Both corticotropin releasing factor and neuropeptide Y are involved in the effect of orexin (hypocretin) on the food intake in rats

Ida, Takanori; Nakahara, Keiko; Kuroiwa, Takatoshi; Fukui, Kuniaki; Nakazato, Masamitsu; Murakami, Takayuki; Murakami, Noboru

doi:10.1016/s0304-3940(00)01498-1

Cited by 72 publications

(47 citation statements)

References 18 publications

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“…Furthermore, hypocretin-1 induces c-Fos expression in the PVN (Ida et al, 2000a) and dose dependently stimulates ACTH and corticosterone release (Hagan et al, 1999;Ida et al, 2000a;Jaszberenyi et al, 2000;Kuru et al, 2000;Samson et al, 2002). Pretreatment with ␣-helical CRF, a CRF antagonist, blocks the corticosterone elevation induced by hcrt (Ida et al, 2000b;Jaszberenyi et al, 2000;Samson et al, 2002). Hypocretindeficient narcoleptic patients have a lower basal ACTH release, suggesting reduced CRF tonus, although cortisol secretion did not differ from that of controls (Kok et al, 2002).…”

Section: Discussionmentioning

confidence: 95%

Interaction between the Corticotropin-Releasing Factor System and Hypocretins (Orexins): A Novel Circuit Mediating Stress Response

Winsky‐Sommerer¹,

Yamanaka²,

Diano³

et al. 2004

J. Neurosci.

412

316

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The hypothalamic neuropeptides hypocretins (orexins) play a crucial role in the stability of arousal and alertness. We tested whether the hypocretinergic system is a critical component of the stress response activated by the corticotropin-releasing factor (CRF). Our results show that CRF-immunoreactive terminals make direct contact with hypocretin-expressing neurons in the lateral hypothalamus and that numerous hypocretinergic neurons express the CRF-R1/2 receptors. We also demonstrate that application of CRF to hypothalamic slices containing identified hypocretin neurons depolarizes membrane potential and increases firing rate in a subpopulation of hypocretinergic cells. CRF-induced depolarization was tetrodotoxin insensitive and was blocked by the peptidergic CRF-R1 antagonist astressin. Moreover, activation of hypocretinergic neurons in response to acute stress was severely impaired in CRF-R1 knock-out mice. Together, our data provide evidence of a direct neuroanatomical and physiological input from CRF peptidergic system onto hypocretin neurons. We propose that, after stressor stimuli, CRF stimulates the release of hypocretins and that this circuit contributes to activation and maintenance of arousal associated with the stress response.

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Section: Discussionmentioning

confidence: 95%

Interaction between the Corticotropin-Releasing Factor System and Hypocretins (Orexins): A Novel Circuit Mediating Stress Response

Winsky‐Sommerer¹,

Yamanaka²,

Diano³

et al. 2004

J. Neurosci.

412

316

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show abstract

“…In the presence of a Y1-specific antagonist, the orexigenic effect of intracerebroventricular injections of hypocretin was reduced, suggesting interactions between hypocretin and NPY systems in the brain (Ida et al, 2000;Yamanaka et al, 2000). One possibility for interactions between these systems is the projection from hypocretin neurons to the arcuate nucleus (Peyron et al, 1998;van den Pol et al, 1998).…”

Section: Npy Depresses Hypocretin Neuron-functional Implicationsmentioning

confidence: 99%

Neuropeptide Y Inhibits Hypocretin/Orexin Neurons by Multiple Presynaptic and Postsynaptic Mechanisms: Tonic Depression of the Hypothalamic Arousal System

Fu¹,

Acuña-Goycolea²,

Pol³

2004

J. Neurosci.

159

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“…It is well documented that orexin-A plays an important role in both normal energy homeostasis and abnormal control of eating behavior such as anorexia nervosa (Baranowska et al, 2008;Bronsky et al, 2011). NPY-containing neurons in the ARC, which have a strong orexigenic effect on feeding, have been shown to express orexin receptors, and much evidence supports that NPYergic signaling mediates orexin-A's appetite-stimulating effect (Dube et al, 2000;Ida et al, 2000;Jain et al, 2000;Yamanaka et al, 2000). However, the precise molecular mechanism that links OX1R with NPYergic function still remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Orexin-A Activates Hypothalamic AMP-Activated Protein Kinase Signaling through a Ca²⁺-Dependent Mechanism Involving Voltage-Gated L-Type Calcium Channel

Zhou

et al. 2013

Mol Pharmacol

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Hypothalamic AMP-activated protein kinase (AMPK) and orexins/ hypocretins are both involved in the control of feeding behavior, but little is known about the interaction between these two signaling systems. Here, we demonstrated that orexin-A elicited significant activation of AMPK in the arcuate nucleus (ARC) of the hypothalamus by elevating cytosolic free Ca 21 involving extracellular calcium influx. Electrophysiological results revealed that orexin-A increased the L-type calcium current via the orexin receptor-phospholipase C-protein kinase C signaling pathway in ARC neurons that produce neuropeptide Y, an important downstream effector of orexin-A's orexigenic effect. Furthermore, the L-type calcium channel inhibitor nifedipine attenuated orexin-A-induced AMPK activation in vitro and in vivo. We found that inhibition of AMPK by either compound C (6-[4-[2-(1-piperidinyl)ethoxy]phenyl]-3-(4-pyridinyl)-pyrazolo[1,5-a]pyrimidine) or the ATPmimetic 9-b-D-arabinofuranoside prevented the appetite-stimulating effect of orexin-A. This action can be mimicked by nifedipine, the blocker of the L-type calcium channel. Our results indicated that orexin-A activates hypothalamic AMPK signaling through a Ca 21 -dependent mechanism involving the voltage-gated L-type calcium channel, which may serve as a potential target for regulating feeding behavior.

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Both corticotropin releasing factor and neuropeptide Y are involved in the effect of orexin (hypocretin) on the food intake in rats

Cited by 72 publications

References 18 publications

Interaction between the Corticotropin-Releasing Factor System and Hypocretins (Orexins): A Novel Circuit Mediating Stress Response

Interaction between the Corticotropin-Releasing Factor System and Hypocretins (Orexins): A Novel Circuit Mediating Stress Response

Neuropeptide Y Inhibits Hypocretin/Orexin Neurons by Multiple Presynaptic and Postsynaptic Mechanisms: Tonic Depression of the Hypothalamic Arousal System

Orexin-A Activates Hypothalamic AMP-Activated Protein Kinase Signaling through a Ca²⁺-Dependent Mechanism Involving Voltage-Gated L-Type Calcium Channel

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Both corticotropin releasing factor and neuropeptide Y are involved in the effect of orexin (hypocretin) on the food intake in rats

Cited by 72 publications

References 18 publications

Interaction between the Corticotropin-Releasing Factor System and Hypocretins (Orexins): A Novel Circuit Mediating Stress Response

Interaction between the Corticotropin-Releasing Factor System and Hypocretins (Orexins): A Novel Circuit Mediating Stress Response

Neuropeptide Y Inhibits Hypocretin/Orexin Neurons by Multiple Presynaptic and Postsynaptic Mechanisms: Tonic Depression of the Hypothalamic Arousal System

Orexin-A Activates Hypothalamic AMP-Activated Protein Kinase Signaling through a Ca2+-Dependent Mechanism Involving Voltage-Gated L-Type Calcium Channel

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Orexin-A Activates Hypothalamic AMP-Activated Protein Kinase Signaling through a Ca²⁺-Dependent Mechanism Involving Voltage-Gated L-Type Calcium Channel