Laboratory of Neuropharmacology, School of Pharmacy, Aichi Gakuin University, Nagoya, 464-8650, Japan.
Laboratory of Neuropharmacology, School of Pharmacy, Aichi Gakuin University, Nagoya, 464-8650, Japan.
J Pharmacol Sci. 2019 Jul;140(3):305-309. doi: 10.1016/j.jphs.2019.07.013. Epub 2019 Aug 3.
The present study evaluated the ability of progesterone to alleviate the synaptic transmission disturbed by hypoxia in the nucleus tractus solitarius (NTS). Hypoxia with N inhibited spontaneous and tractus solitarius-evoked excitatory postsynaptic currents (sEPSCs and eEPSCs) in NTS neurons of the rat brainstem slice. An additional application of progesterone counteracted the hypoxia-induced inhibition of sEPSCs and eEPSCs without affecting the baseline currents. This effect of progesterone occurred rapidly and reversibly. Progesterone had neither effect on sEPSCs nor eEPSCs in normoxia. These results suggest that progesterone restores hypoxia-induced disturbance of the NTS glutamatergic transmission, presumably by a presynaptic, non-genomic mechanism.
本研究评估了孕酮缓解孤束核（NTS）缺氧引起的突触传递障碍的能力。缺氧与 N 抑制了大鼠脑片 NTS 神经元中自发性和孤束束诱发的兴奋性突触后电流（sEPSC 和 eEPSC）。孕酮的额外应用可拮抗缺氧引起的 sEPSC 和 eEPSC 抑制，而不影响基线电流。孕酮的这种作用快速且可逆。孕酮在常氧条件下对 sEPSC 和 eEPSC 均无作用。这些结果表明，孕酮通过一种可能是突触前的非基因组机制来恢复缺氧引起的 NTS 谷氨酸能传递障碍。
