From Wikipedia, the free encyclopedia
Jump to: navigation, search

Physiological stress represents a wide range of physical responses that occur as a direct effect of a stressor causing an upset in the homeostasis of the body. Upon immediate disruption of either psychological or physical equilibrium the body responds by stimulating the nervous, endocrine, and immune systems. The reaction of these systems causes a number of physical changes that have both short and long term effects on the body.

Nervous System[edit]

Peripheral Nervous System (PNS)[edit]

The Peripheral Nervous System (PNS) consists of two subsystems: the sensory-somatic nervous system and the autonomic nervous system. When a physical stressor acts upon the body the sensory-somatic nervous system is triggered through stimulation of the body's sensory nerves. The signal acts as a nerve impulse and travels through the body in a process of electical cell-to-cell communication until it reaches the automatic nervous system. Activation of the automatic nervous system immediately triggers a series of involuntary chemical reactions throughout the body. Preganglionic neurons release the neurotransmitter acetylcholine(ACh). This stimulates postganglionic neurons which release noradrenaline. The noradrenaline flows directly into the bloodstream ensuring that all cells in the body's nervous and endocrine systems have been activated even in areas the ganclionic neurons are unable to reach.

Central Nervous System (CNS)[edit]

The Central Nervous System (CNS) is made up of the brain and the spinal cord. The brain is equipped to process stress in three main areas: the amygdala, the hypocampus, and the prefrontal cortex. Each of these areas is densely packed with stress corticosteroid receptors which process the intensity of physical and psychological stressors acting upon the body through a process of hormone reception. The Mineralocorticoid Receptors (MR) make up the majority of stress corticosteroid receptors and have an extremely high affinity for cortisol. This means that they are atleast partially stimulated at all times and therefore are entirely activated almost immediately when a true stressor is sensed to be disrupting the homeostasis of the body. The second type of receptor, Glucocorticoid Receptors (GR), have a low affinity for cortisol and only begin to become activated as the sensation of stress reaches its peak intensity on the brain.

Stress dramatically reduces the ability of the Blood Brain Barrier (BBB) to block the transfer of chemicals including hormones from entering the brain from the bloodstream. Therefore when corticosteroids are released into the bloodstream – they are immediately able to penetrate the brain and bind to first the MR and then the GR. As the GR begin to become activated, neurons in the amygdala, hypocampus, and prefrontal cortex become over stimulated. This stimulation of the neurons triggers a fight-or-flight response which allows the brain to quickly process information and therefore deal with life threatening situations.

If the stress response continues and becomes chromic, the hyperactivity of the neurons begins to physically change the brain and can have severe damaging effects on one's mental health. As the neurons begin to become stimulated, calcium is released through channels in their cell membranes. Although initially this allows the cells chemical signals to continue to fire allowing nerve cells to remain stimulated, if this continues the cells will become overloaded with calcium and become over excited leading to over-firing of neuron signals. The over-firing of the neurons is seen to the brain as a dangerous malfunction; therefore, triggering the cells to shut down to avoid death due to over stimulation.

Decline in both neuroplasticity and Long Term Potentiation (LTP) has been observed in humans after experiencing levels of high continual stress. To maintain homeostasis the brain is continuously forming new neural connections, reorganizing its neural pathways, and working to fix damages caused by injury and disease. This keeps the brain vital and able to perform cognitive complex thinking. When the brain receives a distress signal it immediately begins to go into overdrive. Neural pathways begin to fire and rewire at hyper-speed to help the brain understand how to handle the task at hand. Often, the brain becomes so intently focused on this one task that it is unable to comprehend, learn, or cognitively understand any other sensory information that is being thrown at it during this time. This over stimulation in specific areas and extreme lack of use in others causes several physiological changes in the brain to take place which overall reduce or even destroy the neuroplasticity of the brain. Dendritic spines found of the dendrite of neurons begin to disappear and many dendrites become shorter and even less complex in structure. Glia cells begin to atrophy and neurogenesis often ceases completely. Without neuroplasticity, the brain loses the ability to form new connections and process new sensory information. Connections between neurons become so weak that it becomes nearly impossible for the brain to effectively encode long term memories; therefore, the LTP of the hippocampus declines dramatically.

Endocrine System[edit]

When a stressor acts upon the body, the endocrine system is triggered by the release of the neurotransmitter, noradreniline, by the automatic nervous system. Noradreniline stimulates the Hypothalamo-Pituitary-Adrenal (HPA) axis which processed the information about the stressor in thehypothalamus. This quickly signals the pituitary gland and finally triggers the adrenal cortex. The adrenal cortex responds by signaling the release of the corticosteroids cortisol and corticotropin releasing hormone (CRH) directly into the bloodstream.

Immune System[edit]

The most important aspect of the immune system are T-cells found in the form of T-helper and T-suppressor cells. Cortisol, once released into the bloodstream, immediately begins to cause division of T-Suppressor cells. This rapid cell division increased the number of T-Supressor cells while at the same time suppressing T-helper cells and therefore reducing immune protection.