Urocortin in the lateral septal area modulates feeding induced by orexin A in the lateral hypothalamus

Wang, Chuanfeng; Kotz, Catherine M.

doi:10.1152/ajpregu.00558.2001

Cited by 62 publications

(55 citation statements)

References 47 publications

(60 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present results are in agreement with those of Kotz and colleagues, who found that deprivation-or hypocretin-induced feeding are reduced by UCN infusion into LS (Wang and Kotz, 2002), and add to the growing body of literature indicating that CRF receptor stimulation in either hypothalamic or extrahypothalamic sites reduces food intake (Ohata et al, 2000;Currie et al, 2001;Wang et al, 2001;Daniels et al, 2004;Jochman et al, 2005;Weitemier and Ryabinin, 2006). The present studies also confirm our previous finding that CRF 1 receptors within the BLA regulate feeding (Jochman et al, 2005).…”

Section: Discussionsupporting

confidence: 93%

“…The present studies addressed these issues and also examined the relative contributions of CRF receptor subtypes to these effects by characterizing the mechanisms through which the CRF 1 /CRF 2 agonist urocortin (UCN) reduces feeding after microinfusion into the lateral septum (LS), a site that has a high concentration of CRF 2 receptors and UCNcontaining terminals and has been found recently to mediate UCN-induced anorexia (Bakshi et al, 2001;Wang and Kotz, 2002).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Stimulation of Lateral Septum CRF₂Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF₁Receptors in Basolateral Amygdala

Bakshi¹,

Newman²,

Smith‐Roe³

et al. 2007

J. Neurosci.

View full text Add to dashboard Cite

The corticotropin-releasing factor (CRF) system is the primary central mediator of stress-like states, coordinating behavioral, endocrine, and autonomic responses to stress. Although induction of anorexia is a well documented effect of CRF receptor agonist administration, the central sites and behavioral processes underlying this phenomenon are poorly understood. The present studies addressed this question by examining the neuroanatomical, behavioral, and pharmacological mechanisms mediating decreases in feeding produced by the CRF 1 /CRF 2 receptor agonist urocortin. Separate groups of food-restricted male Sprague Dawley rats were given infusions of urocortin (0, 50, 125, 250 ng/0.5 l) into the lateral septum (LS) and immediately afterward were rated on a wide array of behaviors (locomotion, rearing, grooming, stereotypies) including a microstructural analysis of ingestive behavior. Intra-LS urocortin infusion dosedependently reduced feeding and drinking while concomitantly increasing grooming, stereotypies, and ethological plus traditional measures of anxiety-like responses in the elevated plus-maze. Urocortin infusion into neighboring sites (lateral ventricle, medial caudate) had no effects. Coinfusion into the LS of the mixed CRF 1 /CRF 2 receptor antagonist D-Phe-CRF (12-41) (0, 100, 1000 ng/0.5 l) or the novel selective CRF 2 receptor antagonist Astressin2B (0, 500, 1000 ng/0.5 l) blocked urocortin-induced effects, but the CRF 1 -selective antagonist NBI27914 (0, 500, 1000 ng/0.5 l) had no effect, although it completely reversed the behavioral sequelae of CRF when infused into the basolateral amygdala. These results indicate that one of the modes through which the CRF system promotes anorexia is the recruitment of stress-like states after stimulation of CRF 2 receptors within the LS.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Stimulation of Lateral Septum CRF₂Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF₁Receptors in Basolateral Amygdala

Bakshi¹,

Newman²,

Smith‐Roe³

et al. 2007

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…CRF injections into the septum also impaired context-and tone-dependent fear conditioning, and this action may be mediated by CRF 2 receptors . Administration of urocortin 1 into the septum significantly decreased feeding in food-deprived rats for 24 h without producing a conditioned taste aversion (Wang and Kotz, 2002). These data suggest that the septal region is an important site for anxiogenic-like, memory-modulatory, and anorectic actions of CRF/urocortin receptor agonists.…”

Section: Neuropharmacological Mechanisms For Crf Systems Local Brain mentioning

confidence: 70%

Corticotropin-Releasing Factor in Brain: A Role in Activation, Arousal, and Affect Regulation

Heinrichs

Koob²

2004

J Pharmacol Exp Ther

323

223

View full text Add to dashboard Cite

Organisms exposed to challenging stimuli that alter the status quo inside or outside of the body are required for survival purposes to generate appropriate coping responses that counteract departures from homeostasis. Identification of an executive control mechanism within the brain capable of coordinating the multitude of endocrine, physiological, and functional coping responses has high utility for understanding the response of the organism to stressor exposure under normal or pathological conditions. The corticotropin-releasing factor (CRF)/urocortin family of neuropeptides and receptors constitutes an affective regulatory system due to the integral role it plays in controlling neural substrates of arousal, emotionality, and aversive processes. In particular, available evidence from pharmacological intervention in multiple species and phenotyping of mutant mice shows that CRF/urocortin systems mediate motor and psychic activation, stimulus avoidance, and threat recognition responses to aversive stimulus exposure. It is suggested that affective regulation is exerted by CRF/urocortin systems within the brain based upon the sensitivity of local brain sites to CRF/urocortin ligand administration and the appearance of hypothalamo-pituitary-adrenocortical activation following stressor exposure. Moreover, these same stress neuropeptides may constitute a mechanism for learning to avoid noxious stimuli by facilitating the formation of so-called emotional memories. A conceptual framework is provided for extrapolation of animal model findings to humans and for viewing CRF/urocortin activation as a continuum measure linking normal and pathological states.Many experimental studies performed in animals support the role of corticotropin-releasing factor (CRF) peptides and receptors as mediators of interoceptive coping reactions to environmental or physiological challenges; however, the advent of small molecule ligands for CRF receptors suitable for administration in human beings raises the question of what insights, if any, anti-stress pharmacology exerted via CRF manipulations in animals provides for human biology and psychopathology. The present review addresses how the evidence for the adaptive utility of CRF systems provides a basis for predicting the consequences of brain CRF system activation or deactivation in man. The thesis most strongly supported by the available experimental evidence is that: 1) activating, 2) avoidant, and 3) learning/memory functions of CRF systems have evolved to serve affective regulatory needs in man and animals. The term affective can be defined as "relating to, arising from, or influencing feelings or emotions" (Webster's Ninth Collegiate Dictionary) whereas the related phrase affective disorder describes a disturbance of mood where mood is defined as a prolonged emotion that colors the whole psychic life (American Psychiatric Association, 1994). The reader familiar with the term homeostasis may be interested in one testable postulate that a certain environmental stimulus intensity...

show abstract

“…In a separate group of animals, the two-bottle preference test was used to determine whether BDNF results in aversive consequences after administration into the VMH. The procedures for the experiment have been previously described (84). In brief, drinking water was allowed only between 10:30 and 11:00 AM for 30 bilaterally VMH-cannulated rats each day for 7 days.…”

Section: Methodsmentioning

confidence: 99%

Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

Wang

Bomberg²,

Levine³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

View full text Add to dashboard Cite

Recent studies show that brainderived neurotrophic factor (BDNF) decreases feeding and body weight after peripheral and ventricular administration. BDNF mRNA and protein, and its receptor TrkB, are widely distributed in the hypothalamus and other brain regions. However, there are few reports on specific brain sites of actions for BDNF. We evaluated the effect of BDNF, given into the ventromedial nucleus of the hypothalamus (VMH), on normal and deprivation-and neuropeptide Y (NPY)-induced feeding behavior and body weight. BDNF injected unilaterally or bilaterally into the VMH of food-deprived and nondeprived rats significantly decreased feeding and body weight gain within the 0-to 24-h and the 24-to 48-h postinjection intervals. Doses effectively producing inhibition of feeding behavior did not establish a conditioned taste aversion. BDNF-induced feeding inhibition was attenuated by pretreatment of the TrkB-Fc fusion protein that blocks binding between BDNF and its receptor TrkB. VMH-injected BDNF significantly decreased VMH NPY-induced feeding at 1, 2, and 4 h after injection. In summary, BDNF in the VMH significantly decreases food intake and body weight gain, by TrkB receptor-mediated actions. Furthermore, the anorectic effects of BDNF in this site appear to be mediated by NPY. These data suggest that the VMH is an important site of action for BDNF in its effects on energy metabolism. food intake; body weight THE VENTROMEDIAL NUCLEUS OF THE HYPOTHALAMUS (VMH) is a brain area important to the regulation of energy metabolism. Early studies indicated that VMH lesions resulted in hyperphagia and obesity (28,38,66), whereas electrical stimulation of the VMH immediately suppressed feeding and induced lipolysis (65). Glucose-sensing neurons (7,27,55,74,75) and receptors for neuropeptides important to energy metabolism have been identified in the VMH, including leptin (13,17,20,22,51), melanocortin (26), neuropeptide Y (NPY) (43), corticotrophin-releasing hormone (49), CCK (12), insulin (33), and orexin (44) receptors. Many biological agents given into the VMH have been demonstrated to affect feeding. Food intake is inhibited by administration of histamine (4, 47), glucagon-like peptide 1 (70), serotonin agonists (25), urocortin (58), CCK (79), leptin (51), and insulin (78), whereas thyroid hormone (3,5,3Ј-triiodothyronine) (40), GABA or GABA agonists (32,34,35), norepinephrine (73), orexin (74), and NPY induce feeding after administration into the VMH (5,9,24,31,43,56,76).Anatomically, the VMH receives inputs from regions important to the regulation of energy metabolism, including the hypothalamic arcuate nucleus (ARC) (2, 14, 23), lateral hypothalamus (18, 67, 80), amygdala (45, 50), and lateral septum. The VMH also projects to ARC (77), paraventricular nucleus (PVN) (42, 52), lateral hypothalamus (72, 80), dorsomedial nucleus of the hypothalamus (46, 80), amygdala (6, 68), lateral septum (68), ventral tegmental area (68), nucleus accumbens (6), and nucleus of the solitary tract (6). These behavioral and neuroanatom...

show abstract

Urocortin in the lateral septal area modulates feeding induced by orexin A in the lateral hypothalamus

Cited by 62 publications

References 47 publications

Stimulation of Lateral Septum CRF₂Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF₁Receptors in Basolateral Amygdala

Stimulation of Lateral Septum CRF₂Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF₁Receptors in Basolateral Amygdala

Corticotropin-Releasing Factor in Brain: A Role in Activation, Arousal, and Affect Regulation

Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

Contact Info

Product

Resources

About

Urocortin in the lateral septal area modulates feeding induced by orexin A in the lateral hypothalamus

Cited by 62 publications

References 47 publications

Stimulation of Lateral Septum CRF2Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF1Receptors in Basolateral Amygdala

Stimulation of Lateral Septum CRF2Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF1Receptors in Basolateral Amygdala

Corticotropin-Releasing Factor in Brain: A Role in Activation, Arousal, and Affect Regulation

Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

Contact Info

Product

Resources

About

Stimulation of Lateral Septum CRF₂Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF₁Receptors in Basolateral Amygdala

Stimulation of Lateral Septum CRF₂Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF₁Receptors in Basolateral Amygdala