{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Keifman E"],"funding":["Fundación Ramón Areces","Agencia Nacional de Promoción Científica y Tecnológica","Ministerio de Sanidad, Servicios Sociales e Igualdad"],"pagination":["2146-2161"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6555865"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["176(13)"],"pubmed_abstract":["<h4>Background and purpose</h4>L-DOPA-induced dyskinesia (LID) remains a major complication of L-DOPA therapy in Parkinson's disease. LID is believed to result from inhibition of substantia nigra reticulata (SNr) neurons by GABAergic striatal projection neurons that become supersensitive to dopamine receptor stimulation after severe nigrostriatal degeneration. Here, we asked if stimulation of direct medium spiny neuron (dMSN) GABAergic terminals at the SNr can produce a full dyskinetic state similar to that induced by L-DOPA.<h4>Experimental approach</h4>Adult C57BL6 mice were lesioned with 6-hydroxydopamine in the medial forebrain bundle. Channel rhodopsin was expressed in striatonigral terminals by ipsilateral striatal injection of adeno-associated viral particles under the CaMKII promot"],"journal":["British journal of pharmacology"],"pubmed_title":["Optostimulation of striatonigral terminals in substantia nigra induces dyskinesia that increases after L-DOPA in a mouse model of Parkinson's disease."],"pmcid":["PMC6555865"],"funding_grant_id":["2015 3687","CIBERNED CB06/05/0055","PICT 2013 1523","OTR02679","172275","PNSD 2016/033"],"pubmed_authors":["Ruiz-DeDiego I","Paz RM","Pafundo DE","Keifman E","Solis O","Murer MG","Moratalla R"],"additional_accession":[]},"is_claimable":false,"name":"Optostimulation of striatonigral terminals in substantia nigra induces dyskinesia that increases after L-DOPA in a mouse model of Parkinson's disease.","description":"<h4>Background and purpose</h4>L-DOPA-induced dyskinesia (LID) remains a major complication of L-DOPA therapy in Parkinson's disease. LID is believed to result from inhibition of substantia nigra reticulata (SNr) neurons by GABAergic striatal projection neurons that become supersensitive to dopamine receptor stimulation after severe nigrostriatal degeneration. Here, we asked if stimulation of direct medium spiny neuron (dMSN) GABAergic terminals at the SNr can produce a full dyskinetic state similar to that induced by L-DOPA.<h4>Experimental approach</h4>Adult C57BL6 mice were lesioned with 6-hydroxydopamine in the medial forebrain bundle. Channel rhodopsin was expressed in striatonigral terminals by ipsilateral striatal injection of adeno-associated viral particles under the CaMKII promot","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jul","modification":"2026-04-07T16:43:18.836Z","creation":"2020-07-04T07:13:35Z"},"accession":"S-EPMC6555865","cross_references":{"pubmed":["30895594"],"doi":["10.1111/bph.14663"]}}