Evidence map›Paper›PMID 9763491›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Nicotine selectively enhances NMDA receptor-mediated synaptic transmission during postnatal development in sensory neocortex.

V B Aramakis, R Metherate

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

56 citing papers in PubMed, 185 citations in OpenAlex.

  1. Article
  2. Cholinergic Activation of Corticofugal Circuits in the Adult Mouse Prefrontal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  3. Nicotine on the developing brain.Pharmacological research · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. α7 nicotinic receptor agonists reduce levodopa-induced dyskinesias with severe nigrostriatal damage.Movement disorders : official journal of the Movement Disorder Society · 2015
    Article
  15. Review
  16. Article
  17. Nicotine recruits glutamate receptors to postsynaptic sites.Molecular and cellular neurosciences · 2015
    Article
  18. Review
  19. Review
  20. Article
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 1 institution in 1 country.

V B AramakisDepartment of Psychobiology, University of California, Irvine, California 92697-4550, USA.
R Metherate
University of California, Irvine · US

Funding

Cellular Mechanisms of Aditory Cortex FunctionR01DC002967 · NIDCD · UNIVERSITY OF CALIFORNIA-IRVINE · PI METHERATE, RAJU · 2003 to 2007
$913k
CELLULAR STUDY OF AUDITORY CORTEX FUNCTIONR29DC002967 · NIDCD · UNIVERSITY OF CALIFORNIA IRVINE · PI METHERATE, RAJU · 1997 to 2001
$226k
CELLULAR MECHANISMS OF AUDITORY CORTEX FUNCTIONR55DC002967 · NIDCD · UNIVERSITY OF CALIFORNIA IRVINE · PI METHERATE, RAJU · 1996 to 1996
–
NIDCD NIH HHS DC02967NIDCD NIH HHS R01 DC002967NIDCD NIH HHS R29 DC002967
6 · The paper itself

Abstract

The neurotransmitters acetylcholine (ACh) and glutamate have been separately implicated in synaptic plasticity during development of sensory neocortex. Here we show that these neurotransmitters can, in fact, act synergistically via their actions at nicotinic ACh receptors (nAChRs) and NMDA receptors, respectively. To determine how activation of nAChRs modifies glutamatergic EPSPs, we made whole-cell recordings from visualized pyramidal neurons in slices of rat auditory cortex. Pulsed (pressure) ejection of nicotine onto apical dendrites selectively enhanced EPSPs mediated by NMDA receptors without affecting AMPA/kainate (AMPA/KA) receptor-mediated EPSPs. The enhancement occurred during a transient, postnatal period of heightened cholinergic function [neurons tested on postnatal day 8-16 (P8-16)], and not in the mature cortex (>P19). Three related findings indicated the mechanism of action: (1) The specific alpha7 nAChR antagonist methyllycaconitine citrate (MLA) blocked the effect of nicotine; (2) pulsed nicotine did not enhance postsynaptic depolarizations induced by iontophoretically applied NMDA; and (3) bath exposure to nicotine for several minutes produced apparent nAChR desensitization and precluded enhancement of EPSPs by pulsed nicotine. Together, the data suggest that nicotine acts at rapidly desensitizing, presynaptic alpha7 nAChRs to increase glutamate release onto postsynaptic NMDA receptors. The synergistic actions mediated by alpha7 nAChRs and NMDA receptors may contribute to experience-dependent synaptic plasticity in sensory neocortex during early postnatal life.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAcetylcholinesteraseAge Factorsalpha7 Nicotinic Acetylcholine ReceptorAnimalsCritical Period, PsychologicalElectrophysiologyExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsFemaleGABA AntagonistsMaleMembrane PotentialsNeuronsNicotine6-Cyano-7-nitroquinoxaline-2,3-dioneAcetylcholinesterasealpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, ratExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsGABA AntagonistsNicotineNicotinic AgonistsN-MethylaspartatePicrotoxinReceptors, NicotinicReceptors, N-Methyl-D-Aspartate

Identifiers

PMID9763491
PMCPMC6792829
OpenAlexW1566487806

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.