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Lecture 11 - Affective Disorders Flashcards

1
Q

Outline statistics in depression

A

Common cold of mental illness
Most widespread
1 in 10 chance least one depressive episode
1 in 20 visits to dr
> 100 per drs list but half unrecognised
20% develop chronic depression

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2
Q

Why may patients not mention depression

A

Embarrassment
Stigma
Avoid lack sympathy

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3
Q

What are the 4 symptoms of depression

A
  1. Mood emotional
  2. Thought cognitive symptoms
  3. Motivational symptoms
  4. Somatic physical symptoms
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4
Q

Outline mood emotional symptoms of depression

A

Hopelessness
Emptiness
Loneliness

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5
Q

Outline thought cognitive symptoms of depression

A

Memory affected

Poorer decision making

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6
Q

Outline motivational symptoms of depression

A

Feelings of rewards attenuated

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7
Q

Outline somatic physical symptoms of depression

A

Manifest differently

Walking slower

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8
Q

Outline Unipolar Depression

A

Mixed anxiety and depression
Recurrent depressive = numerous
Or depressive episode single

Dysthymia persistent and mild = depressive personality

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9
Q

Outline Bipolar disorder

A

Bipolar affective disorder with manic episodes

Cyclothymia persistent instability of mood

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10
Q

Outline affective disorders and creativity

A

Link between affective disorders, bipolar and cyclothymia and creativity

Writers, poets and artists high proportion cyclothymia and major depressive disorder

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11
Q

Outline 3 different systems of brain areas involved in depression

A

Glutamate System

Dopamine system

GABA System

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12
Q

How is the Amygdala associated with depression

A

Associated anxiety

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13
Q

How is the nucleus accumbens involved in depression

A

Important motivation and reward

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14
Q

How is the pre frontal cortex involved in depression

A

Associated cognitive abilities and decision making

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15
Q

How is the hippocampus involved in depression

A

Involved in memory

Hippocampal loss with untreated depression

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16
Q

What is important for the regulation of emotion

A

Increased metabolic activity in amygdala and orbitofrontal cortex

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17
Q

Outline summary of nucleus accumbens brain change in depression

A

Decrease volume
Decrease BOLD in reward related task

Decrease expression synaptic remodelling gene RAC1

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18
Q

Outline summary of hippcampus brain change in depression

A

Decrease volume
Decrease BOLD during positive word encoding task

Decrease synapse density
Decrease glial cell density

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19
Q

Outline summary of basolateral amygdala brain change in depression

A

Decrease volume
Increase resisting state BOLD

Decrease gray matter
Decrease glial cell density

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20
Q

Outline summary of Medial Prefrontal Cortex brain change in depression

A

Decrease volume
Decrease BOLD during reversal learning task

Decrease white matter
Decrease dendritic branching
Decrease glial cell density

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21
Q

How much of depression is inherited Sullivan et al 2000

A

35-70+%

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22
Q

Outline Sullivan et al 2000 twin concordance rate for mood disorders in twins

A

Any mood disorder: MZ 60% DZ 20%

Severe depression MZ 60% DZ 30%

Depression MZ 35% DZ 15%

Bipolar MZ 80% DZ 15%

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23
Q

Outline Seligman 1975 learned helplessness experiment method

A

Dogs in apparatus able shuffle 1 side box to another
Very mild foot shock allowed them escape other side box with no shock

Some prevented from escaping for while then given opportunity to escape

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24
Q

Outline Seligman 1975 learned helplessness experiment findings

A

Instead of escaping didn’t escape learned helplessness

No previous opportunity escape - learned futile and didn’t both

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25
How do learned helplessness animals show Biological features of depression according to Seligman 1975
REM sleep alterations Loss body weight Diminished sexual activity Elevated corticosterone - stress hormone Link cognitive function to biological function
26
Outline recovery in Seligmans learned helplessness 1975 study
Recovery after 48 hours | Due to recovery of hypothalamic noradrenaline levels which is reduced in helpless animals
27
What trophic actions
Increased function and survival of cells | By chronic antidepressant treatment
28
What is the Monoamine Theory Hypothesis of depression
Depression due depletion monoamines - noradrenaline, serotonin, dopamine Originated drugs that depleted such: reserpine (motivational problems in animals)
29
Limitations on Monoamine Theory of depression
Too simplistic | Delayed action of antidepressant drugs
30
How is the Monoamine Theory of depression modified
Include down regulation of NA receptors
31
Outline the effects of Reserpine
Humans: depression Animals: sedation Catecholamines: Vesicular depletion
32
Outline the effects of Amphetamine
Humans: Stimulation Animals: Sedation Catecholamines: Release
33
Outline the effects of MAO inhibitors
Humans: Antidepressant Animals: Prevent Reserpine Catecholamines: Prevent Degradation
34
Outline the effects of Imipramine
Humans: Antidepressant Animals: Prevent Reserpine Catecholamines: Prevents Re-Uptake
35
Outline the effects of DOPA
Humans: Antidepressant Animals: Prevent Reserpine Catecholamines: Increase Precursors
36
Outline Neurochemical hypothesis of depression - Noradrenaline Hypothesis
Respiring depression due reduced levels of NA Supported by effects of antidepressants which increase NA metabolism
37
Problems of the Noradrenaline Hypothesis
Time delay of therapeutic effects of drugs | Uptake BETA receptors takes time to kick in
38
How is the Noradrenaline Hypothesis expanded
Include receptor sensitivity Increased exposure of receptor to NA Eventually sensitivity of receptor is decreased B-Receptors
39
Outline neurochemical Hypothesis of depression - Serotonin 5HT
Serotonin involved: pain sensitivity, emotionality and response negative consequences Metabolite 5HIAA (marker activity serotonin) reduces cerebral spinal fluid
40
How is the serotonin hypotheses of depression refuted
Low 5HIAA associated with aggressive hostile and impulsive behaviour Violent suicide attempts
41
What does the serotonin hypothesis tell us about individual differences of depression
Individuals with different alleles coding for serotonin transporter have different reactivity to stress
42
Outline 5HTT Gene Variation of a human
``` Repeat length polymorphism (abnormal variation genetic code) In promoter (sequence on DNA marks where transcription begins) region ```
43
Outline Biological Phenotype of a human
Altered neural stress and threat circuitry Increase HPA axis response to stress
44
Outline behavioural phenotype of a human
Intermedia phenotypes for depression and anxiety | Increased depression after stressful life events
45
Outline 5HTT Gene Variation of a monkey
Repeat length polymorphism in promotor region
46
Outline Biological phenotype of a Monkey
Altered neural stress and threat circuitry Increased HPA Axis response to stress
47
Outline behavioural phenotype of a monkey
Increased anxiety and stress reactivity after early life stress
48
Outline 5HTT Gene Variation of a Rat
Chemical mutagenesis Knockout
49
Outline Biological Phenotype of a Rat
Increased 5HT signally | Altered 5HT receptor expression and function
50
Outline behavioural phenotype of a Rat
Increased anxiety like behaviour
51
Outline 5HTT Gene Variation of a Mouse
Genetically engineered knockout or over expression
52
Outline Biological Phenotype of a Mouse Knockout
Increased 5HT signalling Altered 5HT receptor expression and function Increased amygdala dendritic spins density and PFC dendritic branching Increased HPA axis response stress
53
Outline Biological Phenotype of a Mouse Over expression
Over expression: Decreased 5HT signalling Altered 5HT
54
Outline behavioural phenotype of a Mouse Knockout
Increased anxiety like behaviour Impaired fear extinction Increased depression related behaviour after multiple stressors
55
Outline behavioural phenotype of a Mouse Over Expression
Decreased anxiety like behaviours
56
Outline Monoamine Oxidase Inhibitors to treat depression
Iproniazid 1950s Interaction certain foods - can’t have wine or cheese Initially non selective, newer selective MAO A or B Atypical depression Inhibit Monoamine enzymes net increase NT
57
Outline Tricyclics used treat depression
Inhibit re uptake of noradrenaline and serotonin Effective, cheap but dose related anticholinergic side effects limit compliance Fatal in overdose
58
Outline SSRIs to treat depression
Inhibit reuptake serotonin - block transporters reuptake increasing levels synaptic cleft Safe overdose Narrow dose range Lack sedation free anti cholinergic side effects
59
Outline Commonly used SSRIs
Prozac Hypericum St Johns Wort
60
Outline the 2 ways different antidepressant act to increase serotonin
1. Inhibit MAO enzyme which breaks down serotonin | 2. Blocking transporter Protein for serotonin reuptake
61
What are Monoamine transporters
Mechanisms controlling extracellular Monoamine dynamics reuptake Achieved through presynaptic neurons via plasma membrane transporters
62
Examples of presynaptic neurons plasma membrane transporters
Dopamine - DAT Serotonin - SERT Noradrenaline - NET
63
How do Monoamine transports though presynaptic neurons plasma membrane transporters act
Remove NTs from outside cells and recycle back into releasing or neighbouring terminals Interfere with transporter function Normal function transporters investigates using gene deletion techniques
64
Outline result of Mice lacking both SERT and DAT
No place preference for cocaine suggesting SERT involvement in cocaine effects on reward
65
What does SNRI stand for
Selective Serotonin Noradrenaline Inhibitors
66
What is an SNRI
New Act via Inhibition of re uptake of 5HT and NA Little action on muscarinic cholinergics and histaminergic receptors - drowsy side effects E.g. Venlafaxine
67
What is the main reason for stopping taking drugs
Side effects
68
How do some drugs work behaviourally by influencing affective bias Harmer et al 2009
Depressed appraise environment differently - biased towards the negative Ppts rate faces happiness slower/later when depressed Treat with Rebourtine increased their recognition of happiness
69
Outline CRF and depression
CRF = major neuropeptide mediator of stress response in CNS Expressed in Paraventricular nucleus of hypothalamus coordinates release ACTH from anterior pituitary CRF increased in CSF if depressed patients
70
Outline HPA Axis - Hypothalamic Pituitary Adrenocortical System
1. CRF release response environmental stressor (uncertainty arousal) 2. ACTH released by pituitary 3. Turn releases cortico-steroids 4. Stressor terminates negative feedback occurs shut down of HPA Axis
71
When are elevated corticosteroids good index of stress
Elevated times threat Elevated chronically at times of loss of control
72
What is the result of long term activation of HPA Axis
Long term damage Depression associated increased activity HPA Axis Enlargement adrenal gland and elevated levels cortisol
73
How do antidepressants act on the HPA Axis
Lower activity
74
How do early experiences affect the activity of HPA Axis
Early experience can bias towards later protracted activity of HPA Maternal separation
75
What is the link between arthritis and depression
Corticosteroids given for Arthritis and cause depression
76
How do reuptake inhibitors boost the HPA System
Improvement in mental state associated with normalisation of HOA activity
77
Outline Cushings Disease
Involves excessive secretion of corticosteroids commonly followed by depression
78
Flow chart of HPA Axis Response
Stress -> Hypothalamus, CRF -> Pituitary, ACTH -> Adrenals, Cortisol
79
Outline neurogenesis and depression
New neurons generation throughout life in hippocampus and olfactory bulb Rodent brain 9000 new cells per day 250,000 per month 50% become neurons
80
Outline protein BDNF neurogenesis and depression
Protein regulates synaptic plasticity and neurogenesis is brain derived neurotrophic factor - BDNF BDNF reduced in depression and following chronic stress Increased by antidepressants and exercise
81
How do we increase neurogenesis
Exercise Environmental enrichment Antidepressants
82
How do we decrease neurogenesis
Stress Sleep deprivation Age

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