International Journal of Cell Biology / 2013 / Article / Fig 4

Review Article

Synaptic Dysfunction in Prion Diseases: A Trafficking Problem?

Figure 4

A role for intracellular PrP retention in NMDAR dysfunction. (a) on the plasma membrane (PM) attenuates NMDAR activity by associating with the NR2D subunit. (b) Owing to misfolding in transport organelles (ER/Golgi), is retained intracellularly. This results in increased NMDAR activation, potentially triggering neurotoxicity. (c) Intracellular retention of misfolded with NR2D and NR1 subunits results in impaired delivery of NMDARs to the cell surface or their abnormal targeting to extrasynaptic sites, leading to loss of NMDAR function and/or activation of neurotoxic stimuli.
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