Evidence map›Paper›PMID 31619450›Full record

ArticleeNeuro

Optogenetically-Induced Population Discharge Threshold as a Sensitive Measure of Network Excitability.

D C Klorig, G E Alberto, T Smith, D W Godwin

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. On brain stimulation in epilepsy.Brain : a journal of neurology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. A Step-by-Step Protocol for Optogenetic Kindling.Frontiers in neural circuits · 2020
    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

4 authors at 1 institution in 2 countries.

D C KlorigDepartment of Neurobiology and Anatomy dklorig@wakehealth.edu neuroptics@gmail.com.ORCID 0000-0001-8756-771X
G E AlbertoDepartment of Neurobiology and Anatomy.
T SmithDepartment of Neurobiology and Anatomy.
D W GodwinDepartment of Neurobiology and Anatomy.
Society for Neuroscience · US

Funding

Wake Forest Translational Alcohol Research Center (WF-TARC)P50AA026117 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Jeffrey L. Weiner · 2018 to 2026
$16.2M
MULTI-DISCIPLINARY TRAINING IN THE BIOLOGY OF ALCOHOLISMT32AA007565 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BRIAN A MCCOOL · 1994 to 2026
$10.1M
Mechanisms of Alcohol WithdrawalR01AA016852 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GODWIN, DWAYNE W · 2008 to 2024
$5.5M
Molecular Mechanism of Hippocampal network excitability in a novel, in vivo model of Tuberous Sclerosis ComplexR01NS105005 · NINDS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RAAB-GRAHAM, KIMBERLY FRANCES · 2018 to 2022
$1.9M
An optogenetic investigation of CNS sensitization following alcohol withdrawalF30AA023708 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ALBERTO, GREGORY ERICK · 2014 to 2019
$228k
T-Channel Dysregulation during Alcohol Withdrawal: Mechanisms and Novel TherapiesF31AA021322 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SMALDINO, MELISSA ANN · 2012 to 2013
$79k
NIAAA NIH HHS F30 AA023708NIAAA NIH HHS F31 AA021322NIAAA NIH HHS P50 AA026117NIAAA NIH HHS R01 AA016852NIAAA NIH HHS T32 AA007565NINDS NIH HHS R01 NS105005
6 · The paper itself

Abstract

Network excitability is governed by synaptic efficacy, intrinsic excitability, and the circuitry in which these factors are expressed. The complex interplay between these factors determines how circuits function and, at the extreme, their susceptibility to seizure. We have developed a sensitive, quantitative estimate of network excitability in freely behaving mice using a novel optogenetic intensity-response procedure. Synchronous activation of deep sublayer CA1 pyramidal cells produces abnormal network-wide epileptiform population discharges (PDs) that are nearly indistinguishable from spontaneously-occurring interictal spikes (IISs). By systematically varying light intensity, and therefore the magnitude of the optogenetically-mediated current, we generated intensity-response curves using the probability of PD as the dependent variable. Manipulations known to increase excitability, such as sub-convulsive doses (20 mg/kg) of the chemoconvulsant pentylenetetrazol (PTZ), produced a leftward shift in the curve compared to baseline. The anti-epileptic drug levetiracetam (LEV; 40 mk/kg), in combination with PTZ, produced a rightward shift. Optogenetically-induced PD threshold (oPDT) baselines were stable over time, suggesting the metric is appropriate for within-subject experimental designs with multiple pharmacological manipulations.

Indexed as

OptogeneticsAction PotentialsAnimalsAnticonvulsantsCA1 Region, HippocampalConvulsantsLevetiracetamMaleMiceMice, TransgenicNerve NetPentylenetetrazolePyramidal CellsAnticonvulsantsConvulsantsLevetiracetamPentylenetetrazoleepilepsyexcitabilityintensity responsenetworkoptogeneticsseizure

Identifiers

PMID31619450
PMCPMC6838688
OpenAlexW2980981605

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.