ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Partial mitochondrial inhibition causes striatal dopamine release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 109 citations in OpenAlex.
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- Endogenous hydrogen peroxide positively regulates secretion of a gut-derived peptide in neuroendocrine potentiation of the oxidative stress response inbioRxiv : the preprint server for biology · 2024Article
- Mitochondrial Hydrogen Peroxide Activates PTEN and Inactivates Akt Leading to Autophagy Inhibition-Dependent Cell Death in Neuronal Models of Parkinson's Disease.Molecular neurobiology · 2023Article
- Glibenclamide alters serotonin and dopamine levels in the rat striatum and hippocampus, reducing cognitive impairment.Psychopharmacology · 2022Article
- NOX2-derived hydrogen peroxide impedes the AMPK/Akt-mTOR signaling pathway contributing to cell death in neuronal cells.Cellular signalling · 2022Article
- Hydrogen peroxide suppresses excitability of gonadotropin-releasing hormone neurons in adult mouse.Frontiers in endocrinology · 2022Article
- Dopamine signaling impairs ROS modulation by mitochondrial hexokinase in human neural progenitor cells.Bioscience reports · 2021Article
- Neonatal Rotenone Administration Induces Psychiatric Disorder-Like Behavior and Changes in Mitochondrial Biogenesis and Synaptic Proteins in Adulthood.Molecular neurobiology · 2021Article
- A New Insight on the Radioprotective Potential of Epsilon-Aminocaproic Acid.Medicina (Kaunas, Lithuania) · 2020Article
- Anti-hypertensive effect of hydrogen peroxide acting centrally.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- The interplay between oxidative stress and bioenergetic failure in neuropsychiatric illnesses: can we explain it and can we treat it?Molecular biology reports · 2020Review
- Dopamine neuronal protection in the mouse Substantia nigra by GHSR is independent of electric activity.Molecular metabolism · 2019Article
- Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction.Neurobiology of aging · 2019Article
- Selective and Mechanically Robust Sensors for Electrochemical Measurements of Real-Time Hydrogen Peroxide Dynamics in Vivo.Analytical chemistry · 2018Article
- Could α-Synuclein Modulation of Insulin and Dopamine Identify a Novel Link Between Parkinson's Disease and Diabetes as Well as Potential Therapies?Frontiers in molecular neuroscience · 2018Review
- Reactive oxygen species increase neuronal excitability via activation of nonspecific cation channel in rat medullary dorsal horn neurons.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- Crosstalk between Ca2+ signaling and mitochondrial H2O2 is required for rotenone inhibition of mTOR signaling pathway leading to neuronal apoptosis.Oncotarget · 2016Article
- Inhibitory and excitatory neuromodulation by hydrogen peroxide: translating energetics to information.The Journal of physiology · 2015Review
- Dopaminergic and cholinergic modulation of striatal tyrosine hydroxylase interneurons.Neuropharmacology · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction is a potential causal factor in Parkinson's disease. We show here that acute exposure to the mitochondrial complex I inhibitor rotenone (30-100 nM; 30 min) causes concentration-dependent suppression of single-pulse evoked dopamine (DA) release monitored in real time with carbon-fiber microelectrodes in guinea pig striatal slices, with no effect on DA content. Suppression of DA release was prevented by the sulfonylurea glibenclamide, implicating ATP-sensitive K+ (KATP) channels; however, tissue ATP was unaltered. Because KATP channels can be activated by hydrogen peroxide (H2O2), as well as by low ATP, we examined the involvement of rotenone-enhanced H2O2 generation. Confirming an essential role for H2O2, the inhibition of DA release by rotenone was prevented by catalase, a peroxide-scavenging enzyme. Striatal H2O2 generation during rotenone exposure was examined in individual medium spiny neurons using fluorescence imaging with dichlorofluorescein (DCF). An increase in intracellular H2O2 levels followed a similar time course to that of DA release suppression and was accompanied by cell membrane depolarization, decreased input resistance, and increased excitability. Extracellular catalase markedly attenuated the increase in DCF fluorescence and prevented rotenone-induced effects on membrane properties; membrane changes were also largely prevented by flufenamic acid, a blocker of transient receptor potential (TRP) channels. Thus, partial mitochondrial inhibition can cause functional DA denervation via H2O2 and KATP channels, without DA or ATP depletion. Furthermore, amplified H2O2 levels and TRP channel activation in striatal spiny neurons indicate potential sources of damage in these cells. Overall, these novel factors could contribute to parkinsonian motor deficits and neuronal degeneration caused by mitochondrial dysfunction.
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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.