Thyrotropin-releasing hormone induces Ca2+ increase in a subset of vagal nodose ganglion neurons

Mamedova, Esmira; Dmytriyeva, Oksana; Rekling, Jens C.

doi:10.1016/j.npep.2022.102261

Cited by 2 publications

(2 citation statements)

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“…Three major PNS neuronal types, sensory (dorsal root ganglia), sympathetic, and enteric neurons, subclassified in clusters according to the expression of multiple molecular markers [98] did not show expression of Trhr. However, the integration of recent and focused organ transcriptomes shows Trhr expression in a cluster corresponding to Gabra expressing neurons from the nodose ganglia [99], coincident with data showing that TRH enhances intracellular Ca 2+ concentration in a subset of neurons of the nodose ganglion in cell culture [100]. Whether these neurons convey an anorexic signal to the brain awaits resolution, so as the endogenous source of TRH acting on the nodose ganglion.…”

Section: Peripheral Trh Effect On Food-intake and Vagus Nerve Or Othe...mentioning

confidence: 60%

Thyrotropin Releasing Hormone and Food-Intake in Mammals: An Update

Vargas,

Castro Tron,

Charli

et al. 2024

Preprint

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Thyrotropin releasing hormone (TRH; pGlu-His-Pro-NH2) is an intercellular signal produced mainly by neurons. Among the multiple pharmacological effects of TRH, that on food-intake is not well understood. We review data that show that peripheral injection of TRH generally produces a transient anorexic effect, discuss the pathways that might initiate this effect, and explain its short half-life. In addition, central administration of TRH can produce anorexic or orexigenic effects, depending on the site of injection, that are likely due to interaction with TRH receptor 1. Anorexic effects are most notable when TRH is injected into the hypothalamus and the nucleus accumbens, while the orexigenic effect has only been detected by injection into the brain stem. Functional evidence suggests that TRH neurons that are prime candidate vectors for TRH action on food-intake include the caudal raphe nuclei projecting to the dorsal motor nucleus of the vagus, and possibly TRH neurons from the tuberal lateral hypothalamus projecting to the tuberomammillary nuclei. For other TRH neurons, the anatomical or physiological context and impact of TRH in each synaptic domain are still poorly understood. The manipulation of TRH expression in well-defined neuron types will facilitate the discovery of its role in food-intake control in each anatomical scene.

show abstract

Section: Peripheral Trh Effect On Food-intake and Vagus Nerve Or Othe...mentioning

confidence: 60%

Thyrotropin Releasing Hormone and Food-Intake in Mammals: An Update

Vargas,

Castro Tron,

Charli

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…Three major PNS neuronal types, sensory (dorsal root ganglia), sympathetic, and enteric neurons, subclassified in clusters according to the expression of multiple molecular markers [ 98 ] did not show expression of Trhr . However, the integration of recent and focused organ transcriptomes shows Trhr expression in a cluster corresponding to Gabra expressing neurons from the nodose ganglia [ 99 ], coincident with data showing that TRH enhances intracellular Ca 2+ concentration in a subset of neurons of the nodose ganglion in cell culture [ 100 ]. Whether these neurons convey an anorexic signal to the brain awaits resolution, as with the endogenous source of TRH acting on the nodose ganglion.…”

Section: Discovery Of the Effects Of Trh A Trh Analogue And Trh Catab...mentioning

confidence: 63%

Thyrotropin-Releasing Hormone and Food Intake in Mammals: An Update

Vargas,

Castro Tron,

Rodríguez Rodríguez

et al. 2024

Metabolites

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Thyrotropin-releasing hormone (TRH; pGlu-His-Pro-NH2) is an intercellular signal produced mainly by neurons. Among the multiple pharmacological effects of TRH, that on food intake is not well understood. We review studies demonstrating that peripheral injection of TRH generally produces a transient anorexic effect, discuss the pathways that might initiate this effect, and explain its short half-life. In addition, central administration of TRH can produce anorexic or orexigenic effects, depending on the site of injection, that are likely due to interaction with TRH receptor 1. Anorexic effects are most notable when TRH is injected into the hypothalamus and the nucleus accumbens, while the orexigenic effect has only been detected by injection into the brain stem. Functional evidence points to TRH neurons that are prime candidate vectors for TRH action on food intake. These include the caudal raphe nuclei projecting to the dorsal motor nucleus of the vagus, and possibly TRH neurons from the tuberal lateral hypothalamus projecting to the tuberomammillary nuclei. For other TRH neurons, the anatomical or physiological context and impact of TRH in each synaptic domain are still poorly understood. The manipulation of TRH expression in well-defined neuron types will facilitate the discovery of its role in food intake control in each anatomical scene.

show abstract

Thyrotropin-releasing hormone induces Ca2+ increase in a subset of vagal nodose ganglion neurons

Cited by 2 publications

References 45 publications

Thyrotropin Releasing Hormone and Food-Intake in Mammals: An Update

Thyrotropin Releasing Hormone and Food-Intake in Mammals: An Update

Thyrotropin-Releasing Hormone and Food Intake in Mammals: An Update

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