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We have demonstrated that i.c.v.‐administered (±)‐epibatidine, a nicotinic ACh receptor (nAChR) agonist, induced secretion of noradrenaline and adrenaline (catecholamines) from the rat adrenal medulla with dihydro‐β‐erythroidin (an α4β2 nAChR antagonist)‐sensitive… Click to show full abstract
We have demonstrated that i.c.v.‐administered (±)‐epibatidine, a nicotinic ACh receptor (nAChR) agonist, induced secretion of noradrenaline and adrenaline (catecholamines) from the rat adrenal medulla with dihydro‐β‐erythroidin (an α4β2 nAChR antagonist)‐sensitive brain mechanisms. Here, we examined central mechanisms for the (±)‐epibatidine‐induced responses, focusing on brain NOS and NO‐mediated mechanisms, soluble GC (sGC) and protein S‐nitrosylation (a posttranslational modification of protein cysteine thiol groups), in urethane‐anaesthetized (1.0 g·kg−1, i.p.) male Wistar rats.
Journal Title: British Journal of Pharmacology
Year Published: 2018
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