Podoplanin Gene Disruption in Mice Promotes in vivo Neural Progenitor Cells Proliferation, Selectively Impairs Dentate Gyrus Synaptic Depression and Induces Anxiety-Like Behaviors.

摘要: Podoplanin (Pdpn), a brain-tumor-related glycoprotein identified in humans and animals, is endogenously expressed several organs critical for life support such as kidney, lung, heart brain. In the brain, Pdpn has been proliferative nestin-positive adult neural progenitor cells neurons of neurogenic hippocampal dentate gyrus (DG), structure associated to anxiety, learning memory functions severely damaged people with Alzheimer's Disease (AD). The vivo role neurogenesis anxiety-like behavior remained however unexplored. Using mice disrupted gene model organism applying combined behavioral, molecular biological electrophysiological assays, we here show that absence selectively impairs long-term synaptic depression DG without affecting CA3-Schaffer's collateral-CA1 synapses. deletion also enhanced capacity diminished survival differentiated neuronal vitro. addition, podoplanin disruption showed increased behaviors experimentally validated behavioral tests compared wild type littermate controls. Together, these findings broaden our knowledge on mechanisms influencing plasticity reveal novel target future studies addressing general anxiety disorder depression-related dysfunctions.