ArticleiScience2026
Thyroid hormones maintain parvalbumin neuron functions in the mouse neocortex.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parvalbumin-expressing GABAergic interneurons are crucial for maintaining excitation/inhibition balance in the neocortex. The postnatal maturation of parvalbumin neurons is highly sensitive to thyroid hormone deficiency. The present study addressed the role of thyroid hormones in mature parvalbumin neurons. Using genetically modified mouse models, we selectively disrupted thyroid hormone signaling in parvalbumin neurons after the onset of parvalbumin expression. Genomic, histological, electrophysiological, sleep, and behavioral analyses were conducted. Mutant mice showed reduced expression of perineuronal net components, decreased neuron excitability, altered gamma oscillations, behavioral hyperactivity, increased wakefulness, delayed sleep onset, and greater susceptibility to seizures. These results demonstrate that thyroid hormones are essential not only for the maturation but also for the maintenance of cortical parvalbumin neuron function after the onset of parvalbumin expression. Disruption of thyroid hormone signaling, during development or adulthood, may thus contribute to neurological and psychiatric disorders involving impaired cortical oscillations.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.