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Hindbrain Noradrenergic Lesions Attenuate Anorexia and Alter Central cFos Expression in Rats after Gastric Viscerosensory Stimulation

Rinaman, L (2003) Hindbrain Noradrenergic Lesions Attenuate Anorexia and Alter Central cFos Expression in Rats after Gastric Viscerosensory Stimulation. Journal of Neuroscience, 23 (31). 10084 - 10092. ISSN 0270-6474

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Abstract

Behavioral, autonomic, and endocrine outputs of the CNS are subject to important feedback modulation by viscerosensory signals that are conveyed initially to the hindbrain nucleus of the solitary tract (NST). In the present study, noradrenergic (NA) neurons [i.e., those that express the NA synthetic enzyme dopamine β hydroxylase (DbH)] in the caudal NST were lesioned to determine their role in mediating anorexic responses to gastric stimulation and in conveying gastric sensory signals to the hypothalamus and amygdala. For this purpose, saporin toxin conjugated to an antibody against DbH was microinjected bilaterally into the caudal NST in adult rats. Control rats received similar microinjections of vehicle. Several weeks later, rats were tested for the ability of systemic cholecystokinin octapeptide (CCK) (0 or 10 μg/kg) to inhibit food intake. CCK-induced anorexia was significantly attenuated in toxin-treated rats. Rats subsequently were used in a terminal cFos study to determine central neural activation patterns after systemic CCK or vehicle and to evaluate lesion extent. Toxin-induced loss of DbH-positive NST neurons was positively correlated with loss of CCK-induced anorexia. Hypothalamic cFos expression was markedly attenuated in lesioned rats after CCK treatment, whereas CCK-induced neural activation in the parabrachial nucleus and amygdala appeared normal. These findings suggest that hindbrain NA neurons are an integral component of brainstem circuits that mediate CCK-induced anorexia and also are necessary for hypothalamic but not parabrachial or amygdala responses to gastric sensory stimulation.

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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Rinaman, Lrinaman@pitt.eduRINAMAN
Date: 5 November 2003
Date Type: Publication
Journal or Publication Title: Journal of Neuroscience
Volume: 23
Number: 31
Page Range: 10084 - 10092
DOI or Unique Handle: 10.1523/jneurosci.23-31-10084.2003
Schools and Programs: Dietrich School of Arts and Sciences > Neuroscience
Refereed: Yes
ISSN: 0270-6474
MeSH Headings: Amygdala--physiology; Animals; Anorexia--chemically induced; Anorexia--physiopathology; Central Nervous System--metabolism; Cholecystokinin--pharmacology; Dopamine beta-Hydroxylase--antagonists & inhibitors; Dopamine beta-Hydroxylase--metabolism; Eating--drug effects; Hypothalamus--physiology; Immunotoxins--pharmacology; Male; Microinjections; Neurons--drug effects; Neurons--metabolism; Norepinephrine--metabolism; Pons--drug effects; Pons--physiology; Proto-Oncogene Proteins c-fos--biosynthesis; Rats; Rats, Sprague-Dawley; Rhombencephalon--physiology; Solitary Nucleus--drug effects; Solitary Nucleus--physiology; Visceral Afferents--drug effects; Visceral Afferents--physiology
PubMed ID: 14602823
Date Deposited: 03 Mar 2016 15:13
Last Modified: 16 Aug 2020 11:55
URI: http://d-scholarship.pitt.edu/id/eprint/26886

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