Norepinephrine is not required for reduction of feeding  induced by cholecystokinin

Cannon, Chase A; Palmiter, Richard D.

doi:10.1152/ajpregu.00689.2002

Cited by 15 publications

(5 citation statements)

References 52 publications

(57 reference statements)

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“…The results also confirmed the anorectic effect of an ID diet, as well as the learning deficit effects . The anorectic effect of CCK-8 has been reported before (Bray, 2000;Asakawa et al, 2002;Cannon and Palmiter, 2003). The increase in blood CCK-8 might explain the anorectic effect of ID diet.…”

Section: Discussionmentioning

confidence: 53%

The Effects of an Essential Fatty Acid Compound and a Cholecystokinin-8 Antagonist on Iron Deficiency Induced Anorexia and Learning Deficits

Yehuda¹,

Mostofsky²

2004

Nutritional Neuroscience

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Iron deficiency (ID) is among the most common nutritional diseases, causing deleterious effects that include decreases in cognitive function and weight loss. The ID also induces a reduction in the number and affinity of dopaminergic D2 receptors. The new finding that ID induces an increase in the pancreas cells, leads to the hypothesis that cholecystokinin-8 (CCK-8) is involved in the ID effects. The level of CCK-8 was higher among ID rats, compared with normal rats. The ID rats in our study were anorectic and performed poorly in learning tests (Morris water maze and passive avoidance learning). Essential fatty acids (EFA) mediate dopamine activity and have been found to rehabilitate learning deficits. Treatment with a fatty acid compound blocked both the learning deficits and the anorexia, while a CCK-8 antagonist was successful only against the anorectic effects.

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Section: Discussionmentioning

confidence: 53%

The Effects of an Essential Fatty Acid Compound and a Cholecystokinin-8 Antagonist on Iron Deficiency Induced Anorexia and Learning Deficits

Yehuda¹,

Mostofsky²

2004

Nutritional Neuroscience

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“…A recent report indicates that systemic CCK retains its anorexic effects in DbH knock-out mice, in which NA signaling is absent (Cannon and Palmiter, 2003). It will be important to determine whether toxin-induced loss of DbH-containing neurons in mice produces effects similar to those observed in the present study in rats, because there may be a species difference.…”

Section: Correlation Between Na Cell Loss and Cck-induced Anorexiamentioning

confidence: 63%

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

2003

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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 beta 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 microg/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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“…These studies, however, cannot differentiate the effects of functional loss of NE signaling from loss of PrRP signaling. Interestingly, DβH knockout mice – which lack NE – continue to display hypophagic responses to systemic CCK (Cannon and Palmiter 2003). In these rodents, NA neurons are not lesioned and maintain the ability to synthesize and release PrRP, suggesting that PrRP signaling may be sufficient for stress-induced hypophagia.…”

Section: Cnts Modulation Of Stress-induced Hypophagiamentioning

confidence: 99%

Interoceptive modulation of neuroendocrine, emotional, and hypophagic responses to stress

Maniscalco

Rinaman

2017

Physiology & Behavior

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Periods of caloric deficit substantially attenuate many centrally mediated responses to acute stress, including neural drive to the hypothalamic-pituitary-adrenal (HPA) axis, anxiety-like behavior, and stress-induced suppression of food intake (i.e., stress hypophagia). It is posited that this stress response plasticity supports food foraging and promotes intake during periods of negative energy balance, even in the face of other internal or external threats, thereby increasing the likelihood that energy stores are repleted. The mechanisms by which caloric deficit alters central stress responses, however, remain unclear. The caudal brainstem contains two distinct populations of stress-recruited neurons [i.e., noradrenergic neurons of the A2 cell group that co-express prolactin-releasing peptide (PrRP+ A2 neurons), and glucagon-like peptide 1 (GLP-1) neurons] that also are responsive to interoceptive feedback about feeding and metabolic status. A2/PrRP and GLP-1 neurons have been implicated anatomically and functionally in the central control of the HPA axis, anxiety-like behavior, and stress hypophagia. The current review summarizes a growing body of evidence that caloric deficits attenuate physiological and behavioral responses to acute stress as a consequence of reduced recruitment of PrRP+ A2 and hindbrain GLP-1 neurons, accompanied by reduced signaling to their brainstem, hypothalamic, and limbic forebrain targets.

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Norepinephrine is not required for reduction of feeding induced by cholecystokinin

Cited by 15 publications

References 52 publications

The Effects of an Essential Fatty Acid Compound and a Cholecystokinin-8 Antagonist on Iron Deficiency Induced Anorexia and Learning Deficits

The Effects of an Essential Fatty Acid Compound and a Cholecystokinin-8 Antagonist on Iron Deficiency Induced Anorexia and Learning Deficits

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

Interoceptive modulation of neuroendocrine, emotional, and hypophagic responses to stress

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