Evidence map›Paper›PMID 28981586›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2018

Gabapentin Prevents Progressive Increases in Excitatory Connectivity and Epileptogenesis Following Neocortical Trauma.

D K Takahashi, Sha Jin, D A Prince

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Gabapentin and cognitive impairment after traumatic brain injury: A multinational cohort of 49,925 patients.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Seizures and epilepsy in patients with ischaemic stroke.Neurological research and practice · 2021
    Review
  7. Article
  8. Review
  9. CurrentCurrent opinion in biomedical engineering · 2020
    Article
  10. Review
  11. Article
  12. 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 1 institution in 1 country.

D K TakahashiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Sha JinDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
D A PrinceDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Stanford University · US

Funding

Effects of pregabalin and thrombospondins on enhanced excitatory connectivity, new synapse formation and epileptogenesis after neocortical injuryR01NS090076 · NINDS · STANFORD UNIVERSITY · PI PRINCE, DAVID ALLAN · 2014 to 2018
$1.9M
Preventing aberrant excitatory connectivity in injured cortex with gabapentinF32NS077623 · NINDS · STANFORD UNIVERSITY · PI TAKAHASHI, DANIEL K. · 2012 to 2012
$54k
NINDS NIH HHS F32 NS077623NINDS NIH HHS R01 NS090076
6 · The paper itself

Abstract

Neocortical injury initiates a cascade of events, some of which result in maladaptive epileptogenic reorganization of surviving neural circuits. Research focused on molecular and organizational changes that occur following trauma may reveal processes that underlie human post-traumatic epilepsy (PTE), a common and unfortunate consequence of traumatic brain injury. The latency between injury and development of PTE provides an opportunity for prophylactic intervention, once the key underlying mechanisms are understood. In rodent neocortex, injury to pyramidal neurons promotes axonal sprouting, resulting in increased excitatory circuitry that is one important factor promoting epileptogenesis. We used laser-scanning photostimulation of caged glutamate and whole-cell recordings in in vitro slices from injured neocortex to assess formation of new excitatory synapses, a process known to rely on astrocyte-secreted thrombospondins (TSPs), and to map the distribution of maladaptive circuit reorganization. We show that this reorganization is centered principally in layer V and associated with development of epileptiform activity. Short-term blockade of the synaptogenic effects of astrocyte-secreted TSPs with gabapentin (GBP) after injury suppresses the new excitatory connectivity and epileptogenesis for at least 2 weeks. Results reveal that aberrant circuit rewiring is progressive in vivo and provide further rationale for prophylactic anti-epileptogenic use of gabapentinoids following cortical trauma.

Indexed as

AnimalsAnimals, NewbornAnticonvulsantsBrain MappingDisease Models, AnimalElectric StimulationEpilepsy, Post-TraumaticExcitatory Amino Acid AgonistsGabapentinGlutamic AcidIn Vitro TechniquesLasersMaleNeocortexNeural PathwaysRatsAnticonvulsantsExcitatory Amino Acid AgonistsGabapentinGlutamic Acid

Identifiers

PMID28981586
PMCPMC6041890
OpenAlexW2695717798

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.