Regulation of feeding by the parabrachial nucleus

2021 ◽  
Author(s):  
Nayla Chaijale
Keyword(s):  
Parabrachial Nucleus

Spino-diencephalic relays through the parabrachial nucleus in the cat

1989 ◽  
Vol 480 (1-2) ◽  
pp. 37-50 ◽  
Author(s):  
Wu Ma ◽  
Anders Blomqvist ◽  
Karen J. Berkley
Keyword(s):  
Parabrachial Nucleus

Electrophysiological identification of neurons in the parabrachial nucleus projecting directly to the hypothalamus in the rat

1984 ◽  
Vol 322 (2) ◽  
pp. 388-392 ◽  
Author(s):  
John Ciriello ◽  
Duncan Lawrence ◽  
Quentin J. Pittman
Keyword(s):  
Parabrachial Nucleus

Projections of the parabrachial nucleus in the pigeon (Columba livia)

1990 ◽  
Vol 293 (4) ◽  
pp. 499-523 ◽  
Author(s):  
J. Martin Wild ◽  
J. J. A. Arends ◽  
H. Philip Zeigler
Keyword(s):  
Columba Livia ◽  
Parabrachial Nucleus

scholarly journals GLP-1 Receptor Stimulation of the Lateral Parabrachial Nucleus Reduces Food Intake: Neuroanatomical, Electrophysiological, and Behavioral Evidence

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4356-4367 ◽  
Author(s):  
Jennifer E. Richard ◽  
Imre Farkas ◽  
Fredrik Anesten ◽  
Rozita H. Anderberg ◽  
Suzanne L. Dickson ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Fluorescent Protein ◽  
Yellow Fluorescent Protein ◽  
Parabrachial Nucleus ◽  
Lateral Parabrachial Nucleus ◽  
Electrophysiological Studies ◽  
Glucagon Like Peptide 1 ◽  
Behavioral Evidence ◽  
Stimulation Of

Abstract The parabrachial nucleus (PBN) is a key nucleus for the regulation of feeding behavior. Inhibitory inputs from the hypothalamus to the PBN play a crucial role in the normal maintenance of feeding behavior, because their loss leads to starvation. Viscerosensory stimuli result in neuronal activation of the PBN. However, the origin and neurochemical identity of the excitatory neuronal input to the PBN remain largely unexplored. Here, we hypothesize that hindbrain glucagon-like peptide 1 (GLP-1) neurons provide excitatory inputs to the PBN, activation of which may lead to a reduction in feeding behavior. Our data, obtained from mice expressing the yellow fluorescent protein in GLP-1-producing neurons, revealed that hindbrain GLP-1-producing neurons project to the lateral PBN (lPBN). Stimulation of lPBN GLP-1 receptors (GLP-1Rs) reduced the intake of chow and palatable food and decreased body weight in rats. It also activated lPBN neurons, reflected by an increase in the number of c-Fos-positive cells in this region. Further support for an excitatory role of GLP-1 in the PBN is provided by electrophysiological studies showing a remarkable increase in firing of lPBN neurons after Exendin-4 application. We show that within the PBN, GLP-1R activation increased gene expression of 2 energy balance regulating peptides, calcitonin gene-related peptide (CGRP) and IL-6. Moreover, nearly 70% of the lPBN GLP-1 fibers innervated lPBN CGRP neurons. Direct intra-lPBN CGRP application resulted in anorexia. Collectively, our molecular, anatomical, electrophysiological, pharmacological, and behavioral data provide evidence for a functional role of the GLP-1R for feeding control in the PBN.

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