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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Blotting, Western, Chronic Disease, Dinoprostone, Disease Models, Animal, Fluorescent Antibody Technique, Glutamate Decarboxylase, Heart Failure, JNK Mitogen-Activated Protein Kinases, Male, Paraventricular Hypothalamic Nucleus, Rats, Rats, Wistar, Real-Time Polymerase Chain Reaction, Receptors, GABA-A, Receptors, Prostaglandin E, EP3 Subtype, Signal Transduction, Sympathetic Nervous System.
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Does c-Jun N-terminal Kinase mediate prostaglandin-induced sympathoexcitation in rats with chronic heart failure by reducing GAD1 and GABRA1 expression? Context: Prostaglandin E2 mediates sympathoexcitation in chronic heart failure (CHF) through EP3 receptors (PTGER3) in the paraventricular nucleus (PVN). The aim of this study was to investigate the role of c-Jun N-terminal kinase (JNK) in expressional regulation of gamma-aminobutyric acid signalling in PVN in CHF rats. Chronic heart failure was induced by left coronary ligation in Wistar rats. Renal sympathetic nerve discharge (RSND) and mean arterial pressure (MAP) responses to the PVN infusion were determined in anaesthetized rats. Osmotic minipumps were used for chronic PVN infusion. PTGER3 expression was examined with immunofluorescence staining, quantitative real-time PCR and Western blot. Chronic heart failure rats had increased JNK activation and decreased glutamate decarboxylase 1 (GAD1) and GABA
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Prostaglandin signalling through upregulated PTGER3 activates JNK which reduces GAD1 and GABRA1 expression in the PVN, and contributes to sympathoexcitation in CHF. Final Decision: yes