Category: Neuroscience Authors: Shahrzad Molavinia Mehrad Nikravesh Marzieh Pashmforoosh Hossein Rajabi Vardanjani Mohammad Javad Khodayar Source Type: research
Zingerone Alleviates Morphine Tolerance and Dependence in Mice by Reducing Oxidative Stress-Mediated NLRP3 Inflammasome Activation
This study provides a novel therapeutic approach to reduce the side effects of MPH.PMID:37864024 | DOI:10.1007/s11064-023-04043-2 (Source: Neurochemical Research)
Source: Neurochemical Research - October 20, 2023 Category: Neuroscience Authors: Shahrzad Molavinia Mehrad Nikravesh Marzieh Pashmforoosh Hossein Rajabi Vardanjani Mohammad Javad Khodayar Source Type: research
Modulation of Cellular Levels of Adenosine Phosphates and Creatine Phosphate in Cultured Primary Astrocytes
Neurochem Res. 2023 Oct 19. doi: 10.1007/s11064-023-04039-y. Online ahead of print.ABSTRACTAdenosine triphosphate (ATP) is the main energy currency of all cells, while creatine phosphate (CrP) is considered as a buffer of high energy-bond phosphate that facilitates rapid regeneration of ATP from adenosine diphosphate (ADP). Astrocyte-rich primary cultures contain ATP, ADP and adenosine monophosphate (AMP) in average specific contents of 36.0 ± 6.4 nmol/mg, 2.9 ± 2.1 nmol/mg and 1.7 ± 2.1 nmol/mg, respectively, which establish an adenylate energy charge of 0.92 ± 0.04. The average specific cellular CrP level was found t...
Source: Neurochemical Research - October 19, 2023 Category: Neuroscience Authors: Gabriele Karger Julius Berger Ralf Dringen Source Type: research
Modulation of Cellular Levels of Adenosine Phosphates and Creatine Phosphate in Cultured Primary Astrocytes
Neurochem Res. 2023 Oct 19. doi: 10.1007/s11064-023-04039-y. Online ahead of print.ABSTRACTAdenosine triphosphate (ATP) is the main energy currency of all cells, while creatine phosphate (CrP) is considered as a buffer of high energy-bond phosphate that facilitates rapid regeneration of ATP from adenosine diphosphate (ADP). Astrocyte-rich primary cultures contain ATP, ADP and adenosine monophosphate (AMP) in average specific contents of 36.0 ± 6.4 nmol/mg, 2.9 ± 2.1 nmol/mg and 1.7 ± 2.1 nmol/mg, respectively, which establish an adenylate energy charge of 0.92 ± 0.04. The average specific cellular CrP level was found t...
Source: Neurochemical Research - October 19, 2023 Category: Neuroscience Authors: Gabriele Karger Julius Berger Ralf Dringen Source Type: research
ATF5-regulated Mitochondrial Unfolded Protein Response Attenuates Neuronal Damage in Epileptic Rat by Reducing Endoplasmic Reticulum Stress Through Mitochondrial ROS
In this study, ATF5 upregulation by lentivirus infection attenuated seizures-induced neuronal damage and apoptosis in a rat model of pilocarpine-induced epilepsy, whereas ATF5 downregulation by lentivirus infection had the opposite effects. ATF5 upregulation potentiated mtUPR by increasing the expression of mitochondrial chaperone heat shock protein 60 (HSP60) and caseinolytic protease proteolytic subunit (ClpP) and reducing mitochondrial ROS generation in pilocarpine-induced seizures in rats. Additionally, upregulation of ATF5 reduced the expression of glucose-regulated protein 78 (GRP78), protein kinase RNA-like endoplas...
Source: Neurochemical Research - October 17, 2023 Category: Neuroscience Authors: Xiaolei Lian Xiaoyi Wang Yinyin Xie Hanqing Sheng Jiao He Tingting Peng Nanchang Xie Cui Wang Yajun Lian Source Type: research
Stabilization and Reduced Cytotoxicity of Amyloid Beta Aggregates in the Presence of Catechol Neurotransmitters
Neurochem Res. 2023 Oct 17. doi: 10.1007/s11064-023-04036-1. Online ahead of print.ABSTRACTOligomeric aggregates of the amyloid-beta (Aβ) peptide have been implicated as the toxic species for Alzheimer's disease by contributing to oxidative cytotoxicity and physical disruption in cell membranes in the brain. Recent evidence points to the ability of the catecholamine neurotransmitter dopamine in the presence of copper ions to both stabilize oligomers and decrease the toxic effects of these oligomers. Based on these results, physical characterization of aggregates and subsequent cell studies with a neuroblastoma line were p...
Source: Neurochemical Research - October 17, 2023 Category: Neuroscience Authors: Mary Alice Allnutt Kathryn Mansfield Matera Source Type: research
ATF5-regulated Mitochondrial Unfolded Protein Response Attenuates Neuronal Damage in Epileptic Rat by Reducing Endoplasmic Reticulum Stress Through Mitochondrial ROS
In this study, ATF5 upregulation by lentivirus infection attenuated seizures-induced neuronal damage and apoptosis in a rat model of pilocarpine-induced epilepsy, whereas ATF5 downregulation by lentivirus infection had the opposite effects. ATF5 upregulation potentiated mtUPR by increasing the expression of mitochondrial chaperone heat shock protein 60 (HSP60) and caseinolytic protease proteolytic subunit (ClpP) and reducing mitochondrial ROS generation in pilocarpine-induced seizures in rats. Additionally, upregulation of ATF5 reduced the expression of glucose-regulated protein 78 (GRP78), protein kinase RNA-like endoplas...
Source: Neurochemical Research - October 17, 2023 Category: Neuroscience Authors: Xiaolei Lian Xiaoyi Wang Yinyin Xie Hanqing Sheng Jiao He Tingting Peng Nanchang Xie Cui Wang Yajun Lian Source Type: research
Stabilization and Reduced Cytotoxicity of Amyloid Beta Aggregates in the Presence of Catechol Neurotransmitters
Neurochem Res. 2023 Oct 17. doi: 10.1007/s11064-023-04036-1. Online ahead of print.ABSTRACTOligomeric aggregates of the amyloid-beta (Aβ) peptide have been implicated as the toxic species for Alzheimer's disease by contributing to oxidative cytotoxicity and physical disruption in cell membranes in the brain. Recent evidence points to the ability of the catecholamine neurotransmitter dopamine in the presence of copper ions to both stabilize oligomers and decrease the toxic effects of these oligomers. Based on these results, physical characterization of aggregates and subsequent cell studies with a neuroblastoma line were p...
Source: Neurochemical Research - October 17, 2023 Category: Neuroscience Authors: Mary Alice Allnutt Kathryn Mansfield Matera Source Type: research
The Role of Circadian Rhythms in Stroke: A Narrative Review
Neurochem Res. 2023 Oct 14. doi: 10.1007/s11064-023-04040-5. Online ahead of print.ABSTRACTStroke, a debilitating condition often leading to long-term disability, poses a substantial global concern and formidable challenge. The increasing incidence of stroke has drawn the attention of medical researchers and neurologists worldwide. Circadian rhythms have emerged as pivotal factors influencing stroke's onset, pathogenesis, treatment, and outcomes. To gain deeper insights into stroke, it is imperative to explore the intricate connection between circadian rhythms and stroke, spanning from molecular mechanisms to pathophysiolo...
Source: Neurochemical Research - October 14, 2023 Category: Neuroscience Authors: Bivek Singh Dongya Huang Source Type: research
