What mechanisms are responsible for the reuptake of levodopa-derived dopamine in parkinsonian striatum?
Levodopa is the most effective medication for motor symptoms in Parkinson’s disease. However, various motor and non-motor complications are associated with levodopa treatment, resulting from altered levodopa-dopamine metabolism with disease progression and long-term use of the drug. The present revi...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2016-12-01
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| Series: | Frontiers in Neuroscience |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnins.2016.00575/full |
| _version_ | 1818850840580980736 |
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| author | Haruo Nishijima Haruo Nishijima Masahiko Tomiyama Masahiko Tomiyama |
| author_facet | Haruo Nishijima Haruo Nishijima Masahiko Tomiyama Masahiko Tomiyama |
| author_sort | Haruo Nishijima |
| collection | DOAJ |
| description | Levodopa is the most effective medication for motor symptoms in Parkinson’s disease. However, various motor and non-motor complications are associated with levodopa treatment, resulting from altered levodopa-dopamine metabolism with disease progression and long-term use of the drug. The present review emphasizes the role of monoamine transporters other than the dopamine transporter in uptake of extracellular dopamine in the dopamine-denervated striatum. When dopaminergic neurons are lost and dopamine transporters decreased, serotonin and norepinephrine transporters compensate by increasing uptake of excessive extracellular dopamine in the striatum. Organic cation transporter-3 and plasma membrane monoamine transporter, low affinity and high capacity transporters, also potentially uptake dopamine when high-affinity transporters do not work normally. Selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors are often administered to patients with Parkinson’s disease presenting with depression, pain or other non-motor symptoms. Thus, it is important to address the potential of these drugs to modify dopamine metabolism and uptake through blockade of the compensatory function of these transporters, which could lead to changes in motor symptoms of Parkinson’s disease. |
| first_indexed | 2024-12-19T06:55:32Z |
| format | Article |
| id | doaj.art-f1450c5c0e4a4a4b82949cb0b4e0e03a |
| institution | Directory Open Access Journal |
| issn | 1662-453X |
| language | English |
| last_indexed | 2024-12-19T06:55:32Z |
| publishDate | 2016-12-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neuroscience |
| spelling | doaj.art-f1450c5c0e4a4a4b82949cb0b4e0e03a2022-12-21T20:31:33ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2016-12-011010.3389/fnins.2016.00575229320What mechanisms are responsible for the reuptake of levodopa-derived dopamine in parkinsonian striatum?Haruo Nishijima0Haruo Nishijima1Masahiko Tomiyama2Masahiko Tomiyama3Aomori Prefectural Central HospitalHirosaki University Graduate School of MedicineAomori Prefectural Central HospitalHirosaki University Graduate School of MedicineLevodopa is the most effective medication for motor symptoms in Parkinson’s disease. However, various motor and non-motor complications are associated with levodopa treatment, resulting from altered levodopa-dopamine metabolism with disease progression and long-term use of the drug. The present review emphasizes the role of monoamine transporters other than the dopamine transporter in uptake of extracellular dopamine in the dopamine-denervated striatum. When dopaminergic neurons are lost and dopamine transporters decreased, serotonin and norepinephrine transporters compensate by increasing uptake of excessive extracellular dopamine in the striatum. Organic cation transporter-3 and plasma membrane monoamine transporter, low affinity and high capacity transporters, also potentially uptake dopamine when high-affinity transporters do not work normally. Selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors are often administered to patients with Parkinson’s disease presenting with depression, pain or other non-motor symptoms. Thus, it is important to address the potential of these drugs to modify dopamine metabolism and uptake through blockade of the compensatory function of these transporters, which could lead to changes in motor symptoms of Parkinson’s disease.http://journal.frontiersin.org/Journal/10.3389/fnins.2016.00575/fullDopamineLevodopaNorepinephrineSerotoninStriatumtransporter |
| spellingShingle | Haruo Nishijima Haruo Nishijima Masahiko Tomiyama Masahiko Tomiyama What mechanisms are responsible for the reuptake of levodopa-derived dopamine in parkinsonian striatum? Frontiers in Neuroscience Dopamine Levodopa Norepinephrine Serotonin Striatum transporter |
| title | What mechanisms are responsible for the reuptake of levodopa-derived dopamine in parkinsonian striatum? |
| title_full | What mechanisms are responsible for the reuptake of levodopa-derived dopamine in parkinsonian striatum? |
| title_fullStr | What mechanisms are responsible for the reuptake of levodopa-derived dopamine in parkinsonian striatum? |
| title_full_unstemmed | What mechanisms are responsible for the reuptake of levodopa-derived dopamine in parkinsonian striatum? |
| title_short | What mechanisms are responsible for the reuptake of levodopa-derived dopamine in parkinsonian striatum? |
| title_sort | what mechanisms are responsible for the reuptake of levodopa derived dopamine in parkinsonian striatum |
| topic | Dopamine Levodopa Norepinephrine Serotonin Striatum transporter |
| url | http://journal.frontiersin.org/Journal/10.3389/fnins.2016.00575/full |
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