Neurobiological mechanisms underlying olfactory bonds

在这项研究中，我们证明：（1）从副嗅球中的二尖瓣细胞内源性释放的谷氨酸通过激活突触前和突触后位点上的代谢型谷氨酸受体mGluR 2来抑制从二尖瓣到颗粒细胞的突触传递，（2）线粒体-（3）包括组蛋白乙酰化在内的表观遗传机制对新生大鼠嗅球线粒体-颗粒细胞突触的厌恶性嗅觉学习和突触可塑性至关重要。

In this study we demonstrate that (1) glutamate endogenously released from mitral cells in the accessory olfactory bulb suppresses synaptic transmission from mitral to granule cells by activating mGluR2, a metabotropic glutamate receptor on the pre- and postsynaptic sites, (2) the activation of the protein kinase PKM zeta and new protein synthesis are required for the late phase of long-term potentiation (L-LTP) at the mitral-to-granule cell synapse and (3) epigenetic mechanisms including histone acetylation are critical for aversive olfactory learning and synaptic plasticity at the mitral-to-granule cell synapse of the olfactory bulb in neonatal rats.