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Articles 1 - 4 of 4
Full-Text Articles in Medical Physiology
Crf Mediates Stress-Induced Pathophysiological High-Frequency Oscillations In Traumatic Brain Injury, Chakravarthi Narla, Paul S. Jung, Francisco Bautista Cruz, Michelle Everest, Julio Martinez-Trujillo, Michael O. Poulter
Crf Mediates Stress-Induced Pathophysiological High-Frequency Oscillations In Traumatic Brain Injury, Chakravarthi Narla, Paul S. Jung, Francisco Bautista Cruz, Michelle Everest, Julio Martinez-Trujillo, Michael O. Poulter
Physiology and Pharmacology Publications
Copyright © 2019 Narla et al. It is not known why there is increased risk to have seizures with increased anxiety and stress after traumatic brain injury (TBI). Stressors cause the release of corticotropin-releasing factor (CRF) both from the hypothalamic pituitary adrenal (HPA) axis and from CNS neurons located in the central amygdala and GABAergic interneurons. We have previously shown that CRF signaling is plastic, becoming excitatory instead of inhibitory after the kindling model of epilepsy. Here, using Sprague Dawley rats we have found that CRF signaling increased excitability after TBI. Following TBI, CRF type 1 receptor (CRFR1)-mediated activity caused …
Interaction Between Angiotensin Ii And Bdnf In Modulating Sympathetic Nerve Activity, Bryan K. Becker
Interaction Between Angiotensin Ii And Bdnf In Modulating Sympathetic Nerve Activity, Bryan K. Becker
Theses & Dissertations
Over activation of the sympathetic nervous system is prevalent in many forms of cardiovascular disease such as chronic heart failure (CHF) and hypertension. Although increased neuronal renin-angiotensin system activity in presympathetic neurons has been well implicated in mediating this sympatho-excitation, many of the neuronal effects of angiotensin II (Ang II) signaling remain poorly understood. One particular mechanism of Ang II-mediated increases in presympathetic neuronal activity is through reductions in voltage-gated K+ currents. Another pathway that has profound effects on neuronal K+ currents and that has been previously implicated in Ang II-signaling is brain-derived neurotrophic factor (BDNF) activity through …
Activation Of Peroxisome Proliferator-Activated Receptor G In Brain Inhibits Inflammatory Pain, Dorsal Horn Expression Of Fos, And Local Edema, Jenny Morgenweck, Omar D. Abdel-Aleem, Katelyn C. Mcnamara, Renee R. Donahue, M Z. Badr, Bradley K. Taylor
Activation Of Peroxisome Proliferator-Activated Receptor G In Brain Inhibits Inflammatory Pain, Dorsal Horn Expression Of Fos, And Local Edema, Jenny Morgenweck, Omar D. Abdel-Aleem, Katelyn C. Mcnamara, Renee R. Donahue, M Z. Badr, Bradley K. Taylor
Renee R. Donahue
Systemic administration of thiazolidinediones reduces peripheral inflammation in vivo, presumablybyacting at peroxisome proliferator-activated receptor g (PPARg) in peripheral tissues. Based on a rapidly growing body of literature indicating the CNS as a functional target of PPARg actions, we postulated that brain PPARg modulates peripheral edema and the processing of inflammatory pain signals in the dorsal horn of the spinal cord. To test this in the plantar carrageenan model of inflammatory pain, we measured paw edema, heat hyperalgesia, and dorsal horn expression of the immediate-early gene c-fos after intracerebroventricular (ICV) administration of PPARg ligands or vehicle. We found that ICV rosiglitazone …
Ranolazine Attenuates Behavioral Signs Of Neuropathic Pain, Harry J. Gould Iii, Colleen J. Garrett, Renee R. Donahue, Dennis Paul, Ivan Diamond, Bradley K. Taylor
Ranolazine Attenuates Behavioral Signs Of Neuropathic Pain, Harry J. Gould Iii, Colleen J. Garrett, Renee R. Donahue, Dennis Paul, Ivan Diamond, Bradley K. Taylor
Renee R. Donahue
Ranolazine modulates the cardiac voltage-gated sodium channel (NaV 1.5) and is approved by the FDA in the treatment of ischemic heart disease. Ranolazine also targets neuronal (NaV 1.7, 1.8) isoforms that are implicated in neuropathic pain. Therefore, we determined the analgesic efficacy of ranolazine in a preclinical animal model of neuropathic pain. Both intraperitoneal and oral administration of ranolazine dose-dependently inhibited the mechanical and cold allodynia associated with spared nerve injury, without producing ataxia or other behavioral side effects. These data warrant clinical investigation of the potential use of ranolazine in the treatment of neuropathic pain.