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Article: Dysregulation of the orexinergic system: A potential neuropeptide target in depression

TitleDysregulation of the orexinergic system: A potential neuropeptide target in depression
Authors
KeywordsOrexin
Depression
Hypothalamus
Issue Date2020
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neubiorev
Citation
Neuroscience & Biobehavioral Reviews, 2020, v. 118, p. 384-396 How to Cite?
AbstractOrexins are highly involved in regulating the circadian rhythm, the brain’s reward mechanism, and the neuroendocrine response to stress. The disruption of orexin regulation is known to be associated with depression. Preclinical studies in rodents have identified the dorsomedial/perifornical and lateral areas of the hypothalamus as the population of orexinergic neurons that are primarily responsible for mediating depression-induced neuroanatomical changes in the brain. There is still no consensus regarding whether hyperactivity or hypoactivity of orexin signaling is responsible for producing depressive-like behaviour. Likewise, clinical studies indicated a general disruption in orexin signaling in depressive patients, but did not report definitive evidence of either hyperactivity or hypoactivity. Nevertheless, given the various reciprocal connections between orexin neurons and multiple brain regions, it is plausible that this involves a differential signaling network with orexin neurons as the coordination center. Here, an overview of preclinical and clinical evidence is provided as a basis for understanding the consequences of altered orexin signaling on neural circuitries modulating different aspects of the physiopathology of depression.
Persistent Identifierhttp://hdl.handle.net/10722/284518
ISSN
2019 Impact Factor: 8.33
2015 SCImago Journal Rankings: 5.290

 

DC FieldValueLanguage
dc.contributor.authorKhairuddin, S-
dc.contributor.authorAquili, L-
dc.contributor.authorHeng, BC-
dc.contributor.authorHoo, TLC-
dc.contributor.authorWong, KH-
dc.contributor.authorLim, LW-
dc.date.accessioned2020-08-07T08:58:48Z-
dc.date.available2020-08-07T08:58:48Z-
dc.date.issued2020-
dc.identifier.citationNeuroscience & Biobehavioral Reviews, 2020, v. 118, p. 384-396-
dc.identifier.issn0149-7634-
dc.identifier.urihttp://hdl.handle.net/10722/284518-
dc.description.abstractOrexins are highly involved in regulating the circadian rhythm, the brain’s reward mechanism, and the neuroendocrine response to stress. The disruption of orexin regulation is known to be associated with depression. Preclinical studies in rodents have identified the dorsomedial/perifornical and lateral areas of the hypothalamus as the population of orexinergic neurons that are primarily responsible for mediating depression-induced neuroanatomical changes in the brain. There is still no consensus regarding whether hyperactivity or hypoactivity of orexin signaling is responsible for producing depressive-like behaviour. Likewise, clinical studies indicated a general disruption in orexin signaling in depressive patients, but did not report definitive evidence of either hyperactivity or hypoactivity. Nevertheless, given the various reciprocal connections between orexin neurons and multiple brain regions, it is plausible that this involves a differential signaling network with orexin neurons as the coordination center. Here, an overview of preclinical and clinical evidence is provided as a basis for understanding the consequences of altered orexin signaling on neural circuitries modulating different aspects of the physiopathology of depression.-
dc.languageeng-
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neubiorev-
dc.relation.ispartofNeuroscience & Biobehavioral Reviews-
dc.subjectOrexin-
dc.subjectDepression-
dc.subjectHypothalamus-
dc.titleDysregulation of the orexinergic system: A potential neuropeptide target in depression-
dc.typeArticle-
dc.identifier.emailLim, LW: limlw@hku.hk-
dc.identifier.authorityLim, LW=rp02088-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neubiorev.2020.07.040-
dc.identifier.pmid32768489-
dc.identifier.scopuseid_2-s2.0-85089413337-
dc.identifier.hkuros312394-
dc.identifier.volume118-
dc.identifier.spage384-
dc.identifier.epage396-
dc.publisher.placeUnited Kingdom-

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