Orexin-A increases cell surface expression of AMPA receptors in the striatum

Shin, Hyun Sung; Cho, Hyeong Seok; Sung, Ki Wug; Yoon, Bong June

doi:10.1016/j.bbrc.2008.11.051

Cited by 31 publications

(27 citation statements)

References 21 publications

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“…By contrast, chronic anti-depressant treatment upregulates CREB, and increasing CREB levels in rodent models resulting in anti-depressant-like behaviors [58]. CREB phosphorylation is also induced by orexin-A in neurons from brain tissue [59], and OX2R activation-induced CREB phosphorylation may be beneficial for the treatment of depression [60].…”

Section: Accepted Manuscriptmentioning

confidence: 93%

Heterodimerization of human orexin receptor 1 and kappa opioid receptor promotes protein kinase A/cAMP-response element binding protein signaling via a Gαs-mediated mechanism

Chen

Zhang

Chen

et al. 2015

Cellular Signalling

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Section: Accepted Manuscriptmentioning

confidence: 93%

Heterodimerization of human orexin receptor 1 and kappa opioid receptor promotes protein kinase A/cAMP-response element binding protein signaling via a Gαs-mediated mechanism

Chen

Zhang

Chen

et al. 2015

Cellular Signalling

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“…Orexin-A increases cell surface expression of ␣-amino-3-hydroxy-5-methyl-4-isoxazole propanoic acid receptors and potentiates ␣-amino-3-hydroxy-5-methyl-4-isoxazole propanoic acid receptors' mediated synaptic transmission in the striatum, providing a potential link between the activation of orexin signaling in the striatum in response to addictive substances and neural adaptations in the reward circuitry. 31 A recent study 32 also revealed that orexin-A, but not orexin B, induces a state-dependent long-term potentiation of synaptic transmission in hippocampal slices from adult mice. Longterm potentiation of synaptic transmission is blocked by pharmacologic inhibition of OX1R and plasticity-related kinases, including serine/threonine (calmodulin kinase II, protein kinase C, protein kinase A, mitogen-activated protein kinase), lipid, phosphatidylinositol 3-kinase, and receptor tyrosine kinases.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Orexin-A Is Mediated by an Increase of Hypoxia-inducible Factor-1 Activity in Rat

Yuan¹,

Dong

Zhang³

et al. 2011

Anesthesiology

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Background: Recent studies suggest that the novel neuropeptide orexin-A may play an essential role during neuronal damage. However, the function of orexin-A during brain ischemia remains unclear. Recently, hypoxia-inducible factor-1␣ (HIF-1␣) was shown to be activated by orexin-A. The aim of the current study is to test the hypothesis that administration of exogenous orexin-A can attenuate ischemia-reperfusion injury through the facilitation of HIF-1␣ expression. Methods: Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion for 120 min. Rats were treated with different doses of orexin-A or vehicle before the ischemia and at the onset of reperfusion. To investigate the action of HIF-1␣ in the neuroprotective effects of orexin-A, the HIF-1␣ inhibitor YC-1 was used alone or combined with orexin-A. Neurologic deficit scores and infarct volume were assessed. Brains were harvested for immunohistochemical staining and western blot analysis. Results: Orexin-A significantly ameliorated neurologic deficit scores and reduced infarct volume after cerebral ischemia reperfusion. Administration of 30 g/kg orexin-A showed optimal neuroprotective effects. This effect was still present 7 days after reperfusion. Furthermore, orexin-A decreased the number of apoptotic cells and significantly enhanced HIF-1␣

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“…Intracellular Ca 21 concentration is elevated through both Ca 21 release and Ca 21 influx, and other potently activated targets include phospholipases C (PLC), D, and A 2 . Mitogen-activated protein kinase pathways ERK1/2 (extracellular signal-regulated kinase 1/2) and p38 may also be important signal relayers in orexin signaling (Hilairet et al, 2003;Ammoun et al, 2006a, b;Shin et al, 2009;reviewed in Kukkonen, 2013). The main G-protein pathway for orexin receptors is assumed to be G q , but other G-protein couplings have also been seen (reviewed in Kukkonen, 2013).…”

Section: Introductionmentioning

confidence: 99%

Autocrine Endocannabinoid Signaling through CB₁Receptors Potentiates OX₁Orexin Receptor Signaling

et al. 2012

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It has been proposed that OX 1 orexin receptors and CB 1 cannabinoid receptors can form heteromeric complexes, which affect the trafficking of OX 1 receptors and potentiate OX 1 receptor signaling to extracellular signal-regulated kinase (ERK). We have recently shown that OX 1 receptor activity releases high levels of the endocannabinoid 2-arachidonoyl glycerol (2-AG), suggesting an alternative route for OX 1 -CB 1 receptor interaction in signaling, for instance, in retrograde synaptic transmission. In the current study, we set out to investigate this possibility utilizing recombinant Chinese hamster ovary K1 cells. 2-AG released from OX 1 receptor-expressing cells acted as a potent paracrine messenger stimulating ERK activity in neighboring CB 1 receptor-expressing cells. When OX 1 and CB 1 receptors were expressed in the same cells, OX 1 stimulation-induced ERK phosphorylation and activity were strongly potentiated. The potentiation but not the OX 1 response as such was fully abolished by specific inhibition of CB 1 receptors or the enzyme responsible for 2-AG generation, diacylglycerol lipase (DAGL). Although the results do not exclude the previously proposed OX 1 -CB 1 heteromerization, they nevertheless unequivocally identify DAGL-dependent 2-AG generation as the pivotal determinant of the OX 1 -CB 1 synergism and thus suggest a functional rather than a molecular interaction of OX 1 and CB 1 receptors.

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Orexin-A increases cell surface expression of AMPA receptors in the striatum

Cited by 31 publications

References 21 publications

Heterodimerization of human orexin receptor 1 and kappa opioid receptor promotes protein kinase A/cAMP-response element binding protein signaling via a Gαs-mediated mechanism

Heterodimerization of human orexin receptor 1 and kappa opioid receptor promotes protein kinase A/cAMP-response element binding protein signaling via a Gαs-mediated mechanism

Neuroprotective Effect of Orexin-A Is Mediated by an Increase of Hypoxia-inducible Factor-1 Activity in Rat

Autocrine Endocannabinoid Signaling through CB₁Receptors Potentiates OX₁Orexin Receptor Signaling

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Orexin-A increases cell surface expression of AMPA receptors in the striatum

Cited by 31 publications

References 21 publications

Heterodimerization of human orexin receptor 1 and kappa opioid receptor promotes protein kinase A/cAMP-response element binding protein signaling via a Gαs-mediated mechanism

Heterodimerization of human orexin receptor 1 and kappa opioid receptor promotes protein kinase A/cAMP-response element binding protein signaling via a Gαs-mediated mechanism

Neuroprotective Effect of Orexin-A Is Mediated by an Increase of Hypoxia-inducible Factor-1 Activity in Rat

Autocrine Endocannabinoid Signaling through CB1Receptors Potentiates OX1Orexin Receptor Signaling

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Autocrine Endocannabinoid Signaling through CB₁Receptors Potentiates OX₁Orexin Receptor Signaling