ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Thyrotropin-releasing hormone increases behavioral arousal through modulation of hypocretin/orexin neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 85 citations in OpenAlex.
- Thyrotropin-releasing hormone as a treatment for cancer-related fatigue: a randomized controlled study.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2012Trial
- Functional Plasticity of Orexin/Hypocretin Neurons Balances Stress States.Biological psychiatry · 2026Review
- Brain-wide mapping and region-specific cellular characterization of Trhr1 reporter-labeled cells in mice using VISoR imaging.Brain structure & function · 2026Article
- Hypothalamic control of arousal.Reviews in endocrine & metabolic disorders · 2026Review
- Body weight and waist circumference are differentially associated with the response to L-thyroxine treatment in primary hypothyroidism.Journal of clinical & translational endocrinology · 2026Article
- Thyrotropin-releasing hormone neurons of different hypothalamic nuclei increase energy expenditure.Nature communications · 2026Article
- Cellular properties and axonal projections of thyrotropin-releasing hormone-expressing neurons in the mouse lateral hypothalamic area.Journal of neurophysiology · 2026Article
- JAK4D, a first-in-class thyrotropin-releasing hormone analogue, reverses scopolamine-induced memory deficits.Brain communications · 2026Article
- The paraventricular nucleus of the hypothalamus: a key node in the control of behavioural states.The Journal of physiology · 2025Review
- Thyrotropin-Releasing Hormone and Food Intake in Mammals: An Update.Metabolites · 2024Review
- Hypothalamic orexinergic neuron changes during the hibernation of the Syrian hamster.Frontiers in neuroanatomy · 2022Article
- Biochemical and physiological insights into TRH receptor-mediated signaling.Frontiers in cell and developmental biology · 2022Review
- Article
- Heterogeneity of Hypocretin/Orexin Neurons.Frontiers of neurology and neuroscience · 2021Review
- A circuit perspective on narcolepsy.Sleep · 2020Article
- Bsx Is Essential for Differentiation of Multiple Neuromodulatory Cell Populations in the Secondary Prosencephalon.Frontiers in neuroscience · 2020Article
- The Thyrotropin-Releasing Hormone-Degrading Ectoenzyme, a Therapeutic Target?Frontiers in pharmacology · 2020Review
- Transgenic Archaerhodopsin-3 Expression in Hypocretin/Orexin Neurons Engenders Cellular Dysfunction and Features of Type 2 Narcolepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Hypocretin as a Hub for Arousal and Motivation.Frontiers in neurology · 2018Review
- Neuronal substrates for initiation, maintenance, and structural organization of sleep/wake states.F1000Research · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Thyrotropin-releasing hormone (TRH) has previously been shown to promote wakefulness and to induce arousal from hibernation. Expression of TRH-R1 (TRH receptor 1) is enriched in the tuberal and lateral hypothalamic area (LHA), brain regions in which the hypocretin/orexin (Hcrt) cells are located. Because the Hcrt system is implicated in sleep/wake control, we hypothesized that TRH provides modulatory input to the Hcrt cells. In vitro electrophysiological studies showed that bath application of TRH caused concentration-dependent membrane depolarization, decreased input resistance, and increased firing rate of identified Hcrt neurons. In the presence of tetrodotoxin, TRH induced inward currents that were associated with a decrease in frequency, but not amplitude, of miniature postsynaptic currents (PSCs). Ion substitution experiments suggested that the TRH-induced inward current was mediated in part by Ca(2+) influx. Although TRH did not significantly alter either the frequency or amplitude of spontaneous excitatory PSCs, TRH (100 nm) increased the frequency of spontaneous inhibitory PSCs by twofold without affecting the amplitude of these events, indicating increased presynaptic GABA release onto Hcrt neurons. In contrast, TRH significantly reduced the frequency, but not amplitude, of miniature excitatory PSCs without affecting miniature inhibitory PSC frequency or amplitude, indicating that TRH also reduces the probability of glutamate release onto Hcrt neurons. When injected into the LHA, TRH increased locomotor activity in wild-type mice but not in orexin/ataxin-3 mice in which the Hcrt neurons degenerate postnatally. Together, these results are consistent with the hypothesis that TRH modulates behavioral arousal, in part, through the Hcrt system.
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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.