Cortisol | EPFL Graph Search

Le cortisol (ou hydrocortisone) est une hormone stéroïde (corticostéroïde et glucocorticoïde) sécrétée par la zone fasciculée du cortex (la partie externe) de la glande surrénale à partir du cholestérol, sous la dépendance de l'ACTH hypophysaire. Cette dernière est connue pour être une hormone du stress physique ou émotionnel. Ses fonctions ou actions principales sont :

l'augmentation de la glycémie par le biais de la néoglucogenèse ;
l'inhibition de certaines réponses du système immunitaire ;
la régulation du métabolisme des lipides, protéines et glucides ;
régulation du cycle circadien (en complément de la mélatonine).

D'un point de vue pathologique, l'hypersécrétion de cortisol – ou hypercortisolisme chronique – définit le syndrome de Cushing, tandis qu'à l'opposé un déficit en cortisol – ou hypocortisolisme – est l'une des formes de l'insuffisance surrénalienne. Différentes formes de corticostéroïdes synthétiques, apparentés au cortisol, sont utilisé

Genetic selection for low glucocorticoid responsiveness recapitulates PTSD-related phenotypes: a behavioral, neuroimaging and sleep-physiology study

Silvia Monari

Humans show inter-individual differences in vulnerability to develop post-traumatic stress disorder (PTSD) following exposure to trauma. Several critical biobehavioral features have been consistently described in PTSD patients, including blunted cortisol levels, smaller hippocampal size, sleep disturbances. However, because of the delay between trauma exposure and the onset of symptoms characteristic of PTSD, only a few longitudinal studies have tried to dissect whether these features constitute pre-trauma risk factors or consequences of the trauma. Enormous effort in animal and human studies has been dedicated to understanding mechanisms of conditioned fear and fear extinction, processes that are at the core of PTSD. However, the same progress has not been translated into psychiatric practice for PTSD. Deepening our understanding of the contribution of key factors to PTSD-related alterations can serve to develop effective treatments.In particular, with regard to low cortisol levels in PTSD pathophysiology, a causative role for blunted glucocorticoid responsiveness in PTSD has not been demonstrated yet.Here, we have addressed this question in lines of Wistar rats genetically-selected for their differential habituation of glucocorticoid responses to stress (LOW-, INTER-, HIGH-CORT Responder rats) and focused on fear extinction, a hallmark of PTSD symptomology, as one of the key features. As a first step, we looked whether divergent trajectories of glucocorticoid responsiveness were associated with brain volume abnormalities, prompted by the influential role of glucocorticoid in brain development. Notably, rats with low or high corticosterone responsiveness exhibit smaller hippocampi, regardless of trauma exposure, compared to rats with normative corticosterone levels. Similarly, the distribution of corticosteroid receptors in the hippocampus presented similarities between the LOW-CR and the HIGH-CR rats with higher mineralocorticoid receptors (MR) and less glucocorticoid receptors (GR). Although LOW- and HIGH-CR rats displayed a similar hippocampal profile at the structural and molecular levels, only LOW-CR male rats exhibited strong deficits in extinction consolidation compared to rats with 'normative' glucocorticoid responses (INTER-CR rats), and showed higher fear response both at few days and at several weeks after trauma exposure. We next tested the causal involvement of corticosterone in the fear extinction consolidation, and found that post-extinction corticosterone treatment markedly prevented the deficits in extinction memory and attenuated fear relapse. In addition, pharmacological inhibition of corticosterone levels during extinction memory consolidation, but not during training, in the INTER-CR rats led to extinction deficits at retrieval one day later. These results indicate that blunted corticosterone levels contribute to confer major vulnerability than having a small hippocampus, and that consolidation processes following extinction are mainly affected by low corticosterone levels.It is well known that glucocorticoids play an important role in memory consolidation processes and that sleep disturbances are a diagnostic criterion of PTSD. Therefore, we investigated in greater detail the sleep architecture in undisturbed condition and during the consolidation period of the extinction phase, which is known to be supported by sleep-dependent processes. In polysomnographic recordings, we found that rats with blunted corticos

EPFL2022

No Scope for Social Modulation of Steroid Levels in a Year-Round Territorial Damselfish

Katarina Damjanovic

Both latitude and mating system have been proposed to shape relationships between steroid hormone levels and social behavior. Recently it has been postulated that species with long lasting non-seasonal territorial behavior have low androgen responsiveness. Tropical damselfishes are an ideal family to test this proposition because they show a large variety in mating systems. Here we contribute to the comparative dataset by measuring the response in steroid levels after social modulation in the banded sergeant, Abudefduf septemfasciatus, a species with non-seasonal territoriality. In highly territorial and brooding males, we found low androgen and cortisol levels that did not increase after experimental intraspecific simulated territorial intrusions (STI tests). No relationship was found between the variation in steroid hormone levels and territorial responses to naturally occurring territorial intrusions. Although steroid levels were low, male A. septemfasciatus were highly territorial both to STI challenges and to fishes that passed the territory. They often chased intruders for several meters away from the territory. This indicates that during nest defence in a non-seasonal territorial damselfish species, territorial behaviors are shown independent of variation in androgen and cortisol levels. J. Exp. Zool. 323A: 80-88, 2015. (c) 2014 Wiley Periodicals, Inc.

Wiley-Blackwell2015

Acute stress alters individual risk taking in a time-dependent manner and leads to anti-social risk

Samuel Bendahan, Lorenz Goette, Fiona Hollis, Leyla Loued-Khenissi, Maria del Carmen Sandi Perez, John Christian Thoresen

Decision-making processes can be modulated by stress, and the time elapsed from stress induction seems to be a crucial factor in determining the direction of the effects. Although current approaches consider the ﬁrst post-stress hour a uniform period, the dynamic pattern of activation of the physiological stress systems (i.e., the sympathetic nervous system and hypothalamic-pitui- tary-adrenal axis) suggests that its neurobehavioural impact might be heterogeneous. Here, we evaluate economic risk prefer- ences on the gain domain (i.e., risk aversion) at three time points following exposure to psychosocial stress (immediately after, and 20 and 45 min from onset). Using lottery games, we examine decisions at both the individual and social levels. We ﬁnd that risk aversion shows a time-dependent change across the ﬁrst post-stress hour, evolving from less risk aversion shortly after stress to more risk averse behaviour at the last testing time. When risk implied an antisocial outcome to a third party, stressed individuals showed less regard for this person in their decisions. Participants’ cortisol levels explained their behaviour in the risk, but not the antisocial, game. Our ﬁndings reveal differential stress effects in self- and other-regarding decision-making and high- light the multidimensional nature of the immediate aftermath of stress for cognition.

2017

Genetic selection for low glucocorticoid responsiveness recapitulates PTSD-related phenotypes: a behavioral, neuroimaging and sleep-physiology study

Silvia Monari

EPFL2022