ArticleNeurobiology of disease2015
The impact of a parkinsonian lesion on dynamic striatal dopamine transmission depends on nicotinic receptor activation.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- GABA uptake transporters support dopamine release in dorsal striatum with maladaptive downregulation in a parkinsonism model.Nature communications · 2020Article
- Plasticity in striatal dopamine release is governed by release-independent depression and the dopamine transporter.Nature communications · 2019Article
- The striatal cholinergic system in L-dopa-induced dyskinesias.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Desynchronization of slow oscillations in the basal ganglia during natural sleep.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Glutamate Cotransmission in Cholinergic, GABAergic and Monoamine Systems: Contrasts and Commonalities.Frontiers in neural circuits · 2018Review
- Review
- Striatal dopamine neurotransmission: regulation of release and uptake.Basal ganglia · 2016Article
- LRRK2 BAC transgenic rats develop progressive, L-DOPA-responsive motor impairment, and deficits in dopamine circuit function.Human molecular genetics · 2016Article
- Dopamine-dependent modulation of rat globus pallidus excitation by nicotine acetylcholine receptors.Experimental brain research · 2016Article
- Preclinical Evidence for a Role of the Nicotinic Cholinergic System in Parkinson's Disease.Neuropsychology review · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Dopamine function is disturbed in Parkinson's disease (PD), but whether and how release of dopamine from surviving neurons is altered has long been debated. Nicotinic acetylcholine receptors (nAChRs) on dopamine axons powerfully govern dopamine release and could be critical contributing factors. We revisited whether fundamental properties of dopamine transmission are changed in a parkinsonian brain and tested the potentially profound masking effects of nAChRs. Using real-time detection of dopamine in mouse striatum after a partial 6-hydroxydopamine lesion and under nAChR inhibition, we reveal that dopamine signals show diminished sensitivity to presynaptic activity. This effect manifested as diminished contrast between DA release evoked by the lowest versus highest frequencies. This reduced activity-dependence was underpinned by loss of short-term facilitation of dopamine release, consistent with an increase in release probability (Pr). With nAChRs active, the reduced activity-dependence of dopamine release after a parkinsonian lesion was masked. Consequently, moment-by-moment variation in activity of nAChRs may lead to dynamic co-variation in dopamine signal impairments in PD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.