Nogo receptor 1 Key to a Plastic Mind
Formation of lasting memories is believed to rely on structural alterations at the synaptic level. We had found that increased neuronal activity down-regulates Nogo receptor-1 (NgR1) in brain regions linked to memory formation and storage, and postulated this to be required for formation of lasting memories. We now show that mice with inducible overexpression of NgR1 in forebrain neurons have normal long-term potentiation and normal 24-h memory, but severely impaired month-long memory in both passive avoidance and swim maze tests. Blocking transgene expression normalizes these memory impairments. Nogo, Lingo-1, Troy, endogenous NgR1, and BDNF mRNA expression levels were not altered by transgene expression, suggesting that the impaired ability to form lasting memories is directly coupled to inability to down-regulate NgR1. Regulation of NgR1 may therefore serve as a key regulator of memory consolidation. Understanding the molecular underpinnings of synaptic rearrangements that carry lasting memories may facilitate development of treatments for memory dysfunction.
Elin Åberg, Cristina M. Bäckman, Stefan Brené, Simone Codeluppi, Barry J. Hoffer, Alexander F. Hoffman, Anna Josephson, Alexandra Karlén, Tobias E. Karlsson, Karin Lundströmer, Carl R. Lupica, Anna Mattsson, Sven Ove Ögren, Lars Olson, Therese M. Pham, Michael A. Sherling, Christian Spenger, Nogo receptor 1 regulates formation of lasting memories (2009 November 13)
Notes
NgR1 found to be key in the formation of long-term memories.
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Keywords
lasting memories, transgene expression, normal long-term potentiation, Plastic Mind NgR1, impaired month-long memory, BDNF mRNA expression, normal 24-h memory, swim maze tests, long-term memories, synaptic rearrangements, memory formation, inducible overexpression
18 more keywords
synaptic level, forebrain neurons, Nogo receptor, structural alterations, neuronal activity, endogenous NgR1, passive avoidance, memory impairments, molecular underpinnings, brain regions, Nogo receptor-1, memory dysfunction, memory consolidation, key regulator, inability, mice, Troy, storage