Freeze, Flight, Fight, Fright, Faint: Adaptationist Perspectives on the Acute Stress Response Spectrum

CNS Spectrums ◽  
2004 ◽  
Vol 9 (9) ◽  
pp. 679-685 ◽  
Author(s):  
H. Stefan Bracha

ABSTRACTThis article reviews the existing evolutionary perspectives on the acute stress response habitual faintness and blood-injection-injury type-specific phobia (BIITS phobia). In this article, an alternative evolutionary perspective, based on recent advances in evolutionary psychology, is proposed. Specifically, that fear–induced faintness (eg, fainting following the sight of a syringe, blood, or following a trivial skin injury) is a distinctHomo sapiens-specific extreme-stress survival response to an inescapable threat. The article suggests that faintness evolved in response to middle paleolithic intra-group and inter-group violence (of con-specifics) rather than as a pan-mammalian defense response, as is presently assumed. Based on recent literature, freeze, flight, fight, fright, faint provides a more complete description of the human acute stress response sequence than current descriptions. Faintness, one of three primary physiological reactions involved in BIITS phobia, is extremely rare in other phobias. Since heritability estimates are higher for faintness than for fears or phobias, the author suggests that trait-faintness may be a useful complement to trait-anxiety as an endophenotype in research on the human fear circuitry. Some implications for the forthcomingDiagnostic and Statistical Manual of Mental Disorders, Fifth Editionas well as for clinical, health services, and transcriptomic research are briefly discussed.

2013 ◽  
Vol 46 (06) ◽  
Author(s):  
I Elbau ◽  
SA Kiem ◽  
A Prosser ◽  
I Eidner ◽  
M Czisch ◽  
...  

Author(s):  
Alexander S. Häusl ◽  
Lea M. Brix ◽  
Jakob Hartmann ◽  
Max L. Pöhlmann ◽  
Juan-Pablo Lopez ◽  
...  

AbstractDisturbed activation or regulation of the stress response through the hypothalamic-pituitary-adrenal (HPA) axis is a fundamental component of multiple stress-related diseases, including psychiatric, metabolic, and immune disorders. The FK506 binding protein 51 (FKBP5) is a negative regulator of the glucocorticoid receptor (GR), the main driver of HPA axis regulation, and FKBP5 polymorphisms have been repeatedly linked to stress-related disorders in humans. However, the specific role of Fkbp5 in the paraventricular nucleus of the hypothalamus (PVN) in shaping HPA axis (re)activity remains to be elucidated. We here demonstrate that the deletion of Fkbp5 in Sim1+ neurons dampens the acute stress response and increases GR sensitivity. In contrast, Fkbp5 overexpression in the PVN results in a chronic HPA axis over-activation, and a PVN-specific rescue of Fkbp5 expression in full Fkbp5 KO mice normalizes the HPA axis phenotype. Single-cell RNA sequencing revealed the cell-type-specific expression pattern of Fkbp5 in the PVN and showed that Fkbp5 expression is specifically upregulated in Crh+ neurons after stress. Finally, Crh-specific Fkbp5 overexpression alters Crh neuron activity, but only partially recapitulates the PVN-specific Fkbp5 overexpression phenotype. Together, the data establish the central and cell-type-specific importance of Fkbp5 in the PVN in shaping HPA axis regulation and the acute stress response.


2011 ◽  
Vol 132 (3) ◽  
pp. 103-109 ◽  
Author(s):  
Toshimitsu Komatsu ◽  
Lucas S. Trindade ◽  
Takuya Chiba ◽  
Hiroko Hayashi ◽  
Tomoko Henmi ◽  
...  

2003 ◽  
Vol 285 (5) ◽  
pp. R1098-R1106 ◽  
Author(s):  
Rogier D. van Anholt ◽  
Tom Spanings ◽  
William Koven ◽  
Sjoerd E. Wendelaar Bonga

The cyclooxygenase (COX) pathway converts arachidonic acid (ArA) into prostaglandins (PGs), which interact with the stress response in mammals and possibly in fish as well. Acetylsalicylic acid (ASA) is a COX inhibitor and was used to characterize the effects of PGs on the release of several hormones and the stress response of tilapia ( Oreochromis mossambicus). Plasma PGE2 was significantly reduced at 100 mg ASA/kg body wt, and both basal PGE2 and cortisol levels correlated negatively with plasma salicylate. Basal plasma 3,5,3′-triiodothyronine (T3) was reduced by ASA treatment, whereas prolactin (PRL)188 increased at 100 mg ASA/kg body wt. ASA depressed the cortisol response to the mild stress of 5 min of net confinement. As expected, glucose and lactate were elevated in the stressed control fish, but the responses were blunted by ASA treatment. Gill Na+-K+-ATPase activity was not affected by ASA. Plasma osmolarity increased after confinement in all treatments, whereas sodium only increased at the high ASA dose. This is the first time ASA has been administered to fish in vivo, and the altered hormone release and the inhibition of the acute stress response indicated the involvement of PGs in these processes.


Sign in / Sign up

Export Citation Format

Share Document