题目：TRP channels: what are they and why are they important for understanding neuronal functions in health and disease

报告人：Baruch Minke ( Departments of Medical Neurobiology, The Institute of Medical Research Israel-Canada (IMRIC), The Edmond and Lily Safra Center for Brain Sciences (ELSC), Faculty of Medicine of the Hebrew University )

时间：2014年04月29日 星期二 13:00-14:30

地点： 生命科学学院 邓佑才报告厅（101室）

邀请人：李沉简

摘要：Transient receptor potential (TRP) channels constitute a large superfamily of polymodal channel proteins with diverse roles in many transduction and sensory pathways. These channels participate in most sensory modalities (e.g. vision, taste, temperature, pain, pheromone detection) and they either open directly in response to ligands or physical stimuli (e.g. temperature, osmotic pressure, or noxious substances) or, indirectly, downstream of a signal transduction cascade. TRP channels form an evolutionary conserved novel cation channel family consisting of seven subfamilies, which include nearly 30 human members. The founding member of this family was found in Drosophila and was designated TRP by Minke. TRP channels are classified into seven related subfamilies designated TRPC (Canonical or classical), TRPM (Melastatin), TRPN (NompC), TRPV (Vanilloid receptor), TRPA (ANKTM1), TRPP (Polycystin) and TRPML (Mucolipin). Our studies in Drosophila shed new light on the properties of the TRP channels by showing that a constitutive ATP-dependent process is required to keep these channels closed in the dark, a requirement that would make them sensitive to metabolic stress. Since mammalian TRP channels are heavily expressed in the brain, neuronal damage due to ischemia may involves activation of TRP channels. Indeed, recent studies have demonstrated that TRPM7 is an essential mediator of anoxic neuronal death that is activated by oxidative stress, in parallel to excitotoxic signal pathways. Thus, future treatment of ischemic brain injury may need to include strategies that inhibit or modulate activity of TRPM7 and possibly other TRP channels.