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. Author manuscript; available in PMC: 2012 Apr 1.
Published in final edited form as: Curr Opin Cell Biol. 2011 Feb 2;23(2):223–230. doi: 10.1016/j.ceb.2010.12.006

Figure 3. Role of chronically activated CaN in synaptic dysfunction.

Figure 3

CaN has been implicated in synaptic abnormalities during neurodegenerative disorders at least in three different ways: (1) Activated CaN dephosphorylates CREB inhibiting its translocation to the nucleus, resulting in the abnormal shut off of CREB regulated gene expression required for neuronal growth and synaptic plasticity; (2) CaN mediates the internalization of AMPA receptor bound to misfolded proteins (particularly Aβ oligomers) inducing synaptic disruption and inhibition of long term potentiation; (3) Inhibition of neurotransmitter release by abrogating synaptic vesicle transport through dephosphorylaton of synapsin I.