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PD.Activator.Office.2013.Win7 __EXCLUSIVE__


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PD.Activator.Office.2013.Win7 __EXCLUSIVE__


One month after an OVX, DA neurons in the midbrain of these female mice begin to die. Thus, we used a midbrain-specific Thy1-ChR2-YFP transgenic mouse line to label DA neurons during the progression of the disease. The fluorescence of the YFP protein in a living neuron was dependent on ChR2 activation. We found that midbrain DA neurons gradually lost their ability to fire action potentials in the majority of mice that were treated with the OVX, indicating that these neurons were nearly completely damaged. At 1 month after the OVX, none of the DA neurons fired action potentials in the absence of ChR2 activation. As estrogen levels rapidly declined during this period, the DA neurons lost their ability to fire action potentials in the majority of the mice. Estrogen treatment 2 months after the OVX partially restored ChR2-induced DA neuron firing. When the estrogen supplement was stopped, ChR2-induced DA neuron firing almost completely disappeared. The ChR2-induced ChAT+ neuron death was also significantly attenuated by the E2 supplement. This study indicated that estrogen has a role in preserving midbrain DA neurons. This role of estrogen might be mediated by modulation of Kir2.1 channels expressed in microglia.


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