Role of TRPM2 cation channels on molecular pathways in neurological cells

Of all the organs in the body, the central nervous system is especially sensitive to free radical damage. its high consumption oxygen, rich content of easily oxidizible fatty acids, relatively low content of antioxidant enzymes and antioxidants, a make it a prime substrate for damage by ros. the na+ and ca2+-permeable melastatin related transient receptor potential 2 (trpm2) cation channels can be gated either by adp-ribose (adpr) in concert with ca2+ or by hydrogen peroxide (h2o2), an experimental model for oxidative stress, binding to the channel’s enzymatic nudix domain. since the mechanisms that lead to trpm2 inhibiting in response to adpr and h2o2 are not understood in neuronal cells, we reviewed the effects of adpr and oxidative stress in neurological cells such as microglia, hippocampus and brain as well as neurological diseases such as bipolar diseases. it was observed that trpm2 cation channels in microglia and hippocampal cells were gated both by adpr and h2o2. in addition, h2o2 seems to responsible activation of trpm2 in neurological diseases. genetic defects may be have important role in etiology of bipolar diseases.