Interaction of noradrenaline and cortisol predicts negative intrusive memories in posttraumatic stress disorder

Nicholson, Emma; Bryant, Richard A.; Felmingham, Kim L.

doi:10.1016/j.nlm.2013.11.018

Cited by 53 publications

(73 citation statements)

References 39 publications

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“…However, it was not possible to find any correlation between ASR1 and the PTSD‐like symptom strength ( P = 0.1223 for ASR34 and P = 0.3662 for CF34, data not shown). Based on recent reports (Salehi et al ., ; Nicholson et al ., ), it was hypothesised that level changes of stress mediators, specifically NE and CORT, serve as predictors for the PTSD endophenotype. Correlations between the stress‐stimulated neurochemical changes or the concurrent hormonal output in the mouse brain and the acute/delayed arousal (ASR1, ASR2 and ASR34) or the strength of aversive memories (CF2 and CF34) induced by FS were evaluated.…”

Section: Discussionmentioning

confidence: 99%

“…Other evidence points to a significant NE and cortisol interaction, but fails to show any independent effects of NE signaling and salivary cortisol levels in the prediction of negative intrusive memories in patients with PTSD (Nicholson et al ., ). It was hypothesised that the assessment of brain NE and corticosterone (CORT) levels is able to predict distinct PTSD outcomes.…”

Section: Introductionmentioning

confidence: 97%

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Norepinephrine and corticosterone in the medial prefrontal cortex and hippocampus predict PTSD‐like symptoms in mice

Kao

Stalla

et al. 2015

Eur J of Neuroscience

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This study measured changes in brain extracellular norepinephrine (NE) and free corticosterone (CORT) levels in a mouse model of post-traumatic stress disorder and related them to hyperarousal and fear memory retention. To this end, microdialysis in the medial prefrontal cortex (mPFC) and the hippocampus (HPC) of male C57BL/6NCrl mice was performed during an acoustic startle response (ASR) and following an electric foot shock (FS), as well as during an ASR and recall of contextual fear (CF) 1 day later. Changes in ASR-stimulated NE levels in the mPFC corresponded to ASR 34 days after FS. Changes in basal and ASR-stimulated extracellular NE levels in the HPC, in contrast, were related to expression of early (day 2) and late (day 34) CF after FS. The increase in extracellular NE levels correlated in a U-shape manner with arousal levels and CF, thus suggesting a non-direct relationship. Stress of different modalities/strength (ASR, FS and CF) caused a similar relative increase in free CORT levels both in the mPFC and the HPC. One day after FS, ASR-induced increases in the CORT content in the mPFC tended to correlate with the FS-potentiated ASR in a U-shape manner. Taken together, these data show that the intracerebral increase in free CORT was likely related to an immediate response to stress, whereas NE neurotransmission in the forebrain predicted arousal and CF 1 month after trauma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Norepinephrine and corticosterone in the medial prefrontal cortex and hippocampus predict PTSD‐like symptoms in mice

Kao

Stalla

et al. 2015

Eur J of Neuroscience

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“…Salivary alpha amylase (sAA) levels are also often considered an indication of the balance of sympathetic nervous system activation and parasympathetic withdrawal (Nater and Rohleder 2009), although their exact relationship with these systems (Bosch et al 2011), versus central (Ehlert et al 2006) or peripheral (Myriam V. Turner and Sugiya 2002) noradrenergic tone in particular, versus other aspects of the stress-response pathway (Myriam V. ) remains unclear. Nonetheless, SAA levels have been repeatedly found to be altered at baseline and following a stressor in populations diagnosed with PTSD (Feldman et al 2013;Nicholson, Bryant, and Felmingham 2014), particularly when circadian patterns of release are assessed (Keeshin et al 2015;Myriam Verena Thoma et al 2012), and correlations between individuals' patterns of sAA have also in some studies been found to correlate with general PTSD symptom intensity and in particular hyperarousal and intrusive symptoms (Chou et al 2014;Keeshin et al 2015).…”

Section: Evidence Of Increased Noradrenergic Tone In Ptsdmentioning

confidence: 99%

Noradrenergic dysregulation in the pathophysiology of PTSD

Hendrickson

Raskind

2016

Experimental Neurology

125

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A central role for noradrenergic dysregulation in the pathophysiology of post-traumatic stress disorder (PTSD) is increasingly suggested by both clinical and basic neuroscience research. Here, we integrate recent findings from clinical and animal research with the earlier literature. We first review the evidence for net upregulation of the noradrenergic system and its responsivity to stress in individuals with PTSD. Next, we trace the evidence that the α noradrenergic receptor antagonist prazosin decreases many of the symptoms of PTSD from initial clinical observations, to case series, to randomized controlled trials. Finally, we review the basic science work that has begun to explain the mechanism for this efficacy, as well as to explore its possible limitations and areas for further advancement. We suggest a view of the noradrenergic system as a central, modifiable link in a network of interconnected stress-response systems, which also includes the amygdala and its modulation by medial prefrontal cortex. Particular attention is paid to the evidence for bidirectional signaling between noradrenaline and corticotropin-releasing factor (CRF) in coordinating these interconnected systems. The multiple different ways in which the sensitivity and reactivity of the noradrenergic system may be altered in PTSD are highlighted, as is the evidence for possible heterogeneity in the pathophysiology of PTSD between different individuals who appear clinically similar. We conclude by noting the importance moving forward of improved measures of noradrenergic functioning in clinical populations, which will allow better recognition of clinical heterogeneity and further assessment of the functional implications of different aspects of noradrenergic dysregulation.

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“…As such, salivary α-amylase (sAA) has been proposed as an indicator of NA levels (Chatterton et al, 1996;Rohleder and Nater, 2009), and has been used in a number of studies to examine the relationship between NA and intrusive memories in PTSD. For example, a recent study found the interaction between sAA and salivary cortisol to predict greater frequency of negative intrusive memories in a sample with PTSD, compared to trauma-exposed and non-exposed controls (Nicholson et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, we were interested in the role of sAA in response to fear conditioning as a moderator between fear extinction learning ability and PTSD symptom severity in a sample with current PTSD, trauma exposure without PTSD, and non-trauma-exposed controls. Based on recent research using sAA as an indicator of NA in intrusive memories (Bryant et al, 2013;Nicholson et al, 2014), and the role of noradrenergic signaling in fear conditioning and extinction (Antov et al, 2015;Antov and Stockhorst, 2014;Soeter and Kindt, 2012), we predicted that sAA levels would moderate the relationship between fear extinction learning and PTSD symptoms. Specifically, we hypothesized that poorer fear extinction learning ability would be associated with greater PTSD symptom severity, and that this relationship would be stronger with lower sAA levels in response to fear conditioning.…”

Section: Introductionmentioning

confidence: 99%

Endogenous salivary α-amylase does not interact with skin conductance response during fear extinction in posttraumatic stress disorder

Zuj

Palmer

Malhi

et al. 2018

Psychiatry Research

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Posttraumatic Stress Disorder (PTSD) is associated with elevated noradrenergic signaling, which has an impact on emotional learning and memory. Fear extinction is thought to underlie the processes of exposure therapy, however the relationship between noradrenaline and extinction in PTSD is unclear. Participants with PTSD (n = 21), trauma-exposure without PTSD (TC; n = 36), and non-trauma-exposed controls (NTC; n = 27) completed a fear conditioning and extinction paradigm, and conditioned fear was indexed by skin conductance response (SCR). Salivary α-amylase (sAA) collected at baseline and immediately post-fear acquisition was used as an index of noradrenaline, and we examined whether sAA in response to fear acquisition was a moderator between fear extinction and PTSD symptoms. While there was a significant increase in sAA from baseline to post-fear acquisition, this was not modulated by group. Compared to TC and NTC, the PTSD group displayed a slower decline in SCRs during early extinction, which generalized across stimulus type, and was not moderated by sAA. These findings suggest that the relationship between fear extinction and PTSD symptoms does not change as a function of sAA levels; however previous research suggests other processes of fear learning may be associated with noradrenergic activity in PTSD.

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Interaction of noradrenaline and cortisol predicts negative intrusive memories in posttraumatic stress disorder

Cited by 53 publications

References 39 publications

Norepinephrine and corticosterone in the medial prefrontal cortex and hippocampus predict PTSD‐like symptoms in mice

Norepinephrine and corticosterone in the medial prefrontal cortex and hippocampus predict PTSD‐like symptoms in mice

Noradrenergic dysregulation in the pathophysiology of PTSD

Endogenous salivary α-amylase does not interact with skin conductance response during fear extinction in posttraumatic stress disorder

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