04. Stress, anxiety, and aggression Flashcards
(27 cards)
What is stress?
- Change that causes physical, emotional, or psychological strain.
What is the Sympathetic-Adrenal-Medullary (SAM) system?
The stress (sympathetic) response
Hypothalamus stimulates the adrenal medulla to release adrenaline/epinephrine (↑blood glucose) and noradrenaline/norepinephrine (↑ blood pressure)
What type of molecules are adrenaline and noradrenaline?
Catecholamines
How does the HPA (Hypothalamic-Pituitary-Adrenal) axis cause the stress response?
Hypothalamus (paraventricular nucleus / PVN) -> pituitary gland (anterior pituitary) -> adrenal cortex
CRH -> ACTH -> Glucocorticoids
- Hypothalamus (spec. paraventricular nucleus or PVN) releases corticotropin-releasing hormone (CRH)
- CRH stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH)
- ACTH enters general circulation and stimulates the adrenal cortex to secrete glucocorticoids (e.g. cortisol) → increases glucose & decreases pain sensitivity
What effect does stress have on the brain?
Stress is toxic
Too much glucocorticoids damages the hippocampus (learning & memory centre)
Rat study showing that stress is toxic
(Diamond et al., 1999)
- rats exposed to the smell and presence of cats
- increased levels of blood glucocorticoids
- impaired primed-burst potentiation in hippocampus
- impaired performance in spatial awareness tasks
What is Post-traumatic stress disorder (PTSD)
- a conditioned response to fear-related stimuli
- responses: flashbacks, hypervigilance, irritability, reactions to sudden noises
PTSD and Pavlov
- Neutral stimulus (helicopter) paired with a salient stimulus/experience (stress from war=US)
- over time, the conditioned stimulus (helicopter) evokes a conditioned fear response
PTSD and brain changes
- Reduced size of hippocampus in PTSD (Bremner et al. 1995; Gurvits et al., 1996; Lindauer et al., 2005)
Are there risk factors for PTSD?
- possibly a smaller hippocampus!
- monozygotic twin study from Vietnam war
- Smaller hippocampus -> less ability to distinguish threats -> PTSD
(Gilbertson et al. 2002)
How do the amygdala and prefrontal cortex (PFC) behave in PTSD?
- PFC is involved in impulse control so normally inhibits the amygdala (Rauch et al. 2006)
- PTSD linked to ↑amygdala and ↓PFC responses to fearful faces (Shin et al. 2005)
- opposite for happy face
How do we treat PTSD?
- Psychotherapy
- ↓amygdala activity, ↑PFC & ↑hippocampus activity (Thomaes et al., 2014)
- Antidepressants (SSRIs)
- Exposure therapy (undoing Pavlovian conditioning - extinction training)
Exposure therapy procedure
- in extinction training, the cue is repeatedly presented without the association, causing extinction of the association
- highly effective (Powers et al., 2010)
What is anxiety?
- normal (unlike stress)
- only concerning when abnormally high
What are anxiety disorders
- intense fear, inappropriate for situation
- likely due to stress
- more common in women
What are panic disorders
- episodic panic attacks
- symptoms: hyperventilation, irregular heart-beat, dizziness, faintness, fear of death & lack of control
- cultural influence: USA rates higher than Asia, Africa and Latin America
Brain changes and anxiety/panic disorders
PETs and fMRIs show:
- increased amygdala activity during panic attack (Pfleiderer et al., 2007)
- increased amygdala activity when presented with negative faces (anger, fear, disgust) (Phan et al., 2005)
- GAD adolescents have increased amygdala and decreased PFC activity (Monk et al., 2008)
- activity correlates with symptoms
Treatments for anxiety
GABAergic drugs (benzodiazepines/BDZs)
- Causes CNS depression, withdrawal & sedation
- Can be abused
- Can cause an anxiolytic overdose
Alcohol
- Not an official treatment (self-medication)
Flumazenil
- Has the opposite effect of BDZ and alcohol
- Disinhibits GABAA & causes panic attacks
- ∴ treatment for BDZ/alcohol overdose
Evidence for GABAergic drugs in reducing anxiety
- animals taking them spend more time in anxiety-inducing situations (elevated & exposed areas on the “elevated plus maze” (EPM))
- reduced amygdala activity looking at negative faces (Paulus et al., 2005)
Why do GABAergic drugs work?
- they increase inhibition by binding to inhibitory GABAA receptors
What are the other treatments for anxiety disorders?
Allopregnanolone
- Increases neurosteroid synthesis (opposite happens in panic attack)
- Reduces panic (Nothdufter et al., 2011)
Fluvoxamine
- SSRI
- Reduces panic attacks (Asnis et al., 2001)
D-cycloserine (DCS)
- Reduces panic attacks (Ressler et al., 2004)
- Facilitates extinction of conditioned fear in animals (Walker et al. 2002)
SSRIs and DCS work alongside therapy, by facilitating learning!
What is Aggression?
Natural urge to enable survival
Behaviours: threat, defense, submission
Where is aggression controlled?
- Brain stem
- Stimulation of periaqueductal grey (PAG) area causes aggressive attack and predation in cats (Gregg and Siegel 2001)
- Medial Hypothalamus→Dorsal PAG: defensive rage
- Lateral Hypothamaus→Ventral PAG: Predatory attack
What reduces aggression? (neurotransmitter)
- Serotonin
- It inhibits both aggression and risk taking
- Either destruction of serotonergic axons (Vergnes et al., 1988) or reducing serotonin synthesis increases aggression (Mosienko et al. 2012)
- Monkeys low in serotonin show greater risk-taking and more fights (Howell et al., 2017)
- Therefore SSRIs (fluoxetine) can reduce aggression
