12.14神経生化学セミナーのご案内/ Neurochemistry Seminar Annoucement
Title: TRPM7 and TRPM2 Channels: The Ischemia-Induced Death of Hippocampal
Lecturer: John F. MacDonald&s_comma; PhD FRSC.
Affiliation: Ernest B. and Leonard B. Smith Professor and Chairman&s_comma; Department
of Physiology&s_comma; University of Toronto
Time: December 14&s_comma; 2007 (Fri) 17：00～18：00
Place: 3rd Floor Lecture Hall&s_comma; Medical Research Building 1 (1-gokan)
Host: Haruhiko Bito&s_comma; Department of Neurochemistry (03-5841-3560)
Supported by Neuroscience Lecture Series&s_comma; Center for Integrated Brain Medical
Science&s_comma; a 21st Century COE Program from MEXT.
Transient receptor potential (TRP) channels represent a highly diverse family of
non-selective cation channels whose functions vary from sensory transduction to
ion homeostasis. The melastatin subfamily of TRP channels (TRPM) is a group of
eight related cation channels for which two members&s_comma; TRPM2 and TRPM7 are
implicated in ischemic cell death&s_comma; Ca2+ entry and stroke. Both TRPM2 and TRPM7
possess enzymatic activity as well as channel function. We have characterized
the role of TRPM7 channels in hippocampal neurons and we have recently shown
that reduction in the expression of TRPM7 protein in the hippocampus&s_comma; through
viral delivery of RNAi targeting this channel&s_comma; provides substantial but not
complete sparing of CA1 pyramidal neurons in an in vivo model of global
ischemia. One possible explanation for the partial sparing of the neurons is a
concurrent activation of TRPM2 channels during reperfusion. TRPM2 channels are
stimulated by oxidative stress or by generation of reactive oxygen species (e.g.
applications of hydrogen peroxide) in various cell lines and have been further
characterized in immunocytes&s_comma; neutrophils and rat islet cells. We have recently
shown large TRPM2-mediated currents in cultured hippocampal neurons and describe
how these channels are activated.
References: Aarts et al. Cell 2003; MacDonald et al. TINS 2006; Wei et al. PNAS
Teｌ: 03-5841-3559 Fax: 03-3814-8154