Evidence map›Paper›PMID 24349346›Full record

ArticlePloS one2013

Nicotine elicits prolonged calcium signaling along ventral hippocampal axons.

Chongbo Zhong, David A Talmage, Lorna W Role

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 49 citations in OpenAlex.

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  9. Effects of nicotine on DARPP-32 and CaMKII signaling relevant to addiction.Advances in pharmacology (San Diego, Calif.) · 2021
    Review
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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

3 authors at 2 institutions in 1 country.

Chongbo ZhongDepartment of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York, United States of America ; Center for Nervous System Disorder, State University of New York at Stony Brook, Stony Brook, New York, United States of America.
David A TalmageCenter for Nervous System Disorder, State University of New York at Stony Brook, Stony Brook, New York, United States of America ; Department of Pharmacological Science, State University of New York at Stony Brook, Stony Brook, New York, United States of America.
Lorna W RoleDepartment of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York, United States of America ; Center for Nervous System Disorder, State University of New York at Stony Brook, Stony Brook, New York, United States of America ; Neuroscience Institute, State University of New York at Stony Brook, Stony Brook, New York, United States of America.
Stony Brook University · USState University of New York · US

Funding

MODULATORY EFFECTS OF SUBSTANCE P ON AUTONOMIC NEURONSR01NS022061 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI PLOTKIN, JOSHUA L · 1985 to 2019
$9.6M
NINDS NIH HHS NS22061NINDS NIH HHS R01 NS022061
6 · The paper itself

Abstract

Presynaptic nicotinic acetylcholine receptors (nAChRs) have long been implicated in the modulation of CNS circuits. We previously reported that brief exposure to low concentrations of nicotine induced sustained potentiation of glutamatergic transmission at ventral hippocampal (vHipp)-striatal synapses. Here, we exploited nAChR subtype-selective antagonists and agonists and α7*nAChR knockout mutant mice (α7-/-) to elucidate the signaling mechanisms underlying nAChR-mediated modulation of synaptic transmission. Using a combination of micro-slices culture from WT and α7-/-mice, calcium imaging, and immuno-histochemical techniques, we found that nicotine elicits localized and oscillatory increases in intracellular Ca(2+) along vHipp axons that persists for up to 30 minutes. The sustained phase of the nicotine-induced Ca(2+) response was blocked by α-BgTx but not by DHβE and was mimicked by α7*nAChR agonists but not by non-α7*nAChR agonists. In vHipp slices from α7-/- mice, nicotine elicited only transient increases of axonal Ca(2+) signals and did not activate CaMKII. The sustained phase of the nicotine-induced Ca(2+) response required localized activation of CaMKII, phospholipase C, and IP3 receptor mediated Ca(2+)-induced Ca(2+) release (CICR). In conclusion, activation of presynaptic nAChRs by nicotine elicits Ca(2+) influx into the presynaptic axons, the sustained phase of the nicotine-induced Ca(2+) response requires that axonal α7*nAChR activate a downstream signaling network in the vHipp axons.

Indexed as

Calcium Signalingalpha7 Nicotinic Acetylcholine ReceptorAnimalsAxonsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Coculture TechniquesHippocampusInositol 1,4,5-Trisphosphate ReceptorsIntracellular SpaceMiceMice, KnockoutNeuronal PlasticityNicotineSynapsesalpha7 Nicotinic Acetylcholine ReceptorCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Inositol 1,4,5-Trisphosphate ReceptorsNicotine

Identifiers

PMID24349346
PMCPMC3857818
OpenAlexW2028486882

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.