scholarly journals Oxidation of KCNB1 Potassium Channels Causes Neurotoxicity and Cognitive Impairment in a Mouse Model of Traumatic Brain Injury

2016 ◽  
Vol 36 (43) ◽  
pp. 11084-11096 ◽  
Author(s):  
W. Yu ◽  
R. Parakramaweera ◽  
S. Teng ◽  
M. Gowda ◽  
Y. Sharad ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Potassium Channels ◽  
Mouse Model

scholarly journals Dietary Energy Restriction Ameliorates Cognitive Impairment in a Mouse Model of Traumatic Brain Injury

2019 ◽  
Vol 67 (4) ◽  
pp. 613-621 ◽  
Author(s):  
V. Rubovitch ◽  
A. Pharayra ◽  
M. Har-Even ◽  
O. Dvir ◽  
M. P. Mattson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Mouse Model ◽  
Energy Restriction ◽  
Dietary Energy ◽  
Dietary Energy Restriction

NEUROPSYCHOLOGICAL CHANGES IN PATIENTS WITH A CONSEQUENCE OF TRAUMATIC BRAIN INJURY

2020 ◽  
Vol 3 (1) ◽  
pp. 44-46
Author(s):  
Istatillo Shodjalilov ◽  
◽  
Saoda Igamova ◽  
Aziza Djurabekova
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Neuropsychological Testing ◽  
Anxiety And Depression ◽  
Psychopathological Symptoms ◽  
Neuropsychological Changes ◽  
The Relationship

The incidence of cognitive impairment in TBI is high, depending on the severity. At the same time, psychopathological symptoms in the form of asthenia, increased anxiety and depression are encountered among patients with TBI. The work studied the relationship between cognitive and psychopathological symptoms in patients with TBI using neuropsychological testing on scales.

scholarly journals Pathologically Entangled: Brain trauma-evoked ROS imbalance disrupts Kir channel function in distant peripheral vessels

Function ◽  
2021 ◽  
Author(s):  
Nick Weir ◽  
Thomas A Longden
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Potassium Channels ◽  
Vascular Function ◽  
Inward Rectifier ◽  
Brain Trauma ◽  
Channel Function ◽  
Inward Rectifier Potassium Channels ◽  
Kir Channel

Abstract A Perspective on "Traumatic Brain Injury Impairs Systemic Vascular Function Through Disruption of Inward-Rectifier Potassium Channels"

scholarly journals Traumatic Brain Injury Impairs Systemic Vascular Function Through Disruption of Inward-Rectifier Potassium Channels

Function ◽  
2021 ◽  
Author(s):  
Adrian M Sackheim ◽  
Nuria Villalba ◽  
Maria Sancho ◽  
Osama F Harraz ◽  
Adrian D Bonev ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Potassium Channels ◽  
Signaling Pathways ◽  
Inward Rectifier ◽  
Pla2 Activity ◽  
Functional Responses ◽  
Channel Function ◽  
Inward Rectifier Potassium Channels ◽  
Kir2.1 Channel

Abstract Trauma can lead to widespread vascular dysfunction, but the underlying mechanisms remain largely unknown. Inward-rectifier potassium channels (Kir2.1) play a critical role in the dynamic regulation of regional perfusion and blood flow. Kir2.1 channel activity requires phosphatidylinositol 4,5-bisphosphate (PIP2), a membrane phospholipid that is degraded by phospholipase A2 (PLA2) in conditions of oxidative stress or inflammation. We hypothesized that PLA2–induced depletion of PIP2 after trauma impairs Kir2.1 channel function. A fluid percussion injury model of traumatic brain injury (TBI) in rats was used to study mesenteric resistance arteries 24 hours after injury. The functional responses of intact arteries were assessed using pressure myography. We analyzed circulating PLA2, hydrogen peroxide (H2O2), and metabolites to identify alterations in signaling pathways associated with PIP2 in TBI. Electrophysiology analysis of freshly-isolated endothelial and smooth muscle cells revealed a significant reduction of Ba2+-sensitive Kir2.1 currents after TBI. Additionally, dilations to elevated extracellular potassium and BaCl2- or ML 133-induced constrictions in pressurized arteries were significantly decreased following TBI, consistent with an impairment of Kir2.1 channel function. The addition of a PIP2 analog to the patch pipette successfully rescued endothelial Kir2.1 currents after TBI. Both H2O2 and PLA2 activity were increased after injury. Metabolomics analysis demonstrated altered lipid metabolism signaling pathways, including increased arachidonic acid, and fatty acid mobilization after TBI. Our findings support a model in which increased H2O2-induced PLA2 activity after trauma hydrolyzes endothelial PIP2, resulting in impaired Kir2.1 channel function.

scholarly journals Acute treatment with TrkB agonist LM22A-4 confers neuroprotection and preserves myelin integrity in a mouse model of pediatric traumatic brain injury

2021 ◽  
Vol 339 ◽  
pp. 113652
Author(s):  
Jessica L. Fletcher ◽  
Larissa K. Dill ◽  
Rhiannon J. Wood ◽  
Sharon Wang ◽  
Kate Robertson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mouse Model ◽  
Acute Treatment ◽  
Pediatric Traumatic Brain Injury

scholarly journals Peroxynitrite-Mediated Protein Nitration and Lipid Peroxidation in a Mouse Model of Traumatic Brain Injury

2004 ◽  
Vol 21 (1) ◽  
pp. 9-20 ◽  
Author(s):  
Edward D. Hall ◽  
Megan R. Detloff ◽  
Kjell Johnson ◽  
Nancy C. Kupina
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Mouse Model ◽  
Protein Nitration

Comparison of Cognitive Impairment Associated With Major Depression Following Stroke Versus Traumatic Brain Injury

2002 ◽  
Vol 43 (4) ◽  
pp. 295-301 ◽  
Author(s):  
Amane Tateno ◽  
Yuichi Murata ◽  
Robert G. Robinson
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Major Depression

The Neuroprotective Effect of Salubrinal in a Mouse Model of Traumatic Brain Injury

2015 ◽  
Vol 17 (1) ◽  
pp. 58-70 ◽  
Author(s):  
Vardit Rubovitch ◽  
Shani Barak ◽  
Lital Rachmany ◽  
Renana Baratz Goldstein ◽  
Yael Zilberstein ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mouse Model ◽  
Neuroprotective Effect
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