ArticleNeuroscience2011
Functional reorganization of the presynaptic dopaminergic terminal in parkinsonism.
Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Serotonin deficiency caused by inactivation of Tph2 in mice leads to widespread sex-dependent changes in cerebral oxidative metabolic activity.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Article
- Dopamine Release Impairments Accompany Locomotor and Cognitive Deficiencies in Rotenone-Treated Parkinson's Disease Model Zebrafish.Chemical research in toxicology · 2022Article
- Review
- MPTP Mouse Model of Preclinical and Clinical Parkinson's Disease as an Instrument for Translational Medicine.Molecular neurobiology · 2018Article
- Regulation of Tyrosine Hydroxylase Expression and Phosphorylation in Dopamine Transporter-Deficient Mice.ACS chemical neuroscience · 2016Article
- Loss of Homeostasis in the Direct Pathway in a Mouse Model of Asymptomatic Parkinson's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- How compensation breaks down in Parkinson's disease: Insights from modeling of denervated striatum.Movement disorders : official journal of the Movement Disorder Society · 2016Review
- The impact of a parkinsonian lesion on dynamic striatal dopamine transmission depends on nicotinic receptor activation.Neurobiology of disease · 2015Article
- Electrochemical Analysis of Neurotransmitters.Annual review of analytical chemistry (Palo Alto, Calif.) · 2015Review
- Methamphetamine-induced neurotoxicity disrupts pharmacologically evoked dopamine transients in the dorsomedial and dorsolateral striatum.Neurotoxicity research · 2014Article
- Methamphetamine-induced neurotoxicity disrupts naturally occurring phasic dopamine signaling.The European journal of neuroscience · 2013Article
- The spontaneously hypertensive and Wistar Kyoto rat models of ADHD exhibit sub-regional differences in dopamine release and uptake in the striatum and nucleus accumbens.Neuropharmacology · 2012Article
- Using in vivo voltammetry to demonstrate drug action: a student laboratory experience in neurochemistry.Journal of undergraduate neuroscience education : JUNE : a publication of FUN, Faculty for Undergraduate Neuroscience · 2012Article
- Dopamine transporter loss in 6-OHDA Parkinson's model is unmet by parallel reduction in dopamine uptake.PloS one · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Whether dopamine (DA) release is compensated during the presymptomatic phase of Parkinson's disease (PD) is controversial. Here we use in vivo voltammetry in the parkinsonian rat and an electrical stimulation protocol established to fatigue nigrostriatal dopaminergic (DAergic) neurons to investigate the plasticity of DA-release mechanisms. Amplitudes of evoked voltammetric signals recorded in intact rat striata decreased with repetitive, high-frequency stimulation (60 Hz, every 5 min/60 min). Strikingly, DA levels were maintained during an identical "fatiguing" protocol in 6-hydroxydopamine-lesioned (<40% denervation) striata in the absence of enhanced DA synthesis. In contrast, more severely lesioned striata (>55% denervation) also appeared to sustain DA release, however, this was demonstrated in the presence of enhanced synthesis. Sustained release was replicated in intact animals after irreversible blockade of the dopamine transporter (DAT) via RTI-76, implicating neuronal uptake as a trigger. We further demonstrate through kinetic analysis that lesions and compromised uptake target a "long-term" (time constant of minutes) presynaptic depression, which underlies the maintenance of release. Taken together, our findings identify a denervation-induced maintenance of DA release that was independent of activated synthesis and driven by altered uptake. This novel neuroadaptation may contribute to early preclinical normalization of function and help resolve discrepant findings regarding compensatory changes in DA release during progression of the parkinsonian state.
Indexed as
Identifiers
What OpenQuestion holds
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.