| First Author | Gantz SC | Year | 2015 |
| Journal | Cell Rep | Volume | 12 |
| Issue | 6 | Pages | 944-54 |
| PubMed ID | 26235617 | Mgi Jnum | J:232898 |
| Mgi Id | MGI:5780392 | Doi | 10.1016/j.celrep.2015.07.005 |
| Citation | Gantz SC, et al. (2015) Depression of Serotonin Synaptic Transmission by the Dopamine Precursor L-DOPA. Cell Rep 12(6):944-54 |
| abstractText | Imbalance between the dopamine and serotonin (5-HT) neurotransmitter systems has been implicated in the comorbidity of Parkinson's disease (PD) and psychiatric disorders. L-DOPA, the leading treatment of PD, facilitates the production and release of dopamine. This study assessed the action of L-DOPA on monoamine synaptic transmission in mouse brain slices. Application of L-DOPA augmented the D2-receptor-mediated inhibitory postsynaptic current (IPSC) in dopamine neurons of the substantia nigra. This augmentation was largely due to dopamine release from 5-HT terminals. Selective optogenetic stimulation of 5-HT terminals evoked dopamine release, producing D2-receptor-mediated IPSCs following treatment with L-DOPA. In the dorsal raphe, L-DOPA produced a long-lasting depression of the 5-HT1A-receptor-mediated IPSC in 5-HT neurons. When D2 receptors were expressed in the dorsal raphe, application of L-DOPA resulted in a D2-receptor-mediated IPSC. Thus, treatment with L-DOPA caused ectopic dopamine release from 5-HT terminals and a loss of 5-HT-mediated synaptic transmission. |
