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Publication : Viscerosensory input drives angiotensin II type 1A receptor-expressing neurons in the solitary tract nucleus.

First Author  Carter DA Year  2018
Journal  Am J Physiol Regul Integr Comp Physiol Volume  314
Issue  2 Pages  R282-R293
PubMed ID  29118020 Mgi Jnum  J:258270
Mgi Id  MGI:6117976 Doi  10.1152/ajpregu.00290.2017
Citation  Carter DA, et al. (2018) Viscerosensory input drives angiotensin II type 1A receptor-expressing neurons in the solitary tract nucleus. Am J Physiol Regul Integr Comp Physiol 314(2):R282-R293
abstractText  Homeostatic regulation of visceral organ function requires integrated processing of neural and neurohormonal sensory signals. The nucleus of the solitary tract (NTS) is the primary sensory nucleus for cranial visceral sensory afferents. Angiotensin II (ANG II) is known to modulate peripheral visceral reflexes, in part, by activating ANG II type 1A receptors (AT1AR) in the NTS. AT1AR-expressing NTS neurons occur throughout the NTS with a defined subnuclear distribution, and most of these neurons are depolarized by ANG II. In this study we determined whether AT1AR-expressing NTS neurons receive direct visceral sensory input, and whether this input is modulated by ANG II. Using AT1AR-GFP mice to make targeted whole cell recordings from AT1AR-expressing NTS neurons, we demonstrate that two-thirds (37 of 56) of AT1AR-expressing neurons receive direct excitatory, visceral sensory input. In half of the neurons tested (4 of 8) the excitatory visceral sensory input was significantly reduced by application of the transient receptor potential vallinoid type 1 receptor agonist, capsaicin, indicating AT1AR-expressing neurons can receive either C- or A-fiber-mediated input. Application of ANG II to a subset of second-order AT1AR-expressing neurons did not affect spontaneous, evoked, or asynchronous glutamate release from visceral sensory afferents. Thus it is unlikely that AT1AR-expressing viscerosensory neurons terminate on AT1AR-expressing NTS neurons. Our data suggest that ANG II is likely to modulate multiple visceral sensory modalities by altering the excitability of second-order AT1AR-expressing NTS neurons.
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