Hypothalamic TRH Mediates Anorectic Effects of Serotonin in Rats

Chávez, Jorge L.; Alcántara-Alonso, Viridiana; García-Luna, Cinthia; Soberanes-Chávez, Paulina; Grammatopoulos, Dimitris; Gortari, Patricia de

doi:10.1523/eneuro.0077-22.2022

Cited by 4 publications

(2 citation statements)

References 65 publications

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“…BNC2 neurons are GABAergic and directly inhibit AGRP/NPY neurons via the GABAA receptor though, as is the case for other feeding neurons, it is possible that neuropeptides also contribute. The snRNA-seq data shows expression of several putative neuropeptides in BNC2 neurons including Scg2, Chga, and Trh, which have been implicated in feeding control and energy balance [54][55][56][57][58][59] . Future studies will be necessary to determine whether in addition to GABA, these neuropeptides mediate some of the effects of BNC2 neurons.…”

Section: Discussionmentioning

confidence: 99%

Leptin Activated Hypothalamic BNC2 Neurons Acutely Suppress Food Intake

Tan,

Yin,

Tan

et al. 2024

Preprint

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Leptin is an adipose tissue hormone that maintains homeostatic control of adipose tissue mass by regulating the activity of specific neural populations controlling appetite and metabolism. Leptin regulates food intake by inhibiting orexigenic agouti-related protein (AGRP) neurons and activating anorexigenic pro-opiomelanocortin (POMC) neurons. However, while AGRP neurons regulate food intake on a rapid time scale, acute activation of POMC neurons has only a minimal effect. This has raised the possibility that there is a heretofore unidentified leptin-regulated neural population that suppresses appetite on a rapid time scale. Here, we report the discovery of a novel population of leptin-target neurons expressing basonuclin 2 (Bnc2) that acutely suppress appetite by directly inhibiting AGRP neurons. Opposite to the effect of AGRP activation, BNC2 neuronal activation elicited a place preference indicative of positive valence in hungry but not fed mice. The activity of BNC2 neurons is finely tuned by leptin, sensory food cues, and nutritional status. Finally, deleting leptin receptors in BNC2 neurons caused marked hyperphagia and obesity, similar to that observed in a leptin receptor knockout in AGRP neurons. These data indicate that BNC2-expressing neurons are a key component of the neural circuit that maintains energy balance, thus filling an important gap in our understanding of the regulation of food intake and leptin action.

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Section: Discussionmentioning

confidence: 99%

Leptin Activated Hypothalamic BNC2 Neurons Acutely Suppress Food Intake

Tan,

Yin,

Tan

et al. 2024

Preprint

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“…The decreased mRNA expression of oxytocin indicated the oxytocin-expressing neurons in the PVN might be parts of the targeting neurons of GABAergic nerve fibers. While the mRNA expression of CRH and TRH in the PVN of WAS-treated rats was increased, it might suggest other stronger endogenous signals modulate their expression after stress stimulation, such as oxytocin and agouti-related protein modulate CRH synthesis, and serotonin regulates TRH secretion [6,25,26]. Although several studies suggest that alterations of central and peripheral CRH induced by stress accelerate colonic motility and transit [27], the lower level of oxytocin is more likely be modulated by the increased GABAergic projection in the PVN of the WAS-treated rats.…”

Section: Discussionmentioning

confidence: 99%

Increased GABAergic projections in the paraventricular nucleus regulate colonic hypersensitivity via oxytocin in a rat model of irritable bowel syndrome

Liu

Guo

et al. 2022

NeuroReport

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Irritable bowel syndrome (IBS) is characterized by gastrointestinal dysmotility and visceral hyperalgesia, and the impaired brain-gut axis is accepted as a crucial cause for the onset of IBS. The objective of this study is to investigate the effects of the adaptive changes in the central neural system induced by stress on IBSlike syndromes in rats. Long-term water avoidance stress (WAS) was used to prepare IBS animals. The changes in neuronal excitation and GABA expression were shown by immunohistochemistry. The mRNA and protein expressions of neurotransmitters were detected with Quantitative reverse-transcription PCR (qRT-PCR) and Enzyme-linked immunosorbent assay (ELISA). The intestinal transit time, fecal moisture content, and abdominal withdrawal reflex scores of rats were recorded to monitor intestinal motility and visceral hyperalgesia. In the WAS-treated rats with enhanced intestinal motility and visceral hypersensitivity, more GABAergic projections were found in the paraventricular nucleus (PVN) of the hypothalamus, which inhibited the firing rate of neurons and decreased the expression of oxytocin. Exogenous oxytocin improved gut motility and decreased AWR scores. The inhibition of oxytocin by the adaptive GABAergic projection in the PVN might be an important mediator of IBS, which indicates a potential novel therapeutic target.

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