ArticleJournal of molecular neuroscience : MN2009
Alternative splicing in the synaptic protein interaction site of rat Ca(v)2.2 (alpha (1B)) calcium channels: changes induced by chronic inflammatory pain.
Article in Journal of molecular neuroscience : MN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- High-Voltage-Activated Calcium Channel in the Afferent Pain Pathway: An Important Target of Pain Therapies.Neuroscience bulletin · 2019Article
- The control of alternative splicing by SRSF1 in myelinated afferents contributes to the development of neuropathic pain.Neurobiology of disease · 2016Article
- Calcium Channel CaVα₁ Splice Isoforms - Tissue Specificity and Drug Action.Current molecular pharmacology · 2015Review
- NFAT1 and NFAT3 cooperate with HDAC4 during regulation of alternative splicing of PMCA isoforms in PC12 cells.PloS one · 2014Article
- Imaging large cohorts of single ion channels and their activity.Frontiers in endocrinology · 2013Review
- Transcriptomic analysis of differentially alternative splicing patterns in mice with inflammatory and neuropathic pain.Molecular painArticle
- Article
- The neuronal splicing factor Nova controls alternative splicing in N-type and P-type CaV2 calcium channels.Channels (Austin, Tex.)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated N-type Ca(2+) channels play a central role in regulation of neurotransmitter release. The II-III linker of N-type calcium channel alpha(1B) subunit (exons 17-21 in rats) contains synaptic protein interaction (synprint) site, which plays a pivotal role in efficient neurotransmission. Using RT-PCR analysis of rat hippocampus and lumbar spinal cord transcripts, the expressions of Ca(v)2.2 exon 18a and a novel Ca(v)2.2 splice variant, which were detected in this study, have been investigated, and they showed tissue-specific pattern. The new variant contains a large deletion in II-III linker that produces a stop codon, which is predicted to produce a two-domain-truncated channel. To study the effect of inflammatory pain on the expression pattern of these variants, animals were treated with intraplantar formalin, and the amount of splice variants in lumbar spinal cord was measured. The results showed that chronic inflammatory pain increases the Ca(v)2.2 mRNA levels lacking exon 18a and decreases the amount of full-length variants, which do not have any deletion. Determining different Ca(v)2.2 splice variants in rat nervous system and the impact of inflammatory pain on the splicing pattern suggest a possible regulatory role for calcium channel alternative splicing.
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.