Event:

While the role of myelin-derived Nogo-A as an inhibitor of axonal regeneration following CNS injury has been thoroughly described, its physiological function in the adult, uninjured CNS is less well known. We recently addressed this question in the rodent hippocampus, where Nogo-A is expressed by neurons as well as oligodendrocytes. Neuronal networks in the brain undergo constant remodeling processes during development and adult learning. These processes involve functional and structural alterations (plastic changes) at synapses and represent cellular mechanisms of learning and memory processes. An accepted model for activity dependent functional plasticity is the induction of Long-term potentiation (LTP) in the CA1 region of the hippocampus by high-frequency stimulation which leads to increased synaptic strength and activates structural growth processes. While the molecular mechanisms positively regulating these functional changes are relatively well described, the molecules controlling the stabilization of synapses and restricting plasticity are still largely unexplored. In search for factors restricting functional as well as structural plasticity processes, we investigated the role of the myelin-associated protein Nogo-A, whose function as negative regulator of structural changes in the CNS is well known. We analyzed synaptic transmission as well as long-term synaptic plasticity (LTP/LTD) in the presence of function blocking anti-NogoA or anti Nogo receptor (NgR) antibodies and in the mature hippocampus of NogoA KO mice.