ArticleMolecular psychiatry2025
Evidence for thyroid hormone regulation of amygdala-dependent fear-relevant memory and plasticity.
Article in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Thyroid hormone levels in patients with bipolar disorder: a systematic review and meta-analysis.BMC endocrine disorders · 2024Pooled it
- Article
- Brain-wide mapping and region-specific cellular characterization of Trhr1 reporter-labeled cells in mice using VISoR imaging.Brain structure & function · 2026Article
- Boldine treatment prevents chronic cognitive impairment and exaggerated fear learning in rats exposed to repetitive low-level blast injury.Frontiers in cellular neuroscience · 2026Article
- Neurological consequences of adult-onset hypothyroidism.Endocrine journal · 2025Review
- Serotonergic and Chemosensory Brain Areas and Sensory Ganglia Expressing Type 3 Deiodinase Mapped With Dio3Cre drivers.Endocrinology · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
The amygdala is an established site for fear memory formation, and clinical studies suggest involvement of hormone signaling cascades in development of trauma-related disorders. While an association of thyroid hormone (TH) status and mood disorders is established, the related brain-based mechanisms and the role of TH in anxiety disorders are unknown. Here we examine the role that TH receptor (TR, a nuclear transcriptional repressor when unbound and a transcriptional activator when bound to TH) may have in mediating the initial formation of fear memories in the amygdala. We identified mRNA levels of TR and other TH pathway regulatory genes, including thyrotropin-releasing hormone (Trh), transthyretin (Ttr), thyrotropin-releasing hormone receptor (Trhr), type 2 iodothyronine deiodinase (Dio2), mediator complex subunit 12 (Med12/Trap230) and retinoid X receptor gamma (Rxrg) to be altered in the amygdala following Pavlovian fear conditioning. Using TH agonist and antagonist infusion into the amygdala, we demonstrated that this pathway is both necessary and sufficient for fear memory consolidation. Inhibition of TH signaling with the TR antagonist 1-850 decreased fear memory consolidation; while activation of TR with T3 (triiodothyronine) resulted in increased memory formation. Using a systemic hypothyroid mouse model, we found that intra-amygdala infusions of T3 were sufficient to rescue deficits in fear memory. Finally, we demonstrated that T3 was sufficient to activate TR-specific gene pathways in the amygdala. These findings on the role of activity-dependent TR modulation support a model in which local TH is a critical regulator of fear memory-related plasticity in the amygdala.
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