Stress, anxiety and aggression Flashcards
What is stress?
Physiological reaction = caused by perception of aversive/ threatening situations
Change = physical, emotional/ psychological strain
Physiological responses help prep = ‘fight or flight’ situ.
Episodic/ continuous
Adaptive but also harmful
What is the physiology of the stress response- SAM system?
Sympathetic Adrenal Medullary system (SAM)
Threats need enhanced activity = need to mobilise energy resources.
Hypothalamus + SNS stimulate adrenal medulla (kidneys) to release the catecholamine transmitters
- epinephrine ↑ blood gluc. 4 muscles
- norepinephrine = ↑ blood pressure 4 blood flow to make movement
Norepinephrine = secreted in brain during stress
How does the HPA-axis respond to stress?
Hypothalamic-Pituitary Adrenal axis = increases glucose to decrease pain sensitivity = helps w/ the fight or flight response
Does this by:
1. Paraventricular nucleus (PVN), hypothalamus releases the peptide corticotropin- releasing hormone/factor (CRH/CRF)
- CRH stimulates anterior pituitary to release adrenocorticotropic hormone (ACTH)
- ACTH enters general circulation +
stimulates adrenal cortex to secrete
glucocorticoids (e.g. cortisol)→ ↑ glucose - CRH also secreted in brain during stress in limbic system
What is the effect of stress on the brain?
Stress can be neurotoxic (Sapolsky)
Hippocampus = involved in
learning and memory (sens. to stress)
Chronic exposure to
glucocorticoids
- destroys hippocampal neurons via
decreased glucose entry
- overstimulation of neurons = glutamate reuptake→ excessive Ca2+ influx and
toxicity
How does Diamond et al. (1999) show evidence supporting stress-induced neurotoxicity?
Rat exposed to car small + presence 4 75mins
Blood glucocorticoids ↑
Impaired primed-burst potentiation (PBP; similar to LTP, synaptic strengthening) in hippocampus (HC)
Impaired in spatial task
How does Uno et al. (1989) show evidence for stress-induced neurotoxicity?
Vervet monkey colonies in Kenya = a hierarchical society:
- Bottom rank monkeys =continuous stress bc upper rank
Results = enlarged adrenal glands
(excessive (nor)epinipherine
production) + hippocampal degeneration
What is post-traumatic stress disorder (PTSD)?
Long-lasting psychological symptoms after traumatic event (e.g. natural disaster, experience of violence) is over
Likelihood is ↑ if traumatic event = danger or violence others (assault, war)
What are the symptoms of PTSD?
Flashbacks, hypervigilance,
irritability, heightened reactions to sudden noises, detachment from social activities
Triggered by cues (e.g. helicopter
sound) related to traumatic event (e.g. war)
Learned, conditioned response
How does PTSD cause the brain to change?
↓ size of hippocampus in combat
veterans + police officers w/ PTSD (Lindauer et al., 2005)
Possible risk factor for PTSD = Monozygotic twin study from
Vietnam war (Gilbertson et al. 2002)
- Smaller hippocampus w/ PTSD
- Possible reason = hippocampus role in distinguishing contexts
- PTSD = Inability to detect threatening vs safe contexts, ‘threat
generalisation’
What areas of the brain is linked to emotional responses?
Prefrontal cortex (PFC) = impulse control + thought to inhibit amygdala - involved in emotional expression (Rauch et al. 2006)
How does PTSD alter the activity of the amygdala?
PTSD assoc. w/ ↑ amygdala + ↓ mPFC activation than controls to fearful face (opposite for happy face) Shin et al. (2005)
PTSD-related changes = show excessive emotional response + ↓ inhibitory control
What are treatments to PTSD?
- Psychotherapy = assoc. w/ ↓ amygdala activity + ↑ PFC (prefrontal cortex) + hippocampal activity (Thomas et al., 2014)
- SSRIs = ↑ hippocampal volume (Bossini et al., 2007)
- Exposure therapy = learned assoc. (cue-stress) + induces condition fear response. Extinction learning reduces cue responding = show cue w/out assoc. H/E extinction didn’t last.
Is exposure therapy effective?
Powers et al (2010) = highly yes bc borrows principle from extinction learning
Repeated cue presentation over weeks in safe therapy context = ↓ response to cue (learning of non-threat, ↓ of fear/anxiety)
What is anxiety?
Apprehensive, uneasiness/ nervousness over impending or anticipated ill.
Normal = unlike stress, doesn’t have an identifiable trigger but some similar responses = faster heartbeat + breathing
What is anxiety disorder?
More intense than common anxiety
Fear/anxiety = inappropriate for circumstance, more than a temp. worry.
Bc cumulative effects of stress contributes to depressive + substance abuse disorders.
Women more likely than men to experience.
May types = panic disorder, agoraphobia, GAD, social anxiety disorder have a known biological component
What is panic disorder?
Episodic attacks of acute (seconds to
hours) anxiety, terror
Symps = hyperventilation (low
CO2), irregular heart-beat, dizziness,
faintness, fear of losing control and
dying
What is agoraphobia?
Intense fear or anxiety abt leaving home, being in open/public areas, being in lines/crowds, etc.
Coping through avoidance bc disproportionate fear/ anxiety
Staying home for years, fear of panic attack
What is GAD?
Excessive, uncontrollable worrying + anxiety from a wide range of
situations + diff. controlling these symptoms
Sense of impending danger, sweating, trembling, difficulty concentrating
More prevalent in women than men
What is social anxiety disorder?
Persistent, excessive fear of being exposed to the scrutiny of others (e.g.
public speaking, group conversations), appearing incompetent
Sweating, blushing
Equally likely in men and women
Is there a cultural component in panic disorder, GAD and social anxiety disorder?
Yes - more prevalent in European descent people
Asian, African, and Latin American Countries have lower rates than e.g. USA (American Psychiatric Association)
How does the brain change because of anxiety disorders?
Using PET + fMRI = showed changes in the prefrontal cortex, anterior
cingulate cortex, + amygdala.
↑ Increased amygdala activity during panic attack (Pfleiderer et al., 2007) + in response to presentations of faces with anger, disgust, and fear in social
anxiety disorder (Phan et al., 2005)
- Activation correlates w/ symps.
Adolescents w/ GAD exhibit ↑ amygdala + ↓ ventrolateral prefrontal cortex (PFC) activation (Monk et al., 2008)
Lack of suppression of amygdala activation via ventromedial prefrontal cortex (vmPFC)
- vmPFC = role in inhibition of fear
How are anxiety treated using GABAergic drugs ?
Benzodiazepines (BDZ) ↓ anxiety
+ anxiety-like bhvrs in animals.
- Less time spent on the ‘anxiogenic’
open arm on the elevated plus maze
(EPM).
Binds to the inhibitory GABAA receptor
as ‘agonist’.
- ↑ Cl- influx
- hyperpolarisation
What do treatments for anxiety do?
BDZ = ↓ amygdala activity when looking @ emotional faces (Paulus et al., 2005)
Flumazenil (antagonist) = disinhibits action at GABAa receptor + produces panic in panic disorder Ps.
- Treats BDZ overdose, acute alcohol intoxication.
Abuse potential = withdrawal + sedation
Better compounds = needed w/ ↓ side effects
How can you treat anxiety by increasing neurosteroid synthesis?
Neuroactive steroids ‘neurosteroids’ (e.g.allpregnaolone) synthesized in periphery + CNS.
They bind to GABAa receptors = ↑ its activity - ↑ chloride coming in + ↑ inhibition
During anxiety attacks, neurosteroid
synthesis is suppressed = GABAA receptor function suppressed
To stop this = XBD173 enhances neurosteroid synthesis + ↓ panic w/out the sedation + withdrawal symptoms from benzodiazepines (Nothdufter et al., 2011)
