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

Overview

1. Children's National Hospital, Washington, DC, United States
2. George Washington University School of Medicine and Health Sciences, Washington, DC, United States

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.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

• geo:GSE145273, at NCBI GEO; found in the text, “Chloride dysregulation and the developmental…”

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 30 September 2026: the first record

Recorded: type, language, journal, volume, pages, dates, 1 author, 8 keywords, 1 funder, 238 references.

Cite

This paper

Hsiao, K. (2026). When the gatekeeper falls: developmental vulnerability of the thalamic reticular nucleus in neonatal and pediatric hypoxic-ischemic brain injury. Frontiers in systems neuroscience, 20, 1753562. https://doi.org/10.3389/fnsys.2026.1753562

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1523/eneuro.0029-26.2026 [code]

Electrical Coupling within Thalamocortical Networks Cumulatively Reduces Cortical Correlation to Sensory Inputs.

Journal: eNeuro

In common: 13 references

[2] doi:10.1371/journal.pbio.3003693 [code]

Thalamic reticular neurons provide cell type-specific modulation of sound processing in the auditory thalamus.

Journal: PLoS biology

In common: 12 references

[3] doi:10.1038/s42003-026-10032-2 [code]

Data-driven mouse motor thalamus model reveals topography and spatial weight scaling govern spindle dynamics.

Journal: Communications biology

In common: 7 references

[4] doi:10.1038/s41398-026-04018-1

Loss of connexin 36 elicits abnormalities in thalamocortical network activity relevant to neuropsychiatric disorders.

Journal: Translational psychiatry

In common: 6 references

[5] doi:10.1038/s41467-026-75162-x [code]

Dyscoordination of thalamic reticular spindles is associated with social memory deficits in mice and humans with autism spectrum disorder.

Journal: Nature communications

In common: 4 references

[6] doi:10.3390/biom16050621

Calretinin and Parvalbumin Trapping of TDP43 and XRCC1 Instructs Neocortical Interneuron Death in Neonatal Hypoxic-Ischemic Encephalopathy.

Journal: Biomolecules

In common: other condition, 3 references

[7] doi:10.1016/j.isci.2026.115878 [code]

Twitching in sleeping premature infants provides a sensitive behavioral assay of early motor control.

Journal: iScience

In common: developmental, 3 references

[8] doi:10.1038/s41598-026-49034-9

Multimodal preclinical study of long-term effects of prenatal ultrasound on the mouse central nervous system.

Journal: Scientific reports

In common: developmental, 3 references

[9] doi:10.1038/s42003-026-10464-w [code]

Quantifying electrostatic control of docking and binding energetics in functional Cx36 gap junctions.

Journal: Communications biology

In common: 3 references

[10] doi:10.3390/ijms27114920

Timing-Dependent Effects of Dexamethasone in a Mouse Model of Neonatal Hypoxic-Ischemic Brain Injury: A Transcriptomic Analysis of Synaptic Signaling and Calcium Homeostasis.

Journal: International journal of molecular sciences

In common: stroke, other condition, 2 references

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.