Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuroscience > Lecture 11 - Affective Disorders > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why may patients not mention depression

A

Embarrassment
Stigma
Avoid lack sympathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 4 symptoms of depression

A
  1. Mood emotional
  2. Thought cognitive symptoms
  3. Motivational symptoms
  4. Somatic physical symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Outline mood emotional symptoms of depression

A

Hopelessness
Emptiness
Loneliness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Outline thought cognitive symptoms of depression

A

Memory affected

Poorer decision making

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Outline motivational symptoms of depression

A

Feelings of rewards attenuated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Outline somatic physical symptoms of depression

A

Manifest differently

Walking slower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Outline Unipolar Depression

A

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

Dysthymia persistent and mild = depressive personality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outline Bipolar disorder

A

Bipolar affective disorder with manic episodes

Cyclothymia persistent instability of mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Outline 3 different systems of brain areas involved in depression

A

Glutamate System

Dopamine system

GABA System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is the Amygdala associated with depression

A

Associated anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is the nucleus accumbens involved in depression

A

Important motivation and reward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is the pre frontal cortex involved in depression

A

Associated cognitive abilities and decision making

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is the hippocampus involved in depression

A

Involved in memory

Hippocampal loss with untreated depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is important for the regulation of emotion

A

Increased metabolic activity in amygdala and orbitofrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How much of depression is inherited Sullivan et al 2000

A

35-70+%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do learned helplessness animals show Biological features of depression according to Seligman 1975

A

REM sleep alterations
Loss body weight
Diminished sexual activity
Elevated corticosterone - stress hormone

Link cognitive function to biological function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Outline recovery in Seligmans learned helplessness 1975 study

A

Recovery after 48 hours

Due to recovery of hypothalamic noradrenaline levels which is reduced in helpless animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What trophic actions

A

Increased function and survival of cells

By chronic antidepressant treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the Monoamine Theory Hypothesis of depression

A

Depression due depletion monoamines - noradrenaline, serotonin, dopamine

Originated drugs that depleted such: reserpine (motivational problems in animals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Limitations on Monoamine Theory of depression

A

Too simplistic

Delayed action of antidepressant drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is the Monoamine Theory of depression modified

A

Include down regulation of NA receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Outline the effects of Reserpine

A

Humans: depression

Animals: sedation

Catecholamines: Vesicular depletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Outline the effects of Amphetamine

A

Humans: Stimulation

Animals: Sedation

Catecholamines: Release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Outline the effects of MAO inhibitors

A

Humans: Antidepressant

Animals: Prevent Reserpine

Catecholamines: Prevent Degradation

34
Q

Outline the effects of Imipramine

A

Humans: Antidepressant

Animals: Prevent Reserpine

Catecholamines: Prevents Re-Uptake

35
Q

Outline the effects of DOPA

A

Humans: Antidepressant

Animals: Prevent Reserpine

Catecholamines: Increase Precursors

36
Q

Outline Neurochemical hypothesis of depression - Noradrenaline Hypothesis

A

Respiring depression due reduced levels of NA

Supported by effects of antidepressants which increase NA metabolism

37
Q

Problems of the Noradrenaline Hypothesis

A

Time delay of therapeutic effects of drugs

Uptake BETA receptors takes time to kick in

38
Q

How is the Noradrenaline Hypothesis expanded

A

Include receptor sensitivity

Increased exposure of receptor to NA

Eventually sensitivity of receptor is decreased
B-Receptors

39
Q

Outline neurochemical Hypothesis of depression - Serotonin 5HT

A

Serotonin involved: pain sensitivity, emotionality and response negative consequences

Metabolite 5HIAA (marker activity serotonin) reduces cerebral spinal fluid

40
Q

How is the serotonin hypotheses of depression refuted

A

Low 5HIAA associated with aggressive hostile and impulsive behaviour
Violent suicide attempts

41
Q

What does the serotonin hypothesis tell us about individual differences of depression

A

Individuals with different alleles coding for serotonin transporter have different reactivity to stress

42
Q

Outline 5HTT Gene Variation of a human

A 
Repeat length polymorphism (abnormal variation genetic code)
In promoter (sequence on DNA marks where transcription begins) region
43
Q

Outline Biological Phenotype of a human

A

Altered neural stress and threat circuitry

Increase HPA axis response to stress

44
Q

Outline behavioural phenotype of a human

A

Intermedia phenotypes for depression and anxiety

Increased depression after stressful life events

45
Q

Outline 5HTT Gene Variation of a monkey

A

Repeat length polymorphism in promotor region

46
Q

Outline Biological phenotype of a Monkey

A

Altered neural stress and threat circuitry

Increased HPA Axis response to stress

47
Q

Outline behavioural phenotype of a monkey

A

Increased anxiety and stress reactivity after early life stress

48
Q

Outline 5HTT Gene Variation of a Rat

A

Chemical mutagenesis Knockout

49
Q

Outline Biological Phenotype of a Rat

A

Increased 5HT signally

Altered 5HT receptor expression and function

50
Q

Outline behavioural phenotype of a Rat

A

Increased anxiety like behaviour

51
Q

Outline 5HTT Gene Variation of a Mouse

A

Genetically engineered knockout or over expression

52
Q

Outline Biological Phenotype of a Mouse Knockout

A

Increased 5HT signalling
Altered 5HT receptor expression and function
Increased amygdala dendritic spins density and PFC dendritic branching
Increased HPA axis response stress

53
Q

Outline Biological Phenotype of a Mouse Over expression

A

Over expression:
Decreased 5HT signalling
Altered 5HT

54
Q

Outline behavioural phenotype of a Mouse Knockout

A

Increased anxiety like behaviour

Impaired fear extinction

Increased depression related behaviour after multiple stressors

55
Q

Outline behavioural phenotype of a Mouse Over Expression

A

Decreased anxiety like behaviours

56
Q

Outline Monoamine Oxidase Inhibitors to treat depression

A

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
Q

Outline Tricyclics used treat depression

A

Inhibit re uptake of noradrenaline and serotonin

Effective, cheap but dose related anticholinergic side effects limit compliance

Fatal in overdose

58
Q

Outline SSRIs to treat depression

A

Inhibit reuptake serotonin - block transporters reuptake increasing levels synaptic cleft

Safe overdose
Narrow dose range
Lack sedation free anti cholinergic side effects

59
Q

Outline Commonly used SSRIs

A

Prozac

Hypericum St Johns Wort

60
Q

Outline the 2 ways different antidepressant act to increase serotonin

A
  1. Inhibit MAO enzyme which breaks down serotonin

2. Blocking transporter Protein for serotonin reuptake

61
Q

What are Monoamine transporters

A

Mechanisms controlling extracellular Monoamine dynamics reuptake

Achieved through presynaptic neurons via plasma membrane transporters

62
Q

Examples of presynaptic neurons plasma membrane transporters

A

Dopamine - DAT

Serotonin - SERT

Noradrenaline - NET

63
Q

How do Monoamine transports though presynaptic neurons plasma membrane transporters act

A

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
Q

Outline result of Mice lacking both SERT and DAT

A

No place preference for cocaine suggesting SERT involvement in cocaine effects on reward

65
Q

What does SNRI stand for

A

Selective Serotonin Noradrenaline Inhibitors

66
Q

What is an SNRI

A

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
Q

What is the main reason for stopping taking drugs

A

Side effects

68
Q

How do some drugs work behaviourally by influencing affective bias Harmer et al 2009

A

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
Q

Outline CRF and depression

A

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
Q

Outline HPA Axis - Hypothalamic Pituitary Adrenocortical System

A
  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
Q

When are elevated corticosteroids good index of stress

A

Elevated times threat

Elevated chronically at times of loss of control

72
Q

What is the result of long term activation of HPA Axis

A

Long term damage
Depression associated increased activity HPA Axis
Enlargement adrenal gland and elevated levels cortisol

73
Q

How do antidepressants act on the HPA Axis

A

Lower activity

74
Q

How do early experiences affect the activity of HPA Axis

A

Early experience can bias towards later protracted activity of HPA

Maternal separation

75
Q

What is the link between arthritis and depression

A

Corticosteroids given for Arthritis and cause depression

76
Q

How do reuptake inhibitors boost the HPA System

A

Improvement in mental state associated with normalisation of HOA activity

77
Q

Outline Cushings Disease

A

Involves excessive secretion of corticosteroids commonly followed by depression

78
Q

Flow chart of HPA Axis Response

A

Stress ->
Hypothalamus, CRF ->
Pituitary, ACTH ->
Adrenals, Cortisol

79
Q

Outline neurogenesis and depression

A

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
Q

Outline protein BDNF neurogenesis and depression

A

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
Q

How do we increase neurogenesis

A

Exercise
Environmental enrichment
Antidepressants

82
Q

How do we decrease neurogenesis

A

Stress
Sleep deprivation
Age

Neuroscience (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions