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Toxics 2015, 3(1), 75-88; doi:10.3390/toxics3010075

L-Dopa and Brain Serotonin System Dysfunction

Department of Neurosciences, University of Toledo College of Medicine, 3000 Arlington Ave, Toledo, OH 43561, USA
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Author to whom correspondence should be addressed.
Academic Editor: Guido Cavaletti
Received: 22 January 2015 / Revised: 16 February 2015 / Accepted: 26 February 2015 / Published: 5 March 2015
(This article belongs to the Special Issue Toxicities of Therapeutic Agents Used in Medicine)
View Full-Text   |   Download PDF [420 KB, uploaded 5 March 2015]

Abstract

L-dopa is used to treat the motor symptoms associated with Parkinson’s disease, a neurodegenerative movement disorder characterized by a loss of dopamine neurons. L-dopa is the precursor to dopamine and crosses the blood-brain barrier to increase dopamine neurotransmission. This review will focus on the findings that dopamine produced from L-dopa is mediated in part by serotonin neurons. Direct evidence will be provided that increases in dopamine cause oxidative stress and damage serotonin neurons. Similarly, chronic L-dopa produces deficits in serotonin neurotransmission, including decreases in both serotonin cell bodies within the dorsal raphe and serotonin neurotransmitter concentrations in several forebrain regions. Since serotonin is involved in many important physiological processes including mood and cognition, L-dopa induced serotonin deficits may play a role in the side-effect symptoms observed in Parkinson’s disease patients treated with L-dopa. View Full-Text
Keywords: 6-hydroxydopamine; dopamine; L-dopa; non-motor symptoms; Parkinson’s disease; serotonin neurons 6-hydroxydopamine; dopamine; L-dopa; non-motor symptoms; Parkinson’s disease; serotonin neurons
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Stansley, B.J.; Yamamoto, B.K. L-Dopa and Brain Serotonin System Dysfunction. Toxics 2015, 3, 75-88.

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