The Docosanoid Neuroprotectin D1 Induces TH-Positive Neuronal Survival in a Cellular Model of XXXX .

@entity1 @entity5212 @entity137 @entity935 @entity3788 @entity19 @entity191 @entity179 @entity9013 @entity528
@entity191 ( @entity191 ) does not manifest clinically until 80 % of striatal @entity935 is reduced, thus most @entity528 takes place before the @entity1 presents clinical symptoms. Therefore, it is important to develop preventive strategies for this disease. In the experimental models of @entity191 , @entity9013 ion (MPP+) and @entity3788 induce @entity137 in dopaminergic neurons. Neuroprotectin D1 (NPD1) displays neuroprotection in cells undergoing proteotoxic and oxidative stress. In the present report, we established an in vitro model using a primary neuronal culture from mesencephalic embryonic @entity19 tissue in which 17-20 % of neurons were TH-positive when differentiated in vitro. NPD1 (100 nM) rescued cells from apoptosis induced by MPP+ and @entity3788 , and the dendritic arbor of surviving neurons was examined using Sholl analysis. @entity3788 , as well as MPP+ and its precursor @entity5212 ( @entity5212 ), severely promoted retraction of dendritic arbor distal segments, thus decreasing the maximum branch order reached. On average, NPD1 counteracted the effects of MPP+ on the dendritic arborization, but failed to do so in the @entity3788 -treated neurons. However, @entity3788 did decrease the Sholl intersection number from radii 25 to 125   m, and NPD1 did restore the pattern to control levels. Similarly, NPD1 partially reverted the dendrite retraction caused by MPP+ and @entity5212 . These results suggest that the apoptosis occurring in mesencephalic TH-positive neurons is not a direct consequence of mitochondrial dysfunction alone and that NPD1 signaling may be counteracting this damage. These findings lay the groundwork for the use of the in vitro model developed for future studies and for the search of specific molecular events that NPD1 targets to prevent @entity179 in @entity191 .
