Evidence map›Paper›PMID 24848473›Full record

ArticleJournal of neurophysiology2014

Cav1.2 and Cav1.3 L-type calcium channels regulate dopaminergic firing activity in the mouse ventral tegmental area.

Yudan Liu, Meghan Harding, Andrea Pittman, Jules Dore, Jörg Striessnig, Anjali Rajadhyaksha, Xihua Chen

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 70 citations in OpenAlex.

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  16. CaScience advances · 2022
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  17. Nonlinear relationship between CAN current andCognitive neurodynamics · 2022
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  18. Review
  19. Tuberous Sclerosis Complex (TSC) Inactivation Increases Neuronal Network Activity by Enhancing CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 4 countries.

Yudan LiuDepartment of Physiology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, Shenyang, Liaoning, China; redfeatherliu@hotmail.com.
Meghan HardingDivision of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland, Canada;
Andrea PittmanDivision of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland, Canada;
Jules DoreDivision of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland, Canada;
Jörg StriessnigDepartment of Pharmacology and Toxicology, Institute of Pharmacy and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria; and.
Anjali RajadhyakshaDivision of Pediatric Neurology, Department of Pediatrics and Brain and Mind Research Institute, Weill Cornell Medical College of Cornell University, New York.
Xihua ChenDivision of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland, Canada;
Memorial University of Newfoundland · CAMIND Research Institute · USShenyang Pharmaceutical University · CNUniversität Innsbruck · AT

Funding

Austrian Science Fund FWF F 4402
6 · The paper itself

Abstract

Dopaminergic projections from the ventral tegmental area (VTA) constitute the mesolimbocortical system that underlies addiction and psychosis primarily as a result of increased dopaminergic transmission. Dopamine release is spike dependent. L-type calcium channels (LTCCs) play an important role in regulating firing activities, but the contribution of specific subtypes remains unclear. This article describes different functions of Cav1.2 and Cav1.3 subtypes in regulating firing properties with two transgenic mouse strains. For basal firing, Cav1.3-deficient (Cav1.3(-/-)) mice had a lower basal firing frequency. The dihydropyridine (DHP) channel blocker nifedipine reduced single-spike firing in mice expressing DHP-insensitive Cav1.2 channels (Cav1.2DHP(-/-) mice), confirming the significant contribution from the Cav1.3 subtype in basal firing. Moreover, the DHP channel activator (S)-(-)-Bay K8644 and the non-DHP channel activator FPL 64176 converted firing patterns from single spiking to bursting in Cav1.2DHP(-/-) mice. Nifedipine inhibited burst firing induced by both activators, suggesting that Cav1.3 also serves an essential role in burst firing. However, FPL 64176 also induced bursting in Cav1.3(-/-) mice. These results indicate that the Cav1.3 subtype is crucial to regulation of basal single-spike firing, while activation of both Cav1.2 and Cav1.3 can support burst firing of VTA neurons.

Indexed as

Action PotentialsAnimalsCalcium Channels, L-TypeDopaminergic NeuronsFemaleMaleMiceMice, Inbred C57BLMice, TransgenicVentral Tegmental AreaCACNA1C protein, mouseCacna1d protein, mouseCalcium Channels, L-Typeaction potentialcalcium channelfiring patternspatch-clamp recordingtransgenic mouse

Identifiers

PMID24848473
PMCPMC4122730
OpenAlexW2049329544

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.