Jurnal Internasional Gangguan Morfologi Somatodendritic yang progresif pada Neuron Dopamin pada Model Tikus Parkinson – Gangguan Gerakan – Lynch
Background:  Parkinson's disease is characterized by the loss of progressive dopamine neurons in the substantia nigra, which causes severe motor deficits. Although this disease may begin to develop for years before observable motor symptoms, certain morphological and functional changes involved are poorly understood.
Purpose: MitoPark mice do not have a gene that encodes the transcription factors of mitochondria A especially in dopamine neurons, which over time produce a progressive decrease in neuronal function and related behavior that phenotypically reflects human parkinsonism. Our previous work identified a progressive decrease in cell capacitance in dopamine neurons from MitoPark mice, possibly indicating reduced membrane surface area. We therefore try to identify and measure somatodendritic parameters in this model across ages.
Method: We used whole cell patch clamp and fluorescent labeling to measure somatodendritic morphology of a single neurobiotin dopamine neurop filled in acute isolated brain pieces from MitoPark mice.
Results: We found that MitoPark mice showed adult onset, age-dependent reduction of neuritic branching and soma size in dopamine neurons. This decrease took place similarly in MitoPark mice of both sexes, but did not begin until after age whose initial decline in ion channel physiology and behavior had previously been observed.
Conclusion: Progressive and severe decline in somatodendritic morphology occurs before cell death, but is not responsible for subtle subtraction seen in the early stages of neurodegeneration. This work can help identify the ideal window of time for special treatments to stop the progression of the disease and prevent debilitating motor deficits in Parkinson's patients. © 2018 International Parkinson and Disorder Society Movement