Serotonergic Regulation of the Orexin/Hypocretin Neurons through the 5-HT<sub>1A</sub>Receptor

Muraki, Yo; Yamanaka, Akihiro; Tsujino, Natsuko; Kilduff, Thomas S.; Goto, Katsutoshi; Sakurai, Takeshi

doi:10.1523/jneurosci.1027-04.2004

Cited by 184 publications

(149 citation statements)

References 61 publications

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“…Basic membrane properties of orexin neurons in V1aR Ϫ/Ϫ mice were not different from our previous reports (Yamanaka et al, 2003a;Muraki et al, 2004). Membrane capacitance, resting membrane potential, and membrane resistance of orexin neurons in V1aR Ϫ/Ϫ ; orexin/EGFP mice were 30.8 Ϯ 3.0 pF (n ϭ 11), Ϫ55.9 Ϯ 0.9 mV (n ϭ 11), and 494.6 Ϯ 58.6 M⍀ (n ϭ 9), respectively.…”

Section: Avp and Oxytocin Failed To Induce An Inward Current In Orexicontrasting

confidence: 72%

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Tsunematsu¹,

Fu²,

Yamanaka³

et al. 2008

J. Neurosci.

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Water homeostasis is a critical challenge to survival for land mammals. Mice display increased locomotor activity when dehydrated, a behavior that improves the likelihood of locating new sources of water and simultaneously places additional demands on compromised hydration levels. The neurophysiology underlying this well known behavior has not been previously elucidated. We report that the anti-diuretic hormone arginine-vasopressin (AVP) is involved in this response. AVP and oxytocin directly induced depolarization and an inward current in orexin/hypocretin neurons. AVP-induced activation of orexin neurons was inhibited by a V1a receptor (V1aR)-selective antagonist and was not observed in V1aR knock-out mice, suggesting an involvement of V1aR. Subsequently activation of phospholipase C␤ triggers an increase in intracellular calcium by both calcium influx through nonselective cation channels and calcium release from calcium stores in orexin neurons. Intracerebroventricular injection of AVP or water deprivation increased locomotor activity in wild-type mice, but not in transgenic mice lacking orexin neurons. V1aR knock-out mice were less active than wild-type mice. These results suggest that the activation of orexin neurons by AVP or oxytocin has an important role in the regulation of spontaneous locomotor activity in mice. This system appears to play a key role in water deprivation-induced hyperlocomotor activity, a response to dehydration that increases the chance of locating water in nature.

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Section: Avp and Oxytocin Failed To Induce An Inward Current In Orexicontrasting

confidence: 72%

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Tsunematsu¹,

Fu²,

Yamanaka³

et al. 2008

J. Neurosci.

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“…4 C and D). Moreover, we found that effects of other inhibitory or excitatory neurotransmitters, 5-hydroxytryptamine (5-HT) (19) or cholecystokinin (CCK) (20) were also decreased (Fig. 4 E and F).…”

Section: Elimination Of Gabab Receptors On Orexin Neurons Results In Anmentioning

confidence: 92%

“…We have previously studied the regulatory mechanisms of orexin neurons in vitro (7,8,19,(23)(24)(25). However, the physiological relevance of the regulatory mechanisms or inputs affecting the activity of orexin neurons remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Selective loss of GABA _B receptors in orexin-producing neurons results in disrupted sleep/wakefulness architecture

Matsuki

Nomiyama

Takahira³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

117

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“…The excitatory glutamatergic input appears to be under presynaptic control by group III metabotropic glutamate receptors , neuropeptide Y2/Y5 receptors (Fu et al, 2004), and GLP-1 receptors (Acuna-Goycolea and van den . Conversely, these neurons can be hyperpolarized by GABA acting on GABA A receptors (Li et al, 2002;Eggermann et al, 2003;Yamanaka et al, 2003a), by serotonin through 5-HT 1A receptors (Muraki et al, 2004) and by neuropeptide Y through Y1 receptors (Fu et al, 2004). Other studies indicate that norepinephrine inhibits (Li et al, 2002;Yamanaka et al, 2003a) and cholinergic activation depolarizes (Yamanaka et al, 2003a) these neurons, but the specific receptors mediating these responses are yet to be identified.…”

Section: Discussionmentioning

confidence: 99%

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.

418

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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Serotonergic Regulation of the Orexin/Hypocretin Neurons through the 5-HT_1AReceptor

Cited by 184 publications

References 61 publications

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Selective loss of GABA _B receptors in orexin-producing neurons results in disrupted sleep/wakefulness architecture

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

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Serotonergic Regulation of the Orexin/Hypocretin Neurons through the 5-HT1AReceptor

Cited by 184 publications

References 61 publications

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Vasopressin Increases Locomotion through a V1a Receptor in Orexin/Hypocretin Neurons: Implications for Water Homeostasis

Selective loss of GABA B receptors in orexin-producing neurons results in disrupted sleep/wakefulness architecture

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

Contact Info

Product

Resources

About

Serotonergic Regulation of the Orexin/Hypocretin Neurons through the 5-HT_1AReceptor

Selective loss of GABA _B receptors in orexin-producing neurons results in disrupted sleep/wakefulness architecture