Posted by CrAzYmEd on May 24, 2010, at 4:24:03 [reposted on May 24, 2010, at 22:44:00 | original URL]
In reply to , posted by on December 31, 1969, at 18:00:00
Personally i beleive that the low dopamine binding in OCD comes from hyperactive glutamate activity (just as glutamate hyperactivity seems to cause low dopamine binding in ALS).
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Decreased striatal dopamine-receptor binding in sporadic ALS: Glutamate hyperactivity?O. J. M. Vogels, MD, PhD, W. J. G. Oyen, MD, PhD, B. G. M. van Engelen, MD, PhD, G. W. A. M. Padberg, MD, PhD and M. W. I. M. Horstink, MD, PhD
From the Departments of Neurology (Drs. Vogels, van Engelen, Padberg, and Horstink) and Nuclear Medicine (Dr. Oyen), University Hospital Nijmegen, the Netherlands.Address correspondence and reprint requests to Dr. O.J.M. Vogels, Department of Neurology, University Hospital Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, the Netherlands.
The pathogenesis of ALS may be related to increased glutamatergic excitotoxicity. The striatum receives massive glutamatergic input. Animal studies suggest that glutamate decreases striatal D2-receptor synthesis. In drug-naïve, sporadic ALS patients we demonstrated decreased striatal D2-receptor binding in vivo that could be partially reversed by the glutamatergic transmission blocker riluzole. Our findings support the glutamatergic excitotoxicity hypothesis in sporadic ALS.
--------------------------------------------Memantine has been shown effective for OCD (it did wonders for wine) while it hasnt got any anti dopaminergic activity, instead it can upregulates dopamine receptors (altough no idea how significant this is in therapeutic relevant doses) and has dopamine agonist properties itself.
But yeah its really complex, and this is my own little theory :p, but i dont buy the too much dopamine theory.
Interesting discussion besides:p.
poster:CrAzYmEd
thread:948688
URL: http://www.dr-bob.org/babble/neuro/20100223/msgs/948730.html