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Publication : Tumor Necrosis Factor α and Interleukin-1β Acutely Inhibit AgRP Neurons in the Arcuate Nucleus of the Hypothalamus.

First Author  Chaves FM Year  2020
Journal  Int J Mol Sci Volume  21
Issue  23 PubMed ID  33255553
Mgi Jnum  J:304994 Mgi Id  MGI:6693881
Doi  10.3390/ijms21238928 Citation  Chaves FM, et al. (2020) Tumor Necrosis Factor alpha and Interleukin-1beta Acutely Inhibit AgRP Neurons in the Arcuate Nucleus of the Hypothalamus. Int J Mol Sci 21(23):8928
abstractText  Obesity-associated low-grade inflammation favors weight gain, whereas systemic infection frequently leads to anorexia. Thus, inflammatory signals can either induce positive or negative energy balance. In this study, we used whole-cell patch-clamp to investigate the acute effects of three important proinflammatory cytokines, tumor necrosis factor alpha (TNF-alpha), interleukin-6, and interleukin-1beta (IL-1beta) on the membrane excitability of agouti-related peptide (AgRP)- or proopiomelanocortin (POMC)-producing neurons. We found that both TNF-alpha and IL-1beta acutely inhibited the activity of 35-42% of AgRP-producing neurons, whereas very few POMC neurons were depolarized by TNF-alpha. Interleukin-6 induced no acute changes in the activity of AgRP or POMC neurons. Our findings indicate that the effect of TNF-alpha and IL-1beta, especially on the activity of AgRP-producing neurons, may contribute to inflammation-induced anorexia observed during acute inflammatory conditions.
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