Leptin increases sympathetic nerve activity via induction of its own receptor in the paraventricular nucleus

Author:

Shi Zhigang1ORCID,Pelletier Nicole E1,Wong Jennifer1,Li Baoxin1,Sdrulla Andrei D2,Madden Christopher J3,Marks Daniel L4ORCID,Brooks Virginia L1ORCID

Affiliation:

1. Department of Physiology and Pharmacology, Portland, United States

2. Department of Anesthesiology and Perioperative Medicine, Portland, United States

3. Department of Neurological Surgery, Portland, United States

4. Department of Pediatrics, Pape Family Pediatric Research Institute, Brenden-Colson Center for Pancreatic Care Oregon Health & Science University, Portland, United States

Abstract

Whether leptin acts in the paraventricular nucleus (PVN) to increase sympathetic nerve activity (SNA) is unclear, since PVN leptin receptors (LepR) are sparse. We show in rats that PVN leptin slowly increases SNA to muscle and brown adipose tissue, because it induces the expression of its own receptor and synergizes with local glutamatergic neurons. PVN LepR are not expressed in astroglia and rarely in microglia; instead, glutamatergic neurons express LepR, some of which project to a key presympathetic hub, the rostral ventrolateral medulla (RVLM). In PVN slices from mice expressing GCaMP6, leptin excites glutamatergic neurons. LepR are expressed mainly in thyrotropin-releasing hormone (TRH) neurons, some of which project to the RVLM. Injections of TRH into the RVLM and dorsomedial hypothalamus increase SNA, highlighting these nuclei as likely targets. We suggest that this neuropathway becomes important in obesity, in which elevated leptin maintains the hypothalamic pituitary thyroid axis, despite leptin resistance.

Funder

National Institutes of Health

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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