Bone morphogenic protein (BMP) has diverse functions in cell signaling from development to cell death. This week, Sun et al. focused on its possible role in synaptic plasticity by targeting the endogenous BMP antagonist chordin. The BMPRII receptor protein was expressed throughout the hippocampus in wild-type mice, as was chordin. Brain slices from mice lacking Chordin (Chrd-/-) had enhanced paired-pulse facilitation and an increased frequency of miniature EPSCs, consistent with a presynaptic site of action for BMP. Nerve terminals in Chrd-/- mice also had an increase in docked vesicles. Perfusion of BMP2 in wild-type slices mimicked the effects seen in slices from Chrd-/- mice. The effects on plasticity and behavior were complex. Long-term potentiation was enhanced in Chrd-/- slices with high-frequency stimulation, but not with theta burst or pairing protocols; and mutant mice showed improved learning in the water maze, but impairment in the Y maze.
Tae Y. Yune, Jee Y. Lee, Gil Y. Jung, Sun J. Kim, Mei H. Jiang, Young C. Kim, Young J. Oh, George J. Markelonis, and Tae H. Oh
Traumatic spinal cord injury (SCI) leads not only to neuronal loss, but also to apoptosis of oligodendrocytes and subsequent demyelination. This week, Yuneet al. tried to connect the dots between neuroprotection afforded by the antibiotic minocycline, inhibition of microglia activation, and apoptotic signaling through the p75 neurotrophin receptor (p75NTR). Five days after a contusion injury at T10/11 in adult rats, the spinal cord showed elevated levels of proNGF (nerve growth factor). Phosphorylated p38 protein-activated mitogen kinase (p-p38MAPK), an indicator of microglia activation, also increased after SCI. In vitro<