Transient receptor potential melastatin-2 and temperature participate in the process of CD38-regulated oxytocin secretion

التفاصيل البيبلوغرافية
العنوان: Transient receptor potential melastatin-2 and temperature participate in the process of CD38-regulated oxytocin secretion
المؤلفون: Wan-Hua Yang, Shuang Ma, Hong-Xiang Liu, Yong Nan
المصدر: Neuroreport. 27(12)
سنة النشر: 2016
مصطلحات موضوعية: 0301 basic medicine, Agonist, endocrine system, medicine.medical_specialty, Pituitary gland, medicine.drug_class, Hypothalamus, TRPM Cation Channels, Oxytocin, Cyclic ADP-ribose, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Pituitary Gland, Posterior, Posterior pituitary, Internal medicine, medicine, Animals, TRPM2, Mice, Inbred ICR, Membrane Glycoproteins, Chemistry, General Neuroscience, Oxytocin secretion, Temperature, ADP-ribosyl Cyclase 1, 030104 developmental biology, Endocrinology, medicine.anatomical_structure, hormones, hormone substitutes, and hormone antagonists, 030217 neurology & neurosurgery, medicine.drug
الوصف: In recent studies, oxytocin showed potential for the treatment of mental diseases. CD38 is essential for oxytocin release, and hence plays a critical role in social behavior. CD38 catalyzes β-NAD into cyclic ADP ribose (cADPR), which could elevate the intracellular Ca by Ca-permeable channels for oxytocin secretion. The temperature-sensitive cation channel, transient receptor potential melastatin-2 (TRPM2), is a cation-nonselective cation and has been shown to affect oxytocin indirectly. The aim of the present study was to verify the participation of temperature and TRPM2 in CD38-regulated oxytocin release. The crude membranes were prepared to isolate the nerve terminals from the posterior pituitary. At 34°C, 37°C, and 39°C, agonists (β-NAD, ADPR, cADPR) and antagonists (8-Br-cADPR, 2-APB) were used to stimulate the nerve terminals. Oxytocin releases were investigated by enzyme-linked immunosorbent assay. In addition, the expression of TRPM2 and CD38 in the hypothalamus and pituitary was detected by western blotting and quantitative PCR. CD38 agonists (β-NAD, cADPR) and antagonist (8-Br-cADPR) could increase or reduce the oxytocin release, respectively. TRPM2 agonist (ADPR) and antagonist (2-APB) alone could also regulate oxytocin release. Furthermore, temperature could increase agonist stimulation and attenuate the antagonist inhibition on oxytocin release. In addition, CD38 and TRPM2 were expressed in the hypothalamus and pituitary at both the mRNA and the protein level. TRPM2 in pituitary nerve terminals plays a role in oxytocin release. Temperature- enhanced oxytocin release by CD38 and TRPM2. TRPM2 might be involved in the process of CD38-regulated oxytocin release.
تدمد: 1473-558X
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ecf35f3d4a002280c92afad0180ff3c6
https://pubmed.ncbi.nlm.nih.gov/27348016
رقم الأكسشن: edsair.doi.dedup.....ecf35f3d4a002280c92afad0180ff3c6
قاعدة البيانات: OpenAIRE