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post-traumatic stress disorder/escopolamina
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6 resultados
Basal and scopolamine-evoked release of hippocampal acetylcholine following traumatic brain injury in rats.
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This study employed in vivo microdialysis in awake, freely-moving Sprague-Dawley rats to examine acetylcholine (ACh) release in the dorsal hippocampus at 14 days following lateral controlled cortical impact. Extracellular levels of ACh were measured prior to and after an intraperitoneal
Influence of pharmacological and epigenetic factors to suppress neurotrophic factors and enhance neural plasticity in stress and mood disorders.
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Stress-induced major depression and mood disorders are characterized by behavioural abnormalities and psychiatric illness, leading to disability and immature mortality worldwide. Neurobiological mechanisms of stress and mood disorders are discussed considering recent findings, and challenges to
Cholinergic Signaling Alters Stress-Induced Sensitization of Hippocampal Contextual Learning.
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Post-traumatic stress disorder (PTSD) has a profound contextual component, and has been demonstrated to alter future contextual learning. However, the mechanism by which a single traumatic event affects subsequent contextual experiences has not been isolated. Acetylcholine (ACh) is an important
Combined therapy affects outcomes differentially after mild traumatic brain injury and secondary forebrain ischemia in rats.
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Muscarinic and NMDA receptors contribute to post-traumatic hypersensitivity to secondary ischemia. However, the effect of these receptor antagonists on behavior and CA1 neuronal death after traumatic brain injury (TBI) with acute (1 h after TBI) forebrain ischemia has not been systematically
EVP-6124, a novel and selective α7 nicotinic acetylcholine receptor partial agonist, improves memory performance by potentiating the acetylcholine response of α7 nicotinic acetylcholine receptors.
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EVP-6124, (R)-7-chloro-N-quinuclidin-3-yl)benzo[b]thiophene-2-carboxamide, is a novel partial agonist of α7 neuronal nicotinic acetylcholine receptors (nAChRs) that was evaluated here in vitro and in vivo. In binding and functional experiments, EVP-6124 showed selectivity for α7 nAChRs and did not
Reduced evoked release of acetylcholine in the rodent neocortex following traumatic brain injury.
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Neocortical acetylcholine (ACh) release was examined in awake, freely-moving rats at 14 days following lateral controlled cortical impact. Extracellular ACh was measured prior to and after an intraperitoneal administration of scopolamine, which evokes ACh release by blocking autoreceptors. At 14
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