Hypothalamic–pituitary–adrenal axis effects on plasma homovanillic acid in man

Posener, Joel A.; Schatzberg, Alan F.; Williams, Gordon H.; Samson, Jacky; McHale, Nancy L; Bessette, Meghan P; Schildkraut, Joseph J.

doi:10.1016/s0006-3223(97)00550-7

Cited by 22 publications

(10 citation statements)

References 33 publications

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“…In schizophrenia, psychotic symptoms have been linked to increased synaptic dopamine function in the associative striatum (Kegeles et al, 2010), and one might speculate whether dysfunctional dopaminergic activity is responsible for secondary psychotic symptoms in PTSD. While PTSD is primarily considered a disorder of serotonin, noradrenalin, and glutamate (Kelmendi et al, 2016), it is also known that stress can increase dopaminergic activity in the central nervous system (Kaneyuki et al, 1991;Lindley, Bengoechea, Schatzberg, & Wong, 1999;Posener et al, 1999). As in our study, PTSD-SP has been linked to increased stress, as suggested by more severe PTSD symptoms (Kaštelan et al, 2007;Pivac et al, 2007Pivac et al, , 2006.…”

Section: Discussionsupporting

confidence: 69%

Associations of neural processing of reward with posttraumatic stress disorder and secondary psychotic symptoms in trauma-affected refugees

Uldall

Nielsen

Carlsson

et al. 2020

European Journal of Psychotraumatology

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Background: Psychological traumatic experiences can lead to posttraumatic stress disorder (PTSD). Secondary psychotic symptoms are not common but may occur. Objectives: Since psychotic symptoms of schizophrenia have been related to aberrant reward processing in the striatum, using the same paradigm we investigate whether the same finding extends to psychotic and anhedonic symptoms in PTSD. Methods: A total of 70 male refugees: 18 PTSD patients with no secondary psychotic symptoms (PTSD-NSP), 21 PTSD patients with secondary psychotic symptoms (PTSD-SP), and 31 healthy controls (RHC) were interviewed and scanned with functional magnetic resonance imaging (fMRI) during a monetary incentive delay task. Using region of interest analysis of the prefrontal cortex and ventral striatum, we investigated reward-related activity.Results: Compared to RHC, participants with PTSD had decreased neural activity during monetary reward. Also, participants with PTSD-SP exhibited decreased activity in the associative striatum relative to participants with PTSD-NSP during processing of motivational reward anticipation which correlated with severity of psychotic symptoms. However, the difference between the two PTSD groups disappeared when PTSD severity and trauma exposure were accounted for. Conclusions: Anhedonia and secondary psychotic symptoms in PTSD are characterized by dysfunctional reward consumption and anticipation processing, respectively. The latter may reflect a mechanism by which abnormal reward signals in the basal ganglia facilitates psychotic symptoms across psychiatric conditions. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 69%

Associations of neural processing of reward with posttraumatic stress disorder and secondary psychotic symptoms in trauma-affected refugees

Uldall

Nielsen

Carlsson

et al. 2020

European Journal of Psychotraumatology

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“…97 In healthy individuals, cortisol has been found to increase serum levels of homovanillic acid, a key dopamine metabolite. 98 Walker 99 has reported that cortisol increases dopamine metabolism in the nucleus accumbens and raises plasma dopamine metabolites, and hypothesizes that this may be a mechanism whereby stress precipitates psychosis. In an animal model of SZ, rats with neonatal hippocampal excitotoxic damage show greatly increased mesolimbic release of dopamine in response to stress.…”

Section: Resultsmentioning

confidence: 99%

Could Stress Cause Psychosis in Individuals Vulnerable to Schizophrenia?

Corcoran¹,

Mujica‐Parodi²,

Yale³

et al. 2002

CNS spectr.

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It has long been considered that psychosocial stress plays a role in the expression of symptoms in schizophrenia (SZ), as it interacts with latent neural vulnerability that stems from genetic liability and early environmental insult. Advances in the understanding of the neurobiology of the stress cascade in both animal and human studies lead to a plausible model by which this interaction may occur: through neurotoxic effects on the hippocampus that may involve synaptic remodeling. Of late, the neurodevelopmental model of SZ etiology has been favored. But an elaboration of this schema that credits the impact of postnatal events and considers a role for neurodegenerative changes may be more plausible, given the evidence for gene-environment interaction in SZ expression and progressive structural changes observed with magnetic resonance imaging. Furthermore, new insights into nongliotic neurotoxic effects such as apoptosis, failure of neurogenesis, and changes in circuitry lead to an expansion of the time frame in which environmental effects may mediate expression of SZ symptoms.

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“…4 eas of the mesocorticolimbic dopamine system in rodents (e.g., Ortiz et al 1996). Stress may also alter dopaminergic activity in human subjects, as indicated by changes in plasma and urine HVA concentrations in response to a variety of psychosocial challenges (e.g., Gruen and Baron 1984;Breier 1989;Sumiyoshi et al 1998;Posener et al 1999). Furthermore, in human subjects the stress induced by acute glucose deprivation causes a reversible decrease in striatal binding to the D2/D3 receptor ligand [ 11 C]raclopride, an effect similar to the lower D2 binding to [ 18 F]FCP observed in subordinate, as compared with dominant, female cynomolgus monkeys (Grant et al 1998;Adler et al 2000).…”

mentioning

confidence: 99%

Central Nervous System Monoamine Correlates of Social Dominance in Cynomolgus Monkeys (Macaca fascicularis)

Kaplan

Manuck

Fontenot³

et al. 2002

Neuropsychopharmacology

100

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Social dominance is a fundamental component of both human and nonhuman primate sociality. However, its neurobiological correlates remain incompletely understood. We evaluated the association between dominance status and monoamine metabolite concentrations in cisternal cerebrospinal fluid (CSF) in adult male (n ϭ 25) and female (n ϭ 21) cynomolgus macaques ( Macaca fascicularis ) housed in unisexual social groups. Concentrations of the metabolites of dopamine (homovanillic acid [HVA]), norepinephrine ) and serotonin Social dominance reflects an asymmetry of relationship among individuals, as defined by the outcomes of dyadic encounters of a competitive or agonistic nature, and has long been thought to represent a fundamental component of sociality in nonhuman primates (Bernstein 1981;Silk 1987;Walters and Seyfarth 1987). Dominance-related behaviors may also comprise a primary axis of interpersonal behavior in the structure of human social relationships (Wiggins and Trapnell 1996). Additionally, this concept is often extended, in people, to include dimensional variation in personality traits such as extraversion or social potency (Wiggins and Pincus 1992;Wiggins and Trapnell 1996). Recent studies also suggest that differences in dominance status in monkeys and dominance-related personality traits in humans partially reflect variation in aspects of central nervous system monoaminergic activity (Raleigh et al. 1983(Raleigh et al. , 1991Depue et al. 1994;Higley et al. 1996aHigley et al. , 1996bShively 1998).In monkeys, serotonin has figured prominently in behavioral research relating to social dominance. For example, male vervet monkeys ( Cercopithecus aethiops ) become dominant in their social groups following treat- Corresponding Author: Jay R. Kaplan, Ph.D., Professor of Pathology (Comparative Medicine), Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1040, Tel.: (336) 716-1522, Fax: (336) 716-1515, E-mail: jkaplan@ wfubmc.edu Received February 12, 2000 revised July 5, 2001; accepted July 25, 2001.Online publication: 7/27/01 at www.acnp.org/citations/Npp 072701155. 432 J.R. Kaplan et al. N EUROPSYCHOPHARMACOLOGY 2002 -VOL . 26 , NO . 4 ment with either the serotonin precursor tryptophan or the serotonin reuptake inhibitor fluoxetine, and take a subordinate position when treated chronically with the serotonin releasing/depleting agent fenfluramine (chronic administration depletes serotonin) (Raleigh et al. 1991). Naturally-occurring differences in cerebrospinal fluid (CSF) concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) also covary positively with dominance rank in female rhesus monkeys ( Macaca mulatta ), although a similar relationship has not been clearly described for adult male rhesus monkeys (Higley et al. 1996a). In contrast, dominant female cynomolgus monkeys ( M. fascicularis ) exhibit lower central serotonergic activity (as indexed by a low prolactin response to the serotonin agonist fenfluramine) than subordinates (Shi...

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Hypothalamic–pituitary–adrenal axis effects on plasma homovanillic acid in man

Cited by 22 publications

References 33 publications

Associations of neural processing of reward with posttraumatic stress disorder and secondary psychotic symptoms in trauma-affected refugees

Associations of neural processing of reward with posttraumatic stress disorder and secondary psychotic symptoms in trauma-affected refugees

Could Stress Cause Psychosis in Individuals Vulnerable to Schizophrenia?

Central Nervous System Monoamine Correlates of Social Dominance in Cynomolgus Monkeys (Macaca fascicularis)

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