Evidence map›Paper›PMID 35401118›Full record

ReviewFrontiers in cellular neuroscience2022

Crosstalk Between GABAergic Neurotransmission and Inflammatory Cascades in the Post-ischemic Brain: Relevance for Stroke Recovery.

Georgios Michalettos, Karsten Ruscher

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Brain Oscillatory Modes as a Proxy of Stroke Recovery.Neurorehabilitation and neural repair · 2025
    Article
  6. Central Dysmyelination in SSADH-Deficient Humans and Mice.Annals of clinical and translational neurology · 2025
    Observational
  7. Differential Roles of Neuro-Inflammatory Regulator, MAPK11 in Cortex and Hippocampus Following Post-Stroke Cognitive Impairments in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
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  19. Review
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.

Georgios MichalettosLaboratory for Experimental Brain Research, Division of Neurosurgery, Department of Clinical Sciences, Wallenberg Neuroscience Center, Lund University, Lund, Sweden.
Karsten RuscherLaboratory for Experimental Brain Research, Division of Neurosurgery, Department of Clinical Sciences, Wallenberg Neuroscience Center, Lund University, Lund, Sweden.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adaptive plasticity processes are required involving neurons as well as non-neuronal cells to recover lost brain functions after an ischemic stroke. Recent studies show that gamma-Aminobutyric acid (GABA) has profound effects on glial and immune cell functions in addition to its inhibitory actions on neuronal circuits in the post-ischemic brain. Here, we provide an overview of how GABAergic neurotransmission changes during the first weeks after stroke and how GABA affects functions of astroglial and microglial cells as well as peripheral immune cell populations accumulating in the ischemic territory and brain regions remote to the lesion. Moreover, we will summarize recent studies providing data on the immunomodulatory actions of GABA of relevance for stroke recovery. Interestingly, the activation of GABA receptors on immune cells exerts a downregulation of detrimental anti-inflammatory cascades. Conversely, we will discuss studies addressing how specific inflammatory cascades affect GABAergic neurotransmission on the level of GABA receptor composition, GABA synthesis, and release. In particular, the chemokines CXCR4 and CX3CR1 pathways have been demonstrated to modulate receptor composition and synthesis. Together, the actual view on the interactions between GABAergic neurotransmission and inflammatory cascades points towards a specific crosstalk in the post-ischemic brain. Similar to what has been shown in experimental models, specific therapeutic modulation of GABAergic neurotransmission and inflammatory pathways may synergistically promote neuronal plasticity to enhance stroke recovery.

Indexed as

chemokineGABAglutamate decarboxylateimmune cellinflammationneurotransmissionstroke recovery

Identifiers

PMID35401118
PMCPMC8983863
OpenAlexW4220833666

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.