Pharmacology of 5-HT2 Modulation of Amygdala &amp; Hypothalamus in Anxiety Disorders

Jiang, Xiaolong; Chen, Aiqin; Smerin, Stanley E.; Zhang, Lei; Li, He

doi:10.5772/22837

Cited by 4 publications

(3 citation statements)

References 88 publications

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“…Normalization of amygdala activity in patients following antidepressant treatment could reflect improvements in depression severity as well as, or alternatively, could be evidence of the effects of SSRI treatment on amygdala responses. The mechanism may be consistent with the density of serotonin receptors within the amygdala (Xu & Pandey, 2000) which are a target of action for SSRIs (Jiang, Chen, Smerin, Zhang, & Li, 2011). Short term administration of SSRIs in both healthy volunteers (Harmer, Mackay, Reid, Cowen, & Goodwin, 2006) and MDD patients (Godlewska, Norbury, Selvaraj, Cowen, & Harmer, 2012) had normalized amygdala responses to negative emotional stimuli, which preceded the clinical improvements (Godlewska et al, 2012), suggesting a therapeutic mechanism of SSRI treatment for MDD.…”

Section: Antidepressant Treatment Effects On Regional Brain Activationsmentioning

confidence: 65%

Psychotherapy and Antidepressant Treatment Effects on the Functional Neuroanatomy of Depression

Sankar

2015

Psychopathology Review

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The present review examines the functional neural correlates of the effects of antidepressant medication as well as psychological therapy in depression. There has been considerable evidence to suggest that antidepressant medications normalize dysfunctional activity in limbic regions, in particular the amygdala, as well as in subcortical and prefrontal regions in patients during processing of emotional and cognitive stimuli. Fewer studies to date have examined psychotherapy related brain changes in patients with depression, with some evidence for amygdalahippocampal reductions following psychological therapies. There may be potential common therapeutic mechanisms of action with antidepressants and psychotherapy. The specificity of effects related to pharmacological and psychological therapies as well as to different classes of pharmacotherapy and effects due to improvements in the severity of depressive symptoms requires further investigation. Anterior cingulate activity as a predictor of clinical response before initiation of antidepressant treatment has been highly replicated, while evidence from CBT has been mixed. In order to derive clinical applications from these findings, machine learning methods have been applied to ascertain diagnosis and prognosis at the individual level with high accuracy. Future research should also aim to investigate whether integration of neuroimaging biomarkers based on multiple neural processes, such as affective and cognitive processing and structural neuroimaging, would achieve more accurate classification. This would help to optimize treatment strategies which are particularly important for those patients who may be less likely to benefit from the usual initial therapies.

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Section: Antidepressant Treatment Effects On Regional Brain Activationsmentioning

confidence: 65%

Psychotherapy and Antidepressant Treatment Effects on the Functional Neuroanatomy of Depression

Sankar

2015

Psychopathology Review

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“…Serotonin, with its receptors, is widely studied in anxiety [92] and is the most widely studied neurochemical in relation to aggression [93]. Increase of serotonin in the midbrain [94], as well as stimulation of serotonergic neurons in the dorsal raphé nucleus, causing release of serotonin in the medial prefrontal cortex among other locations [95], escalates intermale aggression in mice in the resident-intruder paradigm.…”

Section: The Amygdala and Hippocampus In Ptsdmentioning

confidence: 99%

Neurophysiology of Aggression in Posttraumatic Stress Disorder

Smerin

Chen²,

He³

2016

J Psychiatry

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Posttraumatic stress disorder (PTSD) is a universal anxiety disorder, affecting not only soldiers but also victims of every sort of traumatic stress-natural disaster, automobile collision, crime, domestic violence, bereavement. Aggressiveness, stemming from "intermittent explosive anger", is a not infrequent comorbidity of PTSD, with the most serious consequences. The neurophysiology of aggression and anger in general, and PTSD in particular, is a jigsaw puzzle of which we are first gathering the pieces. In this chapter, PTSD is conceptualized as revolving around an idée fix of the traumatic experience, leading to fear and a derivative defensive form of aggression. The history of research in the neurophysiology of aggression and pertinent forms of memory and emotion are then reviewed, leading to a neuronal system that spans the brain. Some basic phenomena in neurophysiology are touched onsynaptic plasticity in the form of long-term potentiation of synaptic transmission, G-protein-coupled receptor modulation thereof, and the theta rhythm of the electroencephalogram-and the path we are following in our attempt to integrate these phenomena into a model of the neurophysiology of aggression in PTSD is described.

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“…traumático y que persiste mucho después de la eliminación de los factores de estrés que participan(Jiang X. , Chen A. , Smerin S. , Zhang L , & H., 2011).…”

Section: Ansiedadunclassified

Interacción de Galphimina-A con los sistemas GABAérgicos y Glutamatérgicos, en modelos de ansiedad y electrofisiología de la amígdala basolateral

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IX 1. Introducción ____________________________________________________________ 2. Antecedentes ___________________________________________________________ 2.1 Ansiedad ________________________________________________________________ 2.1.1 Mecanismos fisiopatológicos de los trastornos de ansiedad _____________________________ 2.2 La amígdala ______________________________________________________________ 2.3 Ácido -amino-butírico (GABA) en la ansiedad __________________________________ 2.4 Glutamato en la ansiedad __________________________________________________ 2.5 Tratamiento de los trastornos de Ansiedad ___________________________________ 2.6 Galphimia glauca Cav, Sinónimo: Thryallis glauca (Cav.) Kuntze __________________ 2.7 Usos y farmacología ______________________________________________________ 3. Planteamiento del problema ______________________________________________ 4. Pregunta de investigación ________________________________________________ 5. Hipótesis ______________________________________________________________ 6. Objetivo general _______________________________________________________ 6.1 Objetivos específicos _____________________________________________________ 7. Material y métodos _____________________________________________________ 7.1 Material vegetal _________________________________________________________ 7.2 Obtención de un pool de galphiminas________________________________________ 7.2.1 Aislamiento e identificación de G-A ________________________________________________ 7.3 Animales _______________________________________________________________ 7.4 Sustancias empleadas ____________________________________________________ 7.5 Laberinto elevado en forma de cruz (LEC), campo abierto (

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Pharmacology of 5-HT2 Modulation of Amygdala & Hypothalamus in Anxiety Disorders

Cited by 4 publications

References 88 publications

Psychotherapy and Antidepressant Treatment Effects on the Functional Neuroanatomy of Depression

Psychotherapy and Antidepressant Treatment Effects on the Functional Neuroanatomy of Depression

Neurophysiology of Aggression in Posttraumatic Stress Disorder

Interacción de Galphimina-A con los sistemas GABAérgicos y Glutamatérgicos, en modelos de ansiedad y electrofisiología de la amígdala basolateral

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