ArticleDevelopmental neuroscience2006
The role of dopamine receptors in the neurobehavioral syndrome provoked by activation of L-type calcium channels in rodents.
Article in Developmental neuroscience, 2006. 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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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
10 citing papers in PubMed, 23 citations in OpenAlex.
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- Neuroinflammation Involving Endothelin-1 and Platelet-Activating Factor Receptors Contributes To Self-Injurious Behaviors Induced by Bay k-8644 in Adolescent Mice.Neurochemical research · 2025Article
- Molecular Pathways, Neural Circuits and Emerging Therapies for Self-Injurious Behaviour.International journal of molecular sciences · 2025Review
- Hypervitaminosis DIranian journal of veterinary research · 2017Article
- Use of vitamin d3 and its metabolites in broiler chicken feed on performance, bone parameters and meat quality.Asian-Australasian journal of animal sciences · 2013Article
- Decreased striatal dopamine receptor binding in primary focal dystonia: a D2 or D3 defect?Movement disorders : official journal of the Movement Disorder Society · 2011Article
- D2 dopamine receptor subtype-mediated hyperactivity and amphetamine responses in a model of ADHD.Neurobiology of disease · 2010Article
- Computational models of neuronal biophysics and the characterization of potential neuropharmacological targets.Current medicinal chemistry · 2008Review
- Neuroanatomical substrates for paroxysmal dyskinesia in lethargic mice.Neurobiology of disease · 2007Article
- Nifedipine suppresses self-injurious behaviors in animals.Developmental neuroscience · 2007Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
In rodents, activation of L-type calcium channels with +/-BayK 8644 causes an unusual behavioral syndrome that includes dystonia and self-biting. Prior studies have linked both of these behaviors to dysfunction of dopaminergic transmission in the striatum. The current studies were designed to further elucidate the relationship between +/-BayK 8644 and dopaminergic transmission in the expression of the behavioral syndrome. The drug does not appear to release presynaptic dopamine stores, since microdialysis of the striatum revealed dopamine release was unaltered by +/-BayK 8644. In addition, the behaviors were preserved or even exaggerated in mice or rats with virtually complete dopamine depletion. On the other hand, pretreatment of mice with D(3) or D(1/5) dopamine receptor antagonists attenuated the behavioral effects of +/-BayK 8644, while pretreatment with D(2) or D(4) antagonists had no effect. In D(3) receptor knockout mice, +/-BayK 8644 elicited both dystonia and self-biting, but these behaviors were less severe than in matched controls. In D(1) receptor knockout mice, behavioral responses to +/-BayK 8644 appeared exaggerated. These results argue that the behavioral effects of +/-BayK 8644 are not mediated by a presynaptic influence. Instead, the behaviors appear to result from a postsynaptic activation of the drug, which does not require but can be modified by D(3) or D(1/5) receptors.
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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.