State-dependent regulation of cortical activity by cortisol: An EEG study

doi:10.1016/j.neulet.2006.05.038

Neuroscience Letters

Volume 404, Issues 1–2, 14 August 2006, Pages 39-43

https://doi.org/10.1016/j.neulet.2006.05.038 Get rights and content

Abstract

In the present study we investigated the effects of cortisol administration on EEG activity in eight healthy volunteers. We administered 35 mg of cortisol in a within-subjects double-blind placebo-controlled design. Cortisol administration caused a global decrease in cortical activity except for an increase frontally at the left, resulting in a significant change in frontal asymmetry. This pattern of results is almost the exact mirror image of one of our previous studies. Comparing subjective activation measures from the present and previous study showed that activation was substantially higher in the present study that was performed in formal testing conditions involving venipuncture, compared to the previous EEG study that was performed in non-formal testing conditions. However, the direction of the present cortisolinduced change in frontal activity asymmetry is consistent with the cortisolinduced change in asymmetric rotation behavior that we recently reported in similar testing conditions. We also found indications that, in contrast to the effects on the EEG measures, effects of cortisol administration on subjective anxiety and plasma oxytocin levels may be sex-dependent. These results are preliminary because of the post-hoc nature and the small number of subjects in the present study. However, they are in line with recent findings by others, suggesting that the effects of cortisol on cortical activity and subjective activation are state dependent and are influenced by testing conditions.

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Thus, the effective screening of free-cortisol levels in physiological fluids is a key factor for both prediction and diagnostic purpose. The existing procedures to diagnose stress-factors include consultations and counseling, [10,11] electroencephalogram [12,13], and electrocardiogram (electrical signals) [14], and/or self-questionnaires [15]. However, these methods are mainly qualitative and can introduce bias in the treatment process.
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Numerous neuroimaging studies have demonstrated opposite affective lateralized processing effects within specific areas of the PFC (see for reviews Miller, Crocker, Spielberg, Infantolino, & Heller, 2013; Wager, Phan, Liberzon, & Taylor, 2003), which could explain these divergent location findings and indicates the need to measure EEG at a high spatial density and combine EEG and fMRI (Davidson, 2004). The finding that FA remained unaffected by stress is at first glance at odds with the study of Lewis et al. (2007) and the prior cortisol administration studies of Tops et al. (2005, 2006). Yet, Lewis et al. (2007) found different results when applying a region or a single electrode analysis and in line with our results, no effect of examination stress was found for the single electrode analysis of F4–F3.
Asymmetry in frontal electrical activity has been suggested to index tendencies in affective responding and thus may be associated with hormonal stress responses. To assess the functional role of frontal asymmetry (FA) in stress, we measured FA at rest and following exposure to acute stress induced with the Maastricht Acute Stress Task (MAST; N = 70) in the standard 8–13 Hz band as well as based on individual alpha frequency (IAF) band. IAF-based resting FA_F4–F3 was associated with the stress-induced neuroendocrine response, such that left individual frontal activity predicted smaller total cortisol increases in response to the MAST. Like previous studies, we found resting left-sided FA_F8–F7 to predict trait behavioural activation measured with the BIS/BAS scales. FA remained unaffected by stress-induced cortisol response. These findings suggest that individual FA might reflect a trait-like characteristic that moderates the stress response. Our results underscore the utility of IAF in studying individual differences in stress responding.
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Depression is accompanied by an array of neurobiological variations, including altered HPA axis activity, monoamine, growth factor and inflammatory immune functioning. In addition, a recent perspective has entertained the possible role for oxytocin in depressive disorders. Given the involvement of oxytocin in prosocial behaviors such as attachment, affiliation, trust, and social support seeking, it is not surprising this neuropeptide might be involved in the development or maintenance of depressive disorders. This view is supported by evidence that oxytocin interacts with various neuroendocrine, neurotransmitter, and inflammatory processes that have previously been implicated in depression. Thus, it might be profitable to consider the contribution of oxytocin in the context of several neurobiological changes provoked by stressors. The current review examines the relation between oxytocin and depression with a specific focus on the interactions between the oxytocinergic system and stressor-provoked biological and psychosocial responses. The possibility is also considered that oxytocin might increase the salience of social cues, such that positive or negative experiences result in exaggerated responses that may influence affective states.
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However, except for the above-mentioned correlations of the participants’ experience with venepunctures and all measures of cortisol responsiveness, none of the significant correlation coefficients presented in Table 3 are robust to a threshold adjustment for multiple testing. As venepuncture procedures have been conceived as “mild pain”, “traumatic” and “potent physiological and psychosocial stressors”, the present article sets out to examine their capability to activate the HPA-axis, and to consequently elicit cortisol responses (Ginsberg et al., 1988; Gunnar et al., 2009; Tops et al., 2006). Although several studies have investigated cortisol changes to venepuncture, an integration of these findings has barely been accomplished to date, promoting the notion that the existence of venepuncture-induced cortisol responses “might appear logical, [but] does not seem to be based on specific findings” (Levine et al., 2007, p. 47).
Venepuncture procedures are frequently employed to continuously monitor humoral stress markers. As such procedures are conceived as “potent psychological and physiological stressors”, there is a need to determine whether venepuncture procedures themselves elicit cortisol responses and if so, how to deal with them appropriately.
In order to assess the rate of cortisol responses to venepuncture, we conducted a literature review, which suggested that venepuncture procedures induce cortisol responses with a probability of approximately 30%. By utilizing Bayesian analysis, this result was integrated with the cortisol data of 18 healthy men who were exposed to a venepuncture procedure twice (time lag: 1 week). The currently observed response rate of 47% differed substantially from the earlier findings, which we attribute to a self-selective sampling of participants. In addition, participants showing a response to the first venepuncture were highly likely to also show a response to the second one. In this regard, we discuss the presumed conditioning of cortisol responses to venepuncture procedures. To prevent the superposition of venepuncture-induced cortisol responses and responses induced by target stressors, we propose a time- and selection-based strategy: cortisol samples taken about 110 min after venepuncture should be virtually adjusted for its superimposing effects. Furthermore, previous experiences of venepuncture were highly predictive for cortisol responsiveness. This association could be utilized in further studies to identify participants who will probably show a cortisol response to venepuncture.

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View full text

State-dependent regulation of cortical activity by cortisol: An EEG study

Abstract

Psychoneuroendocrinology

Trends Neurosci.

Neurosci. Lett.

Neuroimage

Peptides

Biol. Psychol.

Biol. Psychol.

Multiple feedback regulatory loops upon rat hypothalamic corticotropin releasing hormone secretion

J. Clin. Invest.

Different lateralization of trait anxiety and trait fearfulness: evoked potential correlates

Pers. Individ. Dif.

Cortisol-induced impairments of working memory require acute sympathetic activation

Behav. Neurosci.