ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Excitatory effects of thyrotropin-releasing hormone in the thalamus.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 49 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
- L-type calcium channels and MAP kinase contribute to thyrotropin-releasing hormone-induced depolarization in thalamic paraventricular nucleus neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Unmet needs of patients with narcolepsy: perspectives on emerging treatment options.Nature and science of sleep · 2015Review
- Attenuation of inhibitory synaptic transmission by glial dysfunction in rat thalamus.Synapse (New York, N.Y.) · 2011Article
- Recent advances in the treatment of narcolepsy.Current treatment options in neurology · 2011Article
- Excitation of histaminergic tuberomamillary neurons by thyrotropin-releasing hormone.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Thyrotropin-releasing hormone increases behavioral arousal through modulation of hypocretin/orexin neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Stimulation of orexin/hypocretin neurones by thyrotropin-releasing hormone.The Journal of physiology · 2009Article
- The synthetic TRH analogue taltirelin exerts modality-specific antinociceptive effects via distinct descending monoaminergic systems.British journal of pharmacology · 2007Article
- Thyrotropin-releasing hormone increases GABA release in rat hippocampus.The Journal of physiology · 2006Article
- Thalamic T-type Ca2+ channels and NREM sleep.Cell calcium · 2006Review
- Neuronal basis of the slow (<1 Hz) oscillation in neurons of the nucleus reticularis thalami in vitro.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activity of the thalamus is state dependent. During slow-wave sleep, rhythmic burst firing is prominent, whereas during waking or rapid eye movement sleep, tonic, single-spike activity dominates. These state-dependent changes result from the actions of modulatory neurotransmitters. In the present study, we investigated the functional and cellular effects of the neuropeptide thyrotropin-releasing hormone (TRH) on the spontaneously active ferret geniculate slice. This peptide and its receptors are prominently expressed in the thalamic network, yet the role of thalamic TRH remains obscure. Bath application of TRH resulted in a transient cessation of both spindle waves and the epileptiform slow oscillation induced by application of bicuculline. With intracellular recordings, TRH application to the GABAergic neurons of the perigeniculate (PGN) or thalamocortical cells in the lateral geniculate nucleus resulted in depolarization and increased membrane resistance. In perigeniculate neurons, this effect reversed near the reversal potential for K+, suggesting that it is mediated by a decrease in K+ conductance. In thalamocortical cells, the TRH-induced depolarization was of sufficient amplitude to block the generation of rebound Ca2+ spikes, whereas the even larger direct depolarization of PGN neurons transformed these cells from the burst to tonic, single-spike mode of action potential generation. Furthermore, application of TRH prominently enhanced the afterdepolarization that follows rebound Ca2+ spikes, suggesting that this transmitter may also enhance Ca2+-activated nonspecific currents. These data suggest a novel role for TRH in the brain as an intrinsic regulator of thalamocortical network activity and provide a potential mechanism for the wake-promoting and anti-epileptic effects of this peptide.
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