Lesion of medullary catecholaminergic neurons is associated with cardiovascular dysfunction in rotenone-induced Parkinson's disease rats.

Zhang Z, Du X, Xu H, Xie J, Jiang H.
Eur J Neurosci. 2015 Sep;42(6):2346-55. doi: 10.1111/ejn.13012. Epub 2015 Jul 30.

-Direct link here
In this paper, they examined relationships in the loss of dopaminergic neurons in the substantia nigra with loss of catecholaminergic neurons in the RVLM in rat model cases of rotenone-induced Parkinson's Disease (PD). This is an interesting study because symptoms signifying sympathatic disorders (e.g. instability in heart rate and blood pressure, orthostatic intolerance, etc) are frequently linked with PD and are some of the early warning signs of the disease. They gave rats i.p. injections of rotenone, the insectiside that is known to induce a condition highly similar to PD, and examined groups at different time points. They found that, similar to humans, issues with control of blood pressure (and decreases in plasma epinephrine and norepinephrine) arose before the loss of midbrain dopaminergic neurons or the appearance of motor symptoms. They also noted a decreased influence of low frequencies on heart rate after rotenone, suggesting a decrease in sympathetic never activity. Most interestingly, they noted that there was a loss of TH and DBH positive neurons and a decrease of TH and DBH proteins in the RVLM. These changes occurred early, despite the fact that loss of catecholaminergic neurons occurred later and not at all in the CVLM and NTS, respectively.
So the big questions after reading this paper are what makes C1 neurons so sensitive to rotenone and what else wipes them out? Neuroplasticity is one thing, because it can be reversible... but losing them entirely is another. -DH