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Brian I tried attaching to the web site, but didn't have any luck. Could you e-mail a copy of the paper directly to a fellow engineer? Now regarding avoiding Sinemet, I guess I agree that metering the correct dosage is most difficult as the disease progesses. However, there is something that has been bothering me and that is, why should all the symptoms be attributed to loss of dopamine producing cells? Yes the dopamine is produced in the substantia nigra, but it is used by the neurons in the basil ganglia. Each neuron has seven (I think) dopamine receptors which seem to respond as quantizers. Based on the level of dopamine detected by the receptor, a proportionate amount is released to the next neuron across the synapse which activates its receptors. The dopamine is broken down and recaptured by the firing neuron for another shot. Somewhere along the pathway, these dopamine sensitive neurons somehow have a dampening affect ( I postulate the summing node of the feedback loop) on those acetylcholine sensitive neurons which actually activate the muscles. As a system engineer, it seems that there a lot of different failure modes inside the back box that would manifest themselves with the same response outside of this black box. What if my symptoms are caused by failure of dopamine receptors (lose sensitvity)? Or maybe a failure of the transmitter that squirts the dopamine across the synapse. Or maybe the inability to recapture the expended dopamine. Or maybe a failure of the summing node. This last one gets real tricky because I've never seen an explanation as to how the dopamine firing neurons impact the firing of the acetylcholine activated neurons. Just something for you retired guys to ponder. Phil Gesotti 49/46