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Monday, April 21, 2014 2:05:39 PM
About Eltoprazine and its role in dyskinesias
Serotonin neurons are known to be able to convert levodopa to dopamine, as well as store and release dopamine in an activity-dependent manner. In advanced patients, where the dopamine terminals have largely degenerated, serotonin terminals are considered a major source of dopamine release. However, serotonin neurons lack feedback control mechanisms for the release of dopamine, such as the D2 autoreceptor and the dopamine transporter, which normally regulate the synaptic level of dopamine within a physiological range. Administration of levodopa, therefore generates high swings in synaptic dopamine, causing pulsatile stimulation of post-synaptic dopamine receptors, and the appearance of dyskinesia. Preclinical research has shown that removal of the serotonin innervation or activation of pre-synaptic receptors of the serotonin neurons by a combination of 5-HT1A and 5-HT1B receptor agonists produces a suppression of LID. On the basis of these findings it was logical to test eltoprazine in a LID clinical trial.
http://www.businesswire.com/news/home/20120612005589/en/PsychoGenics-Announces-Positive-Efficacy-Data-Levodopa-Induced#.U1VeO_ldXQM
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