Evidence map›Paper›PMID 9705991›Full record

ArticleThe Journal of physiology1998

Encoding properties induced by a persistent voltage-gated muscarinic sodium current in rabbit sympathetic neurones.

M Gola, P Delmas, H Chagneux

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Substance P-mediated modulation of pacemaker properties in the mammalian respiratory network.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  4. 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

3 authors at 2 institutions in 1 country.

M GolaLaboratoire de Neurobiologie, CNRS, Marseille, France. gola@irlnb.cnrs-mrs.fre
P Delmas
H Chagneux
Centre National de la Recherche Scientifique · FRCentre de Recherche en Neurobiologie - Neurophysiologie de Marseille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. A time- and voltage-dependent Na(+)-selective current termed INa,M is activated by muscarinic agonists or splanchnic nerve stimulation in sympathetic neurones of rabbit coeliac and superior mesenteric ganglia. The firing patterns induced by INa,M were investigated in patch-clamped neurones within intact ganglia, and compared with those generated by a neuronal model including INa,M. 2. INa,M was characterized by voltage-dependent low threshold activation and high-threshold inactivation functions. The overlapping functions produced a persistent U-shaped current between -100 and -20 mV, which peaked at the cell resting potential. The activation and inactivation kinetics were fitted to single exponentials with time constants of approximately 100 and 400 ms, respectively. 3. Activating INa,M with muscarinic agonists or nerve stimulation depolarized and fired the neurones. The depolarization was paralleled by an apparent increase in input membrane resistance. The model showed that this paradox resulted from the turning off of INa,M during resistance tests, which also accounted for the all-or-none slow hyperpolarizing responses to current pulses. 4. INa,M gave the neurones an N-shaped I-V relationship capable of producing complex firing patterns. Under given conditions, carbachol-treated neurones could either fire regularly or remain silent at approximately -80 mV, i.e. they displayed bistability. Transitions from one state to the other were triggered with short current pulses. The transitions resulted from the turning on and off of INa,M. 5. Firing reduced INa,M, an effect abolished by blocking Ca2+ channels or adding BAPTA (40 mM) to the pipette. The Ca(2+)-related negative regulation of INa,M may have mediated endogenous bursting activity. Burst firing was generated by the model upon introducing Ca2+ regulation of INa,M. 6. The results demonstrate that INa,M gives prevertebral sympathetic neurones a wide repertoire of firing patterns: pacemaker-like properties, bistability and burst firing capability. They suggest that the INa,M-related encoding properties may provide sympathetic neurotransmission with new potentialities.

Indexed as

AnimalsChelating AgentsEgtazic AcidElectric StimulationElectrophysiologyIn Vitro TechniquesIon Channel GatingMembrane PotentialsMuscarinic AgonistsNeuronsPatch-Clamp TechniquesRabbitsReceptors, MuscarinicSodium ChannelsSympathetic Nervous System1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidChelating AgentsEgtazic AcidMuscarinic AgonistsReceptors, MuscarinicSodium Channels

Identifiers

PMID9705991
PMCPMC2231040
OpenAlexW2026980988

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.