The noradrenergic symptom cluster: clinical expression and neuropharmacology

Pierre Blier1, Mike Briley21Institute of Mental Health Research, University of Ottawa, Ottawa, Ontario, Canada; 2NeuroBiz Consulting and Communication, Castres, FranceAbstract: Signs and symptoms of depression can be linked to one or more monoaminergic systems, specifically the norepinephrine (NE),...

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Autores principales:	Blier P, Briley M
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2011
Materias:	Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/2764a3c41a504310a447238d65c64dbc
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spelling	oai:doaj.org-article:2764a3c41a504310a447238d65c64dbc2021-12-02T06:03:10ZThe noradrenergic symptom cluster: clinical expression and neuropharmacology1176-63281178-2021https://doaj.org/article/2764a3c41a504310a447238d65c64dbc2011-06-01T00:00:00Zhttp://www.dovepress.com/the-noradrenergic-symptom-cluster-clinical-expression-and-neuropharmac-a7599https://doaj.org/toc/1176-6328https://doaj.org/toc/1178-2021Pierre Blier1, Mike Briley21Institute of Mental Health Research, University of Ottawa, Ottawa, Ontario, Canada; 2NeuroBiz Consulting and Communication, Castres, FranceAbstract: Signs and symptoms of depression can be linked to one or more monoaminergic systems, specifically the norepinephrine (NE), the dopamine (DA), and the serotonin (5-HT) systems. In particular, the modulation of energy, vigilance, and arousal can be directly linked to the NE system. There is, however, a great deal of overlap in the modulation of the symptoms of depression between these monoaminergic systems. There are considerable reciprocal interactions between the NE, DA, and the 5-HT systems. When using a selective serotonin reuptake inhibitor (SSRI), for example, 5-HT transmission is enhanced, but at the same time there is a dampening of the activity of NE and DA neurons through inhibitory 5-HT2A and 5-HT2C receptors, respectively. This could explain the residual symptoms of fatigue, lack of energy, and anhedonia, often seen after patients present an overall positive response to a SSRI. Using a dual 5-HT and NE reuptake inhibitor (SNRI), such as milnacipran, would result in an additional increase in NE activity. Futhermore, inhibiting NE reuptake increases DA availability in the frontal cortex since DA is mainly cleared by the NE transporters in several brain regions. A risk inherent in increased NE activity is that of provoking anxiety. This is avoided however by the attenuation of the phasic reactivity of the firing of NE neurons through prolonged administration of SSRI and SNRI.Keywords: norepinephrine, dopamine, serotonin, residual symptoms, norepinephrine paradoxBlier PBriley MDove Medical PressarticleNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol 2011, Iss Supplement 1, Pp 15-20 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429
spellingShingle	Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 Blier P Briley M The noradrenergic symptom cluster: clinical expression and neuropharmacology
description	Pierre Blier1, Mike Briley21Institute of Mental Health Research, University of Ottawa, Ottawa, Ontario, Canada; 2NeuroBiz Consulting and Communication, Castres, FranceAbstract: Signs and symptoms of depression can be linked to one or more monoaminergic systems, specifically the norepinephrine (NE), the dopamine (DA), and the serotonin (5-HT) systems. In particular, the modulation of energy, vigilance, and arousal can be directly linked to the NE system. There is, however, a great deal of overlap in the modulation of the symptoms of depression between these monoaminergic systems. There are considerable reciprocal interactions between the NE, DA, and the 5-HT systems. When using a selective serotonin reuptake inhibitor (SSRI), for example, 5-HT transmission is enhanced, but at the same time there is a dampening of the activity of NE and DA neurons through inhibitory 5-HT2A and 5-HT2C receptors, respectively. This could explain the residual symptoms of fatigue, lack of energy, and anhedonia, often seen after patients present an overall positive response to a SSRI. Using a dual 5-HT and NE reuptake inhibitor (SNRI), such as milnacipran, would result in an additional increase in NE activity. Futhermore, inhibiting NE reuptake increases DA availability in the frontal cortex since DA is mainly cleared by the NE transporters in several brain regions. A risk inherent in increased NE activity is that of provoking anxiety. This is avoided however by the attenuation of the phasic reactivity of the firing of NE neurons through prolonged administration of SSRI and SNRI.Keywords: norepinephrine, dopamine, serotonin, residual symptoms, norepinephrine paradox
format	article
author	Blier P Briley M
author_facet	Blier P Briley M
author_sort	Blier P
title	The noradrenergic symptom cluster: clinical expression and neuropharmacology
title_short	The noradrenergic symptom cluster: clinical expression and neuropharmacology
title_full	The noradrenergic symptom cluster: clinical expression and neuropharmacology
title_fullStr	The noradrenergic symptom cluster: clinical expression and neuropharmacology
title_full_unstemmed	The noradrenergic symptom cluster: clinical expression and neuropharmacology
title_sort	noradrenergic symptom cluster: clinical expression and neuropharmacology
publisher	Dove Medical Press
publishDate	2011
url	https://doaj.org/article/2764a3c41a504310a447238d65c64dbc
work_keys_str_mv	AT blierp thenoradrenergicsymptomclusterclinicalexpressionandneuropharmacology AT brileym thenoradrenergicsymptomclusterclinicalexpressionandneuropharmacology AT blierp noradrenergicsymptomclusterclinicalexpressionandneuropharmacology AT brileym noradrenergicsymptomclusterclinicalexpressionandneuropharmacology
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The noradrenergic symptom cluster: clinical expression and neuropharmacology

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