Evidence map›Paper›PMID 20113344›Full record

ArticleThe European journal of neuroscience2010

Nicotine facilitates long-term potentiation induction in oriens-lacunosum moleculare cells via Ca2+ entry through non-alpha7 nicotinic acetylcholine receptors.

Yousheng Jia, Yoshihiko Yamazaki, Sakura Nakauchi, Ken-Ichi Ito, Katumi Sumikawa

Open access · greenAbstract read
In one paragraph

Article in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 53 citations in OpenAlex.

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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

5 authors at 1 institution in 2 countries.

Yousheng JiaDepartment of Neurobiology and Behavior, University of California, Irvine, CA 92697-4550, USA.
Yoshihiko Yamazaki
Sakura Nakauchi
Ken-Ichi Ito
Katumi Sumikawa
University of California, Irvine · US

Funding

Nicotine Abuse and Memory MechanismsR01DA014542 · NIDA · UNIVERSITY OF CALIFORNIA-IRVINE · PI SUMIKAWA, KATUMI · 2002 to 2010
$1.9M
Maternal nicotine exposure and development of hippocampal circuitsR01DA026458 · NIDA · UNIVERSITY OF CALIFORNIA-IRVINE · PI SUMIKAWA, KATUMI · 2009 to 2013
$1.7M
Maternal smoking and hippocampal circuitsR21DA025269 · NIDA · UNIVERSITY OF CALIFORNIA-IRVINE · PI SUMIKAWA, KATUMI · 2009 to 2010
$421k
NIDA NIH HHS DA014542NIDA NIH HHS DA025269NIDA NIH HHS DA026458NIDA NIH HHS R01 DA014542NIDA NIH HHS R01 DA026458NIDA NIH HHS R21 DA025269
6 · The paper itself

Abstract

Hippocampal inhibitory interneurons have a central role in the control of network activity, and excitatory synapses that they receive express Hebbian and anti-Hebbian long-term potentiation (LTP). Because many interneurons in the hippocampus express nicotinic acetylcholine receptors (nAChRs), we explored whether exposure to nicotine promotes LTP induction in these interneurons. We focussed on a subset of interneurons in the stratum oriens/alveus that were continuously activated in the presence of nicotine due to the expression of non-desensitizing non-alpha7 nAChRs. We found that, in addition to alpha2 subunit mRNAs, these interneurons were consistently positive for somatostatin and neuropeptide Y mRNAs, and showed morphological characteristics of oriens-lacunosum moleculare cells. Activation of non-alpha7 nAChRs increased intracellular Ca(2+) levels at least in part via Ca(2+) entry through their channels. Presynaptic tetanic stimulation induced N-methyl-D-aspartate receptor-independent LTP in voltage-clamped interneurons at -70 mV when in the presence, but not absence, of nicotine. Intracellular application of a Ca(2+) chelator blocked LTP induction, suggesting the requirement of Ca(2+) signal for LTP induction. The induction of LTP was still observed in the presence of ryanodine, which inhibits Ca(2+) -induced Ca(2+) release from ryanodine-sensitive intracellular stores, and the L-type Ca(2+) channel blocker nifedipine. These results suggest that Ca(2+) entry through non-alpha7 nAChR channels is critical for LTP induction. Thus, nicotine affects hippocampal network activity by promoting LTP induction in oriens-lacunosum moleculare cells via continuous activation of non-alpha7 nAChRs.

Indexed as

InterneuronsAnimalsCalciumCalcium Channel BlockersChelating AgentsEgtazic AcidExcitatory Postsynaptic PotentialsHippocampusLong-Term PotentiationNicotineNicotinic AgonistsNifedipinePatch-Clamp TechniquesProtein IsoformsRatsRats, Sprague-Dawley1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidCalciumCalcium Channel BlockersChelating AgentsEgtazic AcidNicotineNicotinic AgonistsNifedipineProtein IsoformsReceptors, NicotinicRyanodine

Identifiers

PMID20113344
PMCPMC2852628
OpenAlexW1988099473

What OpenQuestion holds

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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.