Evidence map›Paper›PMID 10432341›Full record

ArticleThe Journal of physiology1999

Somatic amplification of distally generated subthreshold EPSPs in rat hippocampal pyramidal neurones.

M Andreasen, J D Lambert

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  9. Downregulation of Spermine Augments Dendritic Persistent Sodium Currents and Synaptic Integration after Status Epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
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  17. Intrinsic conductances actively shape excitatory and inhibitory postsynaptic responses in olfactory bulb external tufted cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  18. Article
  19. Neural variability, detection thresholds, and information transmission in the vestibular system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  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.

M AndreasenDepartment of Physiology, University of Aarhus, DK-8000 Arhus C, Denmark. ma@fi.au.dk
J D Lambert
Aarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Intracellular recordings from hippocampal CA1 pyramidal neurones revealed that EPSPs evoked by selective stimulation of the isolated afferent input to the distal third of the apical dendrites were relatively insensitive to changes in dendritic membrane potential (Vm) but amplified by depolarizations of the somatic Vm. The amplification was present at potentials depolarized from resting membrane potential (RMP) but was most marked when the EPSPs were close to threshold for action potential generation. The amplification consisted of a uniform component and a variable component which was only present when the EPSPs were threshold straddling. 2. The somatic amplification was caused by an intrinsic membrane current which was blocked by somatic application of tetrodotoxin (TTX, 10 microM), but was insensitive to bath application of NiCl2 (100-200 microM). We therefore suggest that the amplification of the subthreshold EPSP is due primarily to the activation of a non-inactivating Na+ current (INaP). 3. Injection of 4-aminopyridine (4-AP, 25-50 mM) during intradendritic recordings resulted in amplification of the EPSPs in 37% of the dendrites, which was similar to that observed in somatic recordings. However, in the one case in which somatic application of TTX was tested, dendritic amplification was blocked, suggesting that it is a reflection of the somatic amplification. 4. Because the shift to variable amplification was very abrupt and it is present in only a very narrow voltage range close to threshold, we suggest that the variable component is caused by the regenerative activation of INaP. The variability itself is probably due to the simultaneous activation of different outward K+ currents. 5. The present results indicate that the somatic region of CA1 pyramidal neurones can function as a voltage-dependent amplifier of distally evoked EPSPs and that this is due to the activation of a somatic INaP. The presence of this amplifying mechanism will have important functional consequences for the way in which distally generated EPSPs are integrated.

Indexed as

Afferent PathwaysAnimalsCell MembraneDendritesElectric StimulationElectrophysiologyExcitatory Postsynaptic PotentialsHippocampusIn Vitro TechniquesMaleMembrane PotentialsNickelPotassium ChannelsPyramidal CellsRatsRats, WistarNickelnickel chloridePotassium ChannelsSodium ChannelsTetrodotoxin

Identifiers

PMID10432341
PMCPMC2269499
OpenAlexW1976813093

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.