Evidence map›Paper›PMID 11306610›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Physiological patterns of electrical stimulation can induce neuronal gene expression by activating N-type calcium channels.

T A Brosenitsch, D M Katz

Open access · bronzeAbstract read
PubMed Full text at PMC
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 187 citations in OpenAlex.

  1. Review
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  3. BQ788 reveals glial ETBritish journal of pharmacology · 2023
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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

2 authors at 2 institutions in 1 country.

T A BrosenitschDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
D M Katz
Case Western Reserve University · USUniversity School · US

Funding

VENTROLATERAL PONS SHAPES THE RESPONSE TO HYPOXIAP01HL025830 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI PRABHAKAR, NANDURI R · 1985 to 2006
$11.1M
DEVELOPMENTAL NEUROLOGY TRAINING GRANTT32NS007118 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI LANDMESSER, LYNN T · 1985 to 1998
–
NHLBI NIH HHS HL25830NHLBI NIH HHS P01 HL025830NINDS NIH HHS 5T32NS07118NINDS NIH HHS T32 NS007118
6 · The paper itself

Abstract

Activity-dependent neuronal gene expression is thought to require activation of L-type calcium channels, a view based primarily on studies in which chronic potassium (K(+)) depolarization was used to mimic neuronal activity. However, N-type calcium channels are primarily inactivated during chronic depolarization, and their potential contribution to gene expression induced by physiological patterns of stimulation has not been defined. In the present study, electrical stimulation of dissociated primary sensory neurons at 5 Hz, or treatment with elevated K(+), produced a large increase in the percentage of neurons that express tyrosine hydroxylase (TH) mRNA and protein. However, blockade of L-type channels, which completely inhibited K(+)-induced expression, had no effect on TH expression induced by patterned stimulation. Conversely, blockade of N-type channels completely inhibited TH induction by patterned stimulation, whereas K(+)-induced expression was unaffected. Similar results were obtained for depolarization-induced expression of the immediate early genes Nurr1 and Nur77. In addition, TH induction by patterned stimulation was significantly reduced by inhibitors of PKA and PKC but was unaffected by inhibition of the mitogen-activated protein kinase (MAPK) pathway. On the other hand, K(+)-induced TH expression was significantly reduced by inhibition of the MAPK pathway but was unaffected by inhibitors of PKA or PKC. These results demonstrate that N-type calcium channels can directly link phasic membrane depolarization to gene expression, challenging the view that activation of L-type channels is required for nuclear responses to physiological patterns of activity. Moreover, our data show that phasic and chronic depolarizing stimuli act through distinct mechanisms to induce neuronal gene expression.

Indexed as

AnimalsCalcium Channel BlockersCalcium Channels, L-TypeCalcium Channels, N-TypeCells, CulturedCell SurvivalCyclic AMP-Dependent Protein KinasesDNA-Binding ProteinsElectric StimulationEnzyme InhibitorsFluorescenceGanglia, SensoryGene Expression RegulationMAP Kinase Signaling SystemNeuronsNuclear Receptor Subfamily 4, Group A, Member 1Calcium Channel BlockersCalcium Channels, L-TypeCalcium Channels, N-TypeCyclic AMP-Dependent Protein KinasesDNA-Binding ProteinsEnzyme InhibitorsNr4a1 protein, ratNr4a2 protein, ratNuclear Receptor Subfamily 4, Group A, Member 1Nuclear Receptor Subfamily 4, Group A, Member 2PotassiumProtein Kinase CReceptors, Cytoplasmic and NuclearReceptors, SteroidRNA, MessengerTranscription FactorsTyrosine 3-Monooxygenase

Identifiers

PMID11306610
PMCPMC6762536
OpenAlexW2112659765

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.