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Lecture 10

Lecture 10 notes - WORD FOR WORD what the prof says!

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University of Toronto Scarborough
Rutsuko Ito

NROC61 – Lecture 10 - Stress and Arousal **see the handout AND textbook** There are 2 forms of stresses, 1.Acute and 2.Chronic There are several physiological responses to stress: -Short term response (Alarm phase) -Chronic response (Resistance phase) -Coping Response -Exhaustion (which can eventually lead to death) There is a strong link between stress and illness which we will talk about. We will also talk about PTSD. What is Stress? Your body’s response to any change/event that either disrupts, or threatens to disrupt homeostasis to an unusual degree. Two Types of Stressors 1. Acute stressors: extreme heat/cold; blood volume depletion by heavy bleeding, dehydration; hypoglycaemia; pain; surgical procedures; toxins from a bacterial infection; severe exercise; sleep deprivation; stress that causes a fear reaction -Something that lasts a very short period of time 2. Chronic stressors: Chronic pain, chronic infection; housing problems, marital problems, financial worries, difficulties at work, commuting etc. -Longer-term stress Acute Stressor Stress response system is the body’s natural, adaptive survival system fight or flight response Eg: Consider a gazelle running for its life from a lioness across the Serengeti plains – its stress response system is in full action to divert energy away from storage for use by the muscles, inhibiting non-essential functions such as digestion/reproduction. -When a gazelle is running from a lioness, its system is in full throttle to divert energy away from any non-intentional functions to intentional functionsthat are needed to run (like muscles) and anything that would help the animal be in a state of alertness and running away from the predator. The important thing is that this is a very selective diversion of energy and blood supply from non-relevant functions to organs that really need the blood supply in order to respond to the stressful limit. This is called the flight or fight response and is associated with high arousal. It is an adaptive natural response to stress. Once the stressor has gone, the gazelle’s body returns to its baseline state. -Homeostasis would be re-established. When the stressor is gone you are back to normal. Stress can be good! Nerves/stress before an important job interview, presentation or exam will increase vigilance and attention and improve performance. Adrenaline rush before a sporting event. -A little of stress can be good for you. Think about an exam situation where you are very stressed before and during the exam but actually the stressor can create an adrenaline rush which increases alertness, attention, vigilance and improve overall performance. However, if you have more chronic forms of stress (psychosocial behaviour), The body can tip into a state that is out of control. Chronic Stressors Humans and primates experience forms of stress that are more chronic and psychosocial in nature. This can tip your stress response system out of balance which can be very dangerous. Chronic stressors have the potential to tip the stress response system out of control. Robert Sapolsky -Studies the effect of stress on baboons and humans -monitors baboons behaviour in a pack in South Africa -comments that baboons do not spend most of their time running away from predators but they stress each other out because of their hierarchical group. So the biggest stress for them is their social relationships (similar to humans). •  Study of wild African baboons across 30 years have given insights into factors that make us susceptible to stress-related illnesses. •  Low-ranking male baboons and ‘loner’ females have highest levels of cortisol. -Social interactions are important in inducing stress and helping to cope with stress. ‘They (baboons) are just like us: They're not getting done in by predators and famines, they're getting done in by each other’ Robert Sapolsky, 2007 Chronic Life Stressors -Most of the chronic life stressors are social in nature which shows that social relationships are very important to us. -be mindful of how you manage and respond to stress Physiological Response to Stressors -What happens in the body in response to stress? Hans Selye(1950’s) - Slow Adaptive Response involving Cortisol release -proposed that cortosol release is the slow adaptive response to stresses Walter Cannon (1920’s) – Fast response involving adrenaline/noradrenaline release for ‘fight or flight responses’. -proposed that the stress response is a lot faster and involves adrenaline/noradrenaline Two different theories but we know now that both are true. Adrenaline/Cortisol Response Hypothetical adrenaline and cortisol responses to acute/chronic stressors -Initially in the fight or flight phase, you would see a release of adrenaline in response to an acute stressor. Then you see a slower activation of the cortisol response even when the stressor has gone. -The important thing to note here is: What happens when there are repeated stressors? This is NOT CHRONIC! (chronic would be one straight line). For repeated stressors, there would be the same increase of adrenaline levels and leveling out after the stressor is removed. BUT actually if you look at the cortisol response, because it is a long lasting response throughout, you would see that with repeated exposure to stressors, the cortisol level never really come down back to baseline after each stressful event. So you can end up having elevated cortisol levels continuously in your blood stream. Selye’s General Adaptation Syndrome -Selye came up with a model of stress response. He divided stress response into 3 phases: 1. Alarm phase (flight or fight), 2. The Resistance Phase, and 3. The Exhaustion Phase. Alarm: the body first begins to organize physiological responses (similar to fight-or-flight responses) to threat (stress) Resistance: Stress-activated responses continue, serves to stabilize the body’s adaptations to stress coping responses (there may be neuronal and behavioural coping responses in order to counteract the effects of stress) Exhaustion: The body has depleted its reserves and can no longer maintain responses to the stressors (where you crash – this is dangerous) SHORT –TERM STRESS RESPONSE Alarm phase (Fight or Flight) -This phase is immediate, but very short lived. – you can think of this phase as an arousal phase of a flight-or-fight phase. -‘Counter homeostatic’ – the body is ready to counteract so it is like a feed-forward mechanism. - Aims to mobilise body’s resources (especially if you have glucose) for immediate physical activity. (Like the gazelle running for its life, all the resources need to go into pumping blood around the body to supply energy to the muscles). The hypothalamus coordinates the activation of: (HYPOTHALAMUS IS VERY IMPORTANT) -Respiratory system (increased rate, depth) -Cardiovascular system (increased cardiac output) -Adrenal medulla -Sympathetic nervous sytem Through direct neural connections. -The adrenal medulla activation is one of the key components in very early stress response. 26:43 Adrenal Medulla Activation Adrenal gland is divided into the cortex and the medulla. These areas have different functions and release different substances. Adrenal medullary chromaffin cells have massive stores of catecholamine (adrenaline>noradrenaline).  epinephrine or norepinephrine -there is more adrenaline than noradrenaline being stored in these cells Noradrenaline and adrenaline release is triggered by stress-induces stimulation of preganglionic sympathetic (ACh) nerves (released into the adrenal medulla). Adrenaline/noradrenaline release Hypoxic stress causes rapid massive increase in adrenaline and noradrenalin. - In this experiment they induced hypoxic stress in rats. Hypoxic stress is oxygen deprevation (physical stress) which increases massive amounts of adrenaline and noradrenalin in the blood. Note: - The very rapid increase (rapid release) and the very rapid decrease (adrenaline half-life 10-20 sec) - More adrenaline than noradrenalin is secreted (more adrenaline is stored in the chromaffin cells than noradrenaline). - An acute stress depletes only a small fraction of the stored catecholamine in the chromaffin cells. – with acute stress the chromaffin cells releases only a small amount of noradrenalin and adrenaline so with chronic stress, there would be even more release of adrenalin and nor adrenaline in the chromaffin cells but eventually there will be depletion. Depletion of noradrenaline and adrenaline encourages the increase of sympathetic activity (increase circulation to muscles, circulation to the adrenals, heart, brain.) Physiological Response The secretion of adrenaline and noradrenaliine from the adrenal medulla, combined with increased sympathetic activity: - Increases circulation to muscles, adrenals, heart and brain (via vasodilation) while decreasing circulation to skin, mesentery (via vasoconstriction). o So there is vasodilation but also vasoconstriction to areas of the body which don’t really need the immediate resources (through the blood supply) such as skin and gut system. - Increases energy substrates-promoting catabolism (lipolysis and glycogenolysis) while sparing glucose for CNS. o Adrenaline and noradrenalin also encourage the increased availability of energy substrate. So catabolism is encouraged by lipolysis and glycogenolysis (So breaking down of fatty acids and proteins is encouraged) and we need readily available glucose so as a result of increased circulation to the mesentery, we would have decreased gastrointestinal motility and secreation. - Decreases GI motility and secretion Noradrenaline release in CNS - The sympathetic nervous system activation also leads to the release of noradrenaline from a widely distributed network of central synapses. - These NA pathways originate in the Locus Ceruleus and Reticular Formation. - We know that noradrenalin cannot just release peripherally but also centrally. Nor adrenaline has a very distributed wide network within the CNS. - It enervates all the areas listed below except for the Locus Ceruleus and Reticular formation from which it arises. Noradrenalin - Noradrenalin (is a neurotransmitter in the CNS which) is implicated in arousal, vigilance and selective attention. -> noradrenaline is very important for some of these cognitive functions - Single cell recordings in the LC (cell bodies) show that noradrenalin cells are most responsive to o Intensive properties of stimuli such as brightness o Salient stimuli such as novelty, preferred food and tail-pinch, noxious stimuli - Activation of noradrenalin system in CNS mediates some of the positive effects of the short term stress response upon cognition! - The activation of the noradrenalin system aids in the improved effects in performance and attention as a result of acute stress. (Remember when she said exam stress can be good? The beneficial effects on cognition are mediated by noradrenalin.) RESISTANCE (COPING) PHASE Resistance Phase Reaction - If stress is more long-lasting (only then do we have the activation of the HPA axis) o Prolonged effects of the acute (sympathetic) response o Rapid activation of the hypothalamo-pituitary-adrenal (HPA) axis o This phase is a homeostatic response (to stresses). - (As well as all the other effects of sympathetic activation we had previously described) Sympathetic activation (also) stimulates the kidney to secrete rennin angiotensin II to cause: o Thirst o Aldosterone secretion o Na reabsorption> water retention > maintains high BP and counteracts fluid loss o (basically doing all these things to save resources in order to maintain a high blood pressure and increased blood supply to important muscles for sympathetic activity). HPA axis activation - KNOW THIS IN DETAIL!!! (including full names) -the ultimate aim of the HPA axis activation is the release of glucocorticoids from the adrenal cortex. The presence of glucocorticoids then acts to negatively feedback (or inhibit) further release through hippocampal activation or at different stages of the HPA axis. Negative feedback control of glucocorticoid (corticosterone) secretion. - Parvocellular neurons in the paraventricular nucleus (PVN) of the hypothalamus secrete corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) into the portal vein. - Receptors on pituitary corticotroph cells in the anterior pituitary gland are activated by CRH and AVP release of adrenocorticotropic hormone (ACTH). - ACTH release of corticosteroid hormones from the adrenal cortex such as glucocorticoid, cortisol (corticosteroid in rats). - Glucocorticoids inhibit further release of ACTH by negative feedback, and also inhibit CRH productions in PVN through activation of hippocampus (HPC) corticosteroid receptors. -First there is a stressor. Then somehow parvocellular neurons become activated (not clear how exactly but there are factors such as circadian and metabolic information that leads into the PVN that seems to trigger the HPA response). The activation of PVN neurons leads to the secretion of CRH and vasopressin into the portal vein. Once released into the portal vein, the hormones travel down to the anterior pituitary gland where it activates the release of ACTH. ACTH then acts on the adrenal cortex to release corticosteroid hormones. -Note: cortisol and corticosteroids are the same only cortisol is the terminology used for human corticoids while corticosteroids is the terminology used in relation to rats. -The release of glucocorticoids from the adrenal cortex may have a negative effect on different stations of this pathway either through PVN or through the inhibition of ACTH release and also the reactivation of corticosteroid receptors into the hippocampus. So, the hippocampus has a negative feedback effect upon PVN. Limbic Regulation of HPA Axis -“Push-Pull” regulation – amygdala activation stimulates the HPA system and the stress response. Hippocampal activation, on the other hand, suppresses the HPA system. -In the more systemic picture of HPA axis regulation, we can see that the hippocampus is an important regulator of the HPA axis. The amygdala is also a very big player for regulating the HPA axis so the activation of the hippocampal corticosteroid receptors in the hippocampus leads to inhibition of the HPA axis activity. The activation of the corticosteroids of the amygdala have the opposite effect actually stimulating the HPA axis. This is called the “Push-Pull” regulation of the HPA axis between the amygdala and the hippocampus. This results in the regulation of cortisol release. Actions of Cortisol - What’s so important about cortisol? Half-life of cortisol (in humans) is ~90min – stays much longer in blood than adrenaline (it is a very slow acting, long lasting response). Here are a wide range of actions of cortisol that includes basically the same thing as sympathetic activation which is to encourage the availability of glucose by breaking down amino acids, proteins and fatty acids. Cortisol will also prevent increased capillary permeability (perhaps to maintain solutes in the blood stream). It will also try to maintain the contractility of the cardiac muscle. Cortisol can also inhibit the immune response and by doing that it can reduce inflammation and prevent the inflammation or immune response from becoming disruptive rather than protective. Information can become disruptive so cortisol tries to contain that. - Accelerate lipid and protein catabolism in liver and peripheral tissues; - Accelerate gluconeogenesis in liver; - Increase the sensitivity of blood vessels to vasoconstrictors; - Prevent increased capillary permeability; - Maintain the contractility of cardiac muscle; - Reduce inflammation – prevent it from becoming disruptive rather than protective; - Inhibit the immune response – by an action which damages lymphocytes. Stress and Cognition In the short term, the stress response can enhance cognition -In the short term, cortisol and adrenaline/noradrenalin could directly alter or enhance learning. - Systemic administration of corticosterone, adrenaline and noradrenaline after learning has long been reported to improve retention in rodents (McGaugh group)  action on memory consolidation. - These effects are blocked by lesions of the amygdala (Cahill and McGaugh 1991) and post-training infusion of β-adrenergic receptor antagonists (Liang et al 1986). - Also reports of enhancement of HPC-dependent learning (water maze, working memory, etc). - The McGaugh group looked specifically into the effect of stress response and the neurotransmitter releases associated with stress response on measures of learning. They found that usually if you were to administer cortisol, adrenaline or noradrenalin, AFTER learning episodes, you can actually increase or enhance memory consolidation for that particular learning. They also found that those enhanced effects are blocked by lesions in the amygdala or post-training infusion of the β-adrenergic receptor antagonists. This means that the amygdala and the noradrenalin mechanisms within the amygdala seem to be mediating some of these enhanced effects produced by cortisol and adrenaline and noradrenalin. There have also been reports of enhanced hippocampal-dependent learning despite the fact that the hippocampus is used to suppress the HPA axis, if you were to actually increase cortisol levels in the hippocampus, it seems that spatial working memory is enhanced. -The key is that short term exposure to stress or short term stress response can enhance certain types of learning. -At this stage we are not talking about ACUTE stress but SHORT TERM stress. Coping Responses - Physiological stress response is a form of “coping response” evolved to counter physical stressors. - However, high levels of stress responses (especially increased sympathetic activity) can themselves become stressors. - Thus, in humans one can’t treat stress by activating the HPA axis! - There are other behavioural coping responses that we may resort to. The Physiological stress response at this stage can be considered a sort of coping response or homeostatic mechanism which evolved to counter physical stressors on the body If you think about the HPA axis activation, high levels of cortisol, adrenaline and noradrenalin that get released into the system can themselves become stresses to the body while in a positive feedback loop. So having these kinds of physiological responses is not always beneficial or adaptive to the organism and certainly you cannot try to treat this by trying to activate the HPA axis by release more cortisol, adrenaline or noradrenalin. So we might resort to other behavioural coping responses in order to counter the stress response or stressors effect. Importance of Coping Response - In rats, availability of an avoidance contingency protects against gastric ulceration. In this experiment, it illustrates that the availability of an avoidance contingency or an escape mechanisms really protects against gastric ulceration that can happen with stress exposure. We have 3 groups of animals: There is a control group that is put into a mesh cage but does not receive any shock. There is the Yoked group where the rat will receive shock but there will be no escape so it will be contained within the cage. Finally, the Master group which will receive a shock (like the Yoked group) but they will be able to escape. They measured the total length of gastric lesions in the rats and found: in the control group, the gastric ulceration was quite negligible. In the Yoked group (where they had no availability of escape, they had the huge (length) gastric lesions. This shows that being able to be in control or having control over your stressor is a very important aspect of coping with stress. Other Coping Responses - Availability of another animal elicits a shock-induced fighting response. - Interestingly, a very similar effect of stressing is the availability of another animal in the cage that the shocked animal can fight with or attack, also acts as a coping response for the shock administration or stress exposure. - Initiation of consummatory responses to mild tail pinch stimulation in rats. - Also, if a
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