The Docosanoid Neuroprotectin D1 Induces TH-Positive Neuronal Survival in a Cellular Model of Parkinson’s Disease

• DOI: 10.1007/s10571-015-0206-6
• Publication Date: 2015-06-05T09:26:36Z
• Authors: Jorgelina M. Cala...; Michelle W. Sharp; Nicolas G. Bazan
• Keywords: Neurons; 0303 health sciences; Docosahexaenoic Acids; Tyrosine 3-Monooxygenase; Cell Survival; Cell Biology; Rats; 3. Good health; Rats, Sprague-Dawley; Cellular and Molecular Neuroscience; 03 medical and health sciences; Parkinsonian Disorders; Mesencephalon; Rotenone; Animals; Cells, Cultured; Original Research

Parkinson's disease (PD) does not manifest clinically until 80 % of striatal dopamine is reduced, thus most neuronal damage takes place before the patient presents clinical symptoms. Therefore, it important to develop preventive strategies for this disease. In experimental models PD, 1-methyl-4-phenylpyridinium ion (MPP+) and rotenone induce toxicity in dopaminergic neurons. Neuroprotectin D1 (NPD1) displays neuroprotection cells undergoing proteotoxic oxidative stress. present report, we established an vitro model using a primary culture from mesencephalic embryonic mouse tissue which 17-20 neurons were TH-positive when differentiated vitro. NPD1 (100 nM) rescued apoptosis induced by MPP+ rotenone, dendritic arbor surviving was examined Sholl analysis. Rotenone, as well its precursor 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), severely promoted retraction distal segments, decreasing maximum branch order reached. On average, counteracted effects on arborization, but failed do so rotenone-treated However, did decrease intersection number radii 25 125 µm, restore pattern control levels. Similarly, partially reverted dendrite caused MPTP. These results suggest that occurring direct consequence mitochondrial dysfunction alone signaling may be counteracting damage. findings lay groundwork use developed future studies search specific molecular events targets prevent early neurodegeneration PD.