Corticotropin-releasing hormone projections from the paraventricular nucleus of the hypothalamus to the nucleus of the solitary tract increase blood pressure

• DOI: 10.1152/jn.00623.2018
• Publication Date: 2018-12-19T09:22:22Z
• Authors: Lei A. Wang; Dianna H. Nguyen; Steve W. Mifflin
• Keywords: Corticotropin-releasing hormone; Solitary nucleus; Solitary tract; Kynurenic acid

Activation of corticotropin-releasing hormone (CRH) type 2 receptors (CRHR2) in the nucleus solitary tract (NTS) contributes to development hypertension, but source CRH inputs NTS that increases blood pressure remains unknown. This study tested hypothesis activation CRH-containing projections from paraventricular hypothalamus (PVN) increase pressure. We expressed channelrhodopsin (ChR2), a light-sensitive ion channel, into neurons PVN. was achieved by injecting Cre-inducible virus expressing ChR2 PVN CRH-Cre mice. mice are genetically modified Cre recombinase only producing CRH. found optogenetic stimulation somas or fibers originating significantly increased and heart rate. Microinjection K-41498 (CRHR2 antagonist) attenuated pressor tachycardiac responses induced In vitro loose-patch recordings revealed discharge frequency neurons. effect pretreatment abolished kynurenic acid (nonselective glutamate receptor antagonist). These results suggest PVN-NTS The cardiovascular may be mediated at least part corelease axons NEW & NOTEWORTHY Optogenetic (CRH)-containing Corelease contribute elicited somas.