Lecture 12: Stress & Anxiety Flashcards
adaptive stress and anxiety
contribute to our survival
maladaptive stress and anxiety
can cause deterioration of the body, which, if prolonged, can lead to harmful changes in physiology
physiological changes caused by stress
the heart beats faster, blood pressure increases, and stress hormones (including cortisol) are released
stressor
something that produces stress at any time
Hans Selye definition of stress
“the non-specific response of the body to any stressor”
general adaptation syndrome
a three stage process
- the general alarm response occurs in the first 6-48 hours and is characterized by numerous physiological changes (fight/flight physiology)
- resistance (coping with stressors) occurs from about 48 hours after the stressor
- exhaustion (if stress persists) and therefore the initial stress response is evident (leads to stress as a pathological state with continuation of this phase)
Kim and Diamond three-point definition of stress
- stress requires increased irritability or excitement
- stress must also be experienced as negative (excitement can increase under both pleasurable and negative conditions)
- manageability
the reactivity hypothesis
originally proposed that physiological responses to stress, if frequent and intense, could cause physical harm
- has been criticized for failing to account for the prolonged physiological effects of stress, which often extend beyond the immediate stressful event
prolonged activation model
suggests that physiological responses to stress become harmful when they persist long after the stressor has ended, or when the body’s physiological activity is triggered by anticipation of the stressor before it occurs
- can persist during periods of worry, rumination, and anticipatory anxiety
- introduced to address the limitations of the reactivity hypothesis
perseverative cognition hypothesis
- the autonomic nervous system (ANS) recovers much more quickly from physical stressors (e.g. running up a flight of stairs) than from psychological stressors (e.g. worry or rumination)
- humans have the unique ability to mentally stimulate future events or reflect on past experiences, thereby prolonging the stress response
- this ability allows us to anticipate future stressors or dwell on past ones, which can prolong physiological responses long before or after the stressful event, a phenomenon known as perseverative cognition
physiological profile of perseverative cognition
includes decreased heart rate variability, increased blood pressure, and prolonged cortisol responsiveness (reflecting a sustained state of physiological arousal
- additionally decreased activity in the prefrontal cortex and increased activity in the amygdala
psychological profile of perseverative cognition
characterized by increased anxiety, depression, neuroticism, impaired cognitive functions such as decision making and inhibitory control
complex network of signalling systems
the central nervous system (CNS), endocrine system, and immune system all interact with the body’s response to stress
hypothalamic-pituitary-adrenal (HPA) axis
when a stressor is detected, the CNS, particularly the hypothalamus, activates the HPA axis resulting in the release of stress hormones such as cortisol
central nervous system (CNS)
serves as the control center for processing and integrating sensory information about stressors and initiating the the physiological stress response
endocrine system (including HPA axis)
releases corticotropin-releasing hormone (CHRI), which stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH)
- ACTH then stimulates the adrenal glands to secrete cortisol
immune system
also involved as cortisol affects immune functioning by regulating inflammatory responses and promoting lymphocyte maturation
- chronic stress and prolonged cortisol secretion can suppress the immune system resulting in poor immune function
the body’s stress response
begins with the detection of a stressor
- sensory pathways send information about the stressor to the CNS
- CNS processes input and initiates fight-or-flight response
- HPA axis becomes activated and the paraventricular nucleus of the hypothalamus releases CRH, stimulating the pituitary gland to release ACTH
- ACTH stimulates the adrenal glands to produce glucocorticoids including cortisol
- these hormones prepare the body to cope with the stressor by increasing energy availability, suppressing non-essential functions such as digestion and reproduction, and enhancing memory/sensory functions
acute stressors effects on the immune system
can enhance natural immunity by preparing the body to respond to immediate threats
chronic stressors effects on the immune system
suppresses both the general and specific immune systems, making the body more susceptible to disease and impairing functions such as wound healing
Marucha et al. (1998)
showed that stress during exam periods can slow wound healing compared to stress-free periods such as summer vacations
role of sympathetic nervous system (part of the CNS) in response to stress
triggers rapid physical changes (increased heart rate and blood pressure)
cortisol
the primary stress hormone produced by the HPA axis
- critical for regulating various functions during stress
- increases glucose availability, modulates immune function, and adjusts physiological properties such as suppressing reproduction and digestion
- follows a circadian rhythm
homeostasis vs allostasis
homeostasis
- refers to the maintenance of physiological balance or equilibrium in response to stressors
allostasis
- the process by which the body achieves stability through physiological or behavioral changes
when stress persists over time, the body moves from homeostasis to allostasis, where set points for balance are adjusted to meet long-term demands
allostatic load
refers to the cumulative wear and tear on the body when systems are over-activated in response to chronic stress
- prolonged activation of physiological systems due to stress can lead to pathology, which affects health by causing conditions such as weakened immune function, delayed wound healing, and chronic disease
allostatic load effects on the immune system
- acute stress boosts natural immunity by increasing neutrophils and NK cells to prepare the body for injury or infection
- chronic stress suppresses both innate and specific immunicty, making the body more susceptible to disease
effect of positive psychological factors
positive psychological factors such as social support and optimism can protect health
neurobiology of anxiety
involves several neurotransmitter systems, with a focus on gamma-aminobutyric acid (GABA), norepinephrine, and serotonin
- help regulate the activity in the brain associated with fear and anxiety
- GABA is particularly important as it plays a key role in inhibiting overactivity in the brain regions associated with anxiety
GABA
an inhibitory neurotransmitter that reduces neuronal excitability by making the cell membrane more negative (hyperpolarized)
- reduces likelihood of an action potential, effectively calming the brain and reducing anxiety
- GABA-A receptor received most attention due to it being the target of several anxiolytic drugs such as benzodiazepines
norepinephrine (adrenaline)
primarily in the locus coeruleus, and is involved in arousal and the body’s stress response
- dysregulation of the system is associated with increased anxiety
serotonin
located primarily in the amygdala and dorsal raphe nuclei, serotonin plays a role in mood regulation and emotional responses
- low serotonin levels associated with anxiety disorders
how GABA functions
reduces anxiety by transporting chloride (Cl-) ions into the cell
- hyperpolarizes the neuron, making it less likely to fire an action potential
benzodiazepines
drugs commonly used to reduce anxiety by enhancing the inhibitory effect of GABA
- act as positive allosteric modulators by binding to the benzodiazepine site on the GABA-A receptor
- allows for a greater influx of Cl- ions into the cell
barbiturates
originally developed for their sedative and hypnotic effects
- classified as CNS depressants (e.g. diethylbarbituric acid (barbital) and phenobarbital)
- can induce sleep and have anxiolytic properties at moderate doses
- mimick GABA even in the absence of GABA by increasing Cl- conductance
- highly addictive with many risks (respiratory/cardiovascular depression, coma, and death)
- rarely used
flumazenil
acts as an antagonist at the benzodiazepine binding site on the GABA-A receptor
- prevents benzodiazepines from potentiating the GABAergic effect
- GABA can still bind to its receptor, but the influx of Cl- ions is significantly less than in the presence of benzodiazepines
- used to counteract benzodiazepine overdose
inverse agonists
binds to the benzodiazepine site but has the opposite effect of benzodiazepines
- decrease the flow of Cl- ions into the cell
- depolarizes neuron, increasing the likelihood of an action potential and leading to more neuronal activity
- anxiogenic (cause anxiety by reducing the inhibitory effects of GABA
full agonists
such as benzodiazepines, fully activate the GABA-A receptor, resulting in maximum Cl- ion influx and complete inhibition of neural activity
partial agonists
do not fully activate the receptor and therefore produce a weaker response
- induce less Cl- influx and provide less inhibition
alpha-2-adrenoceptors
receptors in the locus coeruleus, which when blocked increases the release of noradrenaline and decreases the release of noradrenaline when stimulated
clonidine
an antihypertensive drug that has been used to treat panic attacks and suppress symptoms of anxiety during nicotine withdrawal
beta-adrenoceptors
postsynaptic receptors in which blockade is anxiolytic
- effects appear to be mediated by peripheral receptors
propranolol
a beta-adrenoceptor antagonist that can treat some of the symptoms of anxiety
- particularly autonomic symptoms such as sweating, tremors, and tachycardia
beta-adrenergic receptor antagonists
able to block the peripheral effects of anxiety
- do not block the conscious experience of anxiety
low serotonin with high norepinephrine
produces anxiety
enhancement vs reduction of serotonergic neurotransmission
enhancement increases anxiety, while reduction reduces anxiety
- opposite for depression (low serotonin, higher depression)
