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Lecture 19

PSYC 3F20 Lecture 19: PSYC 3F20 March 7th Bipolar

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Andrew Dane

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PSYC 3F20 Abnormal Psychology Section 1 March 7th, 2017.
Lecture 18
w/ = with ppl = people ex., or eg., = example
b/w = between q = question ie., = in other words
w/o = without ps = participant
Depressie Disorders ontd
Emotion Regulation: HPA Axis, Hippocampus, and Negative Feedback
Cortisol (stress hormone) released by HPA axis
Binds to receptors on hippocampus
Negative feedback from hippocampus regulates cortisol levels (like a thermostat)
HPA Axis and Depression: Another Problem with Emotion Regulation
Cortisol levels are elevated in individuals with depression (Barlow et al., 2013).
May be due to dysfunctional negative feedback function in hippocampus (broken
Post-mortem analyses of hippocampus showed that abused suicide victims had less transcription
of genes that code for cortisol receptors compared to non-suicide comparison participants
(McGowan et al., 2009).
Healthy girls whose mothers are depressed have shown reduced hippocampal volume (Chen et
al., 2010)
Chronic stress and exposure to cortisol leads to atrophy of hippocampal cells and reduced
hippocampal volume (Herbert et al., 2006).
Dexamethasone Suppression Test (see next slides)
Hippocampus, HPA Axis, and Broken Thermostat
Dexamethasone suppression test
individuals with depression and history of abuse show less suppression of cortisol release when
cortisol levels are high
Results of Heim et al. (2008): Dexamethasone Suppression Test
- depressed group w/ history of abuse show abnormal in ACTH and cortisol
- eperietal eidee of roke therostat here hippoapus is ot properl
engaging in negative feedback
Dysregulated HPA Axis and responses to threat: Emotion regulation problems (Cicchetti, 2011)
Thus, individuals with a depressive disorder may have excessive emotional and physical
reactions to perceived stressors due in part to a dysfunctional HPA axis
Can have many effects
reduced cortisol-mediated negative feedback from hippocampus to HPA axis
Increased cortisol levels may increase noradrenergic stimulation (fear system; triggers SNS) of the
amygdala (i.e., the fear system) (Wolf, 2008
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Summary of Evidence for Biological Vulnerability
Depressive Disorders
Emotional processing biased toward negative information, amplified negative emotionality,
decreased positive emotionality
fMRI evidence re: amygdala and striatum
EEG resting frontal asymmetry (right side more active) associated w/ generation of more
negative emotions
Poor emotion regulation
Difficulty dampening negative emotions
Low functional connectivity between PFC and amygdala
Dysregulated HPA axis
Twin Studies and Mood Disorders: Genetic Basis for Biological Vulnerability? (McGuffin et al.,
- twins that share 100% of genes are more similar in depression compared to fraternal
- genetic info partially why some ppl are more vulnerable to depression
Depression and the Short Serotonin Transporter allele (Caspi et al., 2011).
Carriers of the short-version of the 5-HTT gene are more sensitive to stress
Greater risk of Depression and Suicide.
Emotion processing impairments
fMRI shows that amygdala (activates fear response) is more responsive to threatening stimuli
such as angry faces
More Neuroticism (emotional reactivity); more social blushing
Emotion regulation deficits
Weaker connections between prefrontral cortex (cognitive control centre) and amygdala
associated with reduced volume of gray matter in ACC (cognitive control system)
Psychosocial Etiological Factors
Psychological factors
Behavioural theories
Reduction in positive reinforcers
Cognitive theories
Bek’s egatie ogitie triad sheas, ogitie errors
Reformulated learned helplessness theory; hopelessness theory
Ruminative response styles theory
Social factors
Stressful life events
Social support
Behavioural Theory (Lewinsohn & Gotlib, 1995)
Risk of depression increases when the experience of positive reinforcement is reduced
and there is an increase in aversive events.
Stressful life events predict initial depressive episodes (Lewinsohn et al., 1999)
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