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The fight-or-flight or the fight-flight-or-freeze[1] (also called hyperarousal or the acute stress response) is a physiological reaction that occurs in response to a perceived harmful event, attack, or threat to survival.[2] It was first described by Walter Bradford Cannon.[a][3] His theory states that animals react to threats with a general discharge of the sympathetic nervous system, preparing the animal for fighting or fleeing.[4] More specifically, the adrenal medulla produces a hormonal cascade that results in the secretion of catecholamines, especially norepinephrine and epinephrine.[5] The hormones estrogen, testosterone, and cortisol, as well as the neurotransmitters dopamine and serotonin, also affect how organisms react to stress.[6] The hormone osteocalcin might also play a part.[7][8]

This response is recognised as the first stage of the general adaptation syndrome that regulates stress responses among vertebrates and other organisms.[9]

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Physiology

Autonomic nervous system

The autonomic nervous system is a control system that acts largely unconsciously and regulates heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. This system is the primary mechanism in control of the fight-or-flight response and its role is mediated by two different components: the sympathetic nervous system and the parasympathetic nervous system.[10]

Sympathetic nervous system

The sympathetic nervous system originates in the spinal cord and its main function is to activate the physiological changes that occur during the fight-or-flight response. The sympathetic nervous system transfers signals from the dorsal hypothalamus, which activates the heart, increases vascular resistance, and increases blood flow, especially to the muscle, heart, and brain tissues. It activates the adrenal medulla, releasing catecholamines that amplify the sympathetic response. Additionally, this component of the autonomic nervous system utilizes and activates the release of norepinephrine in by the adrenal glands in the reaction.[11]

Parasympathetic nervous system

The parasympathetic nervous system originates in the sacral spinal cord and medulla, physically surrounding the sympathetic origin, and works in concert with the sympathetic nervous system. Its main function is to activate the "rest and digest" response and return the body to homeostasis after the fight or flight response. This system utilizes and activates the release of the neurotransmitter acetylcholine.[12]


Evolutionary perspective[edit]

An evolutionary psychology explanation is that early animals had to react to threatening stimuli quickly and did not have time to psychologically and physically prepare themselves. The fight or flight response provided them with the mechanisms to rapidly respond to threats against survival.

Examples[edit]

A typical example of the stress response is a grazing zebra. If the zebra sees a lion closing in for the kill, the stress response is activated as a means to escape its predator. The escape requires intense muscular effort, supported by all of the body's systems. The sympathetic nervous system's activation provides for these needs. A similar example involving fight is of a cat about to be attacked by a dog. The cat shows accelerated heartbeat, piloerection (hair standing on end), and pupil dilation, all signs of sympathetic arousal. Note that the zebra and cat still maintain homeostasis in all states.

In July 1992, Behavioral Ecology published experimental research conducted by biologist Lee A. Dugatkin where guppies were sorted into "bold", "ordinary", and "timid" groups based upon their reactions when confronted by a smallmouth bass (i.e. inspecting the predator, hiding, or swimming away) after which the guppies were left in a tank with the bass. After 60 hours, 40 percent of the timid guppies and 15 percent of the ordinary guppies survived while none of the bold guppies did.

References

Adamo, S. A. (2014). The Effects of Stress Hormones on Immune Function May be Vital for the Adaptive Reconfiguration of the Immune System During Fight-or-Flight Behavior. Integrative and Comparative Biology, 54(3), 419–426. https://doi.org/10.1093/icb/icu005[13]

  1. ^ Walker, Peter (2013). Complex PTSD: From Surviving to Thriving : a Guide and Map for Recovering from Childhood Trauma. ISBN 9781492871842.
  2. ^ Cannon, Walter (1932). Wisdom of the Body. United States: W.W. Norton & Company. ISBN 978-0393002058.
  3. ^ Walter Bradford Cannon (1915). Bodily changes in pain, hunger, fear, and rage. New York: Appleton-Century-Crofts. p. 211.
  4. ^ Jansen, A; Nguyen, X; Karpitsky, V; Mettenleiter, M (27 October 1995). "Central Command Neurons of the Sympathetic Nervous System: Basis of the Fight-or-Flight Response". Science Magazine. 5236 (270): 644–6. Bibcode:1995Sci...270..644J. doi:10.1126/science.270.5236.644. PMID 7570024. S2CID 38807605.
  5. ^ Walter Bradford Cannon (1915). Bodily Changes in Pain, Hunger, Fear and Rage: An Account of Recent Researches into the Function of Emotional Excitement. Appleton-Century-Crofts.
  6. ^ "Adrenaline, Cortisol, Norepinephrine: The Three Major Stress Hormones, Explained". Huffington Post. April 19, 2014. Retrieved 16 August 2014.
  7. ^ Kwon, Diana. "Fight or Flight May Be in Our Bones". Scientific American. Retrieved 2020-06-22.
  8. ^ "Bone, not adrenaline, drives fight or flight response". phys.org. Retrieved 2020-06-22.
  9. ^ Gozhenko, A; Gurkalova, I.P.; Zukow, W; Kwasnik, Z (2009). PATHOLOGY – Theory. Medical Student's Library. Radom. pp. 270–275.
  10. ^ Schmidt, A; Thews, G (1989). "Autonomic Nervous System". In Janig, W (ed.). Human Physiology (2 ed.). New York, NY: Springer-Verlag. pp. 333–370.
  11. ^ Chudler, Eric. "Neuroscience For Kids". University of Washington. Retrieved 19 April 2013.
  12. ^ Chudler, Eric. "Neuroscience For Kids". University of Washington. Retrieved 19 April 2013.
  13. ^ Adamo, S. A. (2014-09-01). "The Effects of Stress Hormones on Immune Function May be Vital for the Adaptive Reconfiguration of the Immune System During Fight-or-Flight Behavior". Integrative and Comparative Biology. 54 (3): 419–426. doi:10.1093/icb/icu005. ISSN 1540-7063.


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