2024-06-062024-06-062021-12-010143-4179https://doi.org/10.1016/j.npep.2021.102186https://hdl.handle.net/11452/41787We recently demonstrated that peripheral and central administration of nesfatin-1 in fasting and satiety states generate hyperventilation activity by increasing tidal volume (TV), respiratory rate (RR), and respiratory minute ventilation (RVM). The present study aimed to investigate the mediation of central cholinergic receptors effective in respiratory control in the hyperventilation activity of nesfatin-1. Besides this, we intended to determine possible changes in blood gases due to hyperventilation activity caused by nesfatin-1 and investigate the mediation of central cholinergic receptors in these changes.Intracerebroventricular (ICV) administration of nesfatin-1 revealed a hyperventilation response with an increase in TV, RR, RMV, and pO(2) and a decrease in pCO(2) in saturated Sprague Dawley rats. ICV pretreatment with the muscarinic receptor antagonist atropine partially blocked the RR, RMV, pO(2), and pCO(2) responses produced by nesfatin-1 while completely blocking the TV response. However, central pretreatment with nicotinic receptor antagonist mecamylamine blocked the respiratory and blood gas responses induced by nesfatin-1.The study's conclusion demonstrated that nesfatin-1 had active hyperventilation effects resulting in an increase in pO(2) and a decrease in pCO(2). The critical finding of the study was that activation of central cholinergic receptors was involved in nesfatin-1-evoked hyperventilation and blood gas responses.eninfo:eu-repo/semantics/openAccessCdp-cholineRespiratory systemArachidonic-acidSolitary tractNucleusNeuronsBrainReceptorNesfatin-1Cholinergic muscarinic and nicotinic receptorsRespiratory parametersPartial oxygen and carbon dioxide pressureIntracerebroventricularScience & technologyLife sciences & biomedicineEndocrinology & metabolismNeurosciencesEndocrinology & metabolismNeurosciences & neurologyArticle0007442554000079010.1016/j.npep.2021.102186