Blockade of soluble epoxide hydrolase attenuates post-ischemic neuronal hyperexcitation and confers resilience against stroke with TrkB activation

Keyphrases

• Resilience 100%
• Tropomyosin Receptor Kinase B 100%
• Soluble Epoxide Hydrolase 100%
• Neuronal Hyperexcitation 100%
• Acid Treatment 37%
• Ureido 37%
• Dodecanoic Acid 37%
• Transient Middle Cerebral Artery Occlusion (tMCAO) 25%
• KO Mice 25%
• Acid Soluble 25%
• Ischemic Long-term Potentiation 25%
• Microvasculature 12%
• Knock-in Mouse Model 12%
• Attenuation 12%
• Wild Mice 12%
• Immunohistochemistry 12%
• Neuronal Transmission 12%
• Gene Deletion 12%
• Infarct 12%
• Oxygen-glucose Deprivation 12%
• Neuroprotective Effect 12%
• Neurovascular Unit 12%
• Neuroprotective Mechanisms 12%
• Neurological Deficit 12%
• Neurotrophin Signaling 12%
• Deprivation Theory 12%
• Brain Infarction 12%
• Infarction 12%
• Hydrolase Activity 12%
• Experimental Ischemic Stroke 12%
• Soluble Epoxide Hydrolase Inhibitor 12%
• Middle Cerebral Artery Occlusion Model 12%
• Sensorimotor Recovery 12%
• Glutamate Receptors 12%
• Peri-infarct 12%
• Epoxyeicosatrienoic Acids 12%
• Neuroexcitation 12%

Neuroscience

• Kinase 100%
• Tropomyosin 100%
• Epoxide Hydrolase 100%
• Cerebrovascular Accident 100%
• Receptor 100%
• Lauric Acid 33%
• Amantadine 33%
• Middle Cerebral Artery 22%
• Long-Term Potentiation 22%
• Neuroprotective Agent 22%
• In Vivo 11%
• Immunohistochemistry 11%
• Synaptic Transmission 11%
• Brain Ischemia 11%
• Gene Deletion 11%
• Vasoactive 11%
• Epoxyeicosatrienoic Acid 11%
• Glutamate Receptor 11%
• Microvessel 11%
• Hydrolase Inhibitor 11%