Evidence map›Paper›PMID 41884089›Full record

ReviewFrontiers in systems neuroscience2026

When the gatekeeper falls: developmental vulnerability of the thalamic reticular nucleus in neonatal and pediatric hypoxic-ischemic brain injury.

Kuangfu Hsiao

Abstract readReview
In one paragraph

Review in Frontiers in systems neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Kuangfu HsiaoChildren's National Hospital, Washington, DC, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The thalamic reticular nucleus orchestrates thalamocortical oscillations and sensory gating. Its early development features a unique confluence of depolarizing GABA signaling, immature chloride regulation, and transient electrical coupling via connexin-36 gap junctions. These developmental specializations, essential for synchronizing cortical maturation, also render thalamocortical networks vulnerable to hypoxic-ischemic insults such as perinatal asphyxia or pediatric cardiac arrest. Following cellular ATP depletion, rapid chloride imbalance eliminates fast synaptic inhibition, permitting abnormal network activity to propagate via gap-junction coupling that persists when chemical inhibition collapses. The resulting electrical hypersynchrony, exacerbated by depolarizing GABAergic currents and impaired chloride extrusion, promotes excitotoxicity and thalamocortical dysrhythmia. This review synthesizes recent evidence to establish a framework that accounts for the selective vulnerability of the immature brain. Understanding these mechanisms may inform strategies to preserve developmental integrity and promote circuit resilience after pediatric asphyxial events.

Indexed as

cardiac arrestchloride homeostasisconnexin-36developmental neurophysiologyGABAA receptorhypoxia–ischemiapediatricsthalamic reticular nucleus

Identifiers

PMID41884089
PMCPMC13008923

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.