ArticleMetabolic brain disease2001
Effects of voltage-sensitive calcium channel blockers on extracellular dopamine levels in rat striatum.
Article in Metabolic brain disease, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- 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
- Impaired striatal dopamine output of homozygous Wfs1 mutant mice in response to [K+] challenge.Journal of physiology and biochemistry · 2011Article
- Presynaptic control of serotonin on striatal dopamine function.Psychopharmacology · 2011Review
- Low concentrations of methamphetamine can protect dopaminergic cells against a larger oxidative stress injury: mechanistic study.PloS one · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various subtypes of voltage-sensitive calcium channels (VSCCs) support the release of dopamine (DA) in the central nervous system. Using in vivo microdialysis, we investigate the influence of these subtypes of calcium channels on dopaminergic terminals in the rat striatum. L-type (nifedipine-sensitive), N-type (omega-conotoxin GVIA-sensitive), or N- and P/Q-type (omega-conotoxin MVIIC-sensitive) Ca2+ channels were blocked using selective antagonists injected locally, and K+-evoked DA release was measured in freely moving animals. K+ (100 mM) induced a massive increase of basal DA extracellular levels (930%) and was without significant effect on extracellular levels of DA metabolites DOPAC and HVA, and on the serotonin metabolite 5HIAA. Omega-conotoxin GVIA (1 microM) and omega-conotoxin MVIIC (1 microM) significantly reduced the K+-evoked DA release by 55 and 62%, respectively. The simultaneous application of the two conotoxins at the same concentration reduced K+-evoked DA release by 66%. Nifedipine (10 microM) had no significant effect on K-evoked DA release, while neomycin, a nonspecific VSCC blocker, produced a highly significant decrease when applied at 250 and 500 microM (56 and 75%, respectively). The compounds. however, had no effect on basal DA release and on the levels of extracellular DOPAC, HVA, and 5HIAA. These results suggest that under high and persistent conditions of membrane depolarization (15 min, 10 mM K+), striatal DA release is mainly mediated by N-type VSCCs.
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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.