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MTB x > week 12 > Flashcards

week 12 Flashcards

1
Q

Define Anxiety

A

An adaptive state of increased apprehension that helps an animal avoid potential danger, and it is associated with muscle tension and vigilance

An cautious or avoidant behaviours

Includes panic

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2
Q

Define Fear

A

Emotional response to real or perceived imminent threat

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3
Q

What does fear include?

A

surges of autonomic arousal necessary for fight or flight

Thoughts of immediate danger, and escape behaviours

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4
Q

What is anxiety related to?

A

Fear

It is not the same

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5
Q

What is anxiety a umbrella term for?

A

A variety of disorders

within DSM-5

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6
Q

What are the manifestations of anxiety disorder?

A

Both psychological and physical

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7
Q

What are examples of potential stressors?

A
  1. Failures
  2. Personal losses
  3. Frightening events
  4. Time precursors
  5. Insults
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8
Q

When the potential stressors are perceived as a threat, what is it subdivided into?

A
  1. Bodily effects

2. Upsetting thoughts

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9
Q

What are examples of bodily effects?

A
  1. Autonomic emergency response
  2. Shallow breathing
  3. Pounding heart
  4. Tense muscles
  5. Digestive problems
  6. Sleep disturbances
  7. Fatigue
  8. Psychosomatic illness
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10
Q

What are examples of upsetting thoughts?

A
  1. Anger
  2. Fears
  3. Preoccupations
  4. Self-doubts
  5. Negative self-talk
  6. Repeated ‘‘danger’’ thoughts
  7. Worry about body reactions and health
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11
Q

What does bodily effects and upsetting thoughts lead to?

A

Ineffective behaviour

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12
Q

What is an example of ineffective behaviour?

A
  1. Escape
  2. Avoidance
  3. Indecision
  4. Aggression
  5. Inflexible responses
  6. Poor judgement
  7. Inefficiency
  8. Drug use
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13
Q

What is ineffective behaviour’?

A

Behaviour you engage that has no actual purpose or produce no result

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14
Q

What is fear processing?

A
  1. Thalamus projects to amygdala
  2. Indirectly via the cortex (long pathway)
  3. Directly (short route)
  4. Amygdala connects hypothalamus: bodily manifestations of feat
  5. Output: run/freeze
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15
Q

Where is sensory stimulation interpreted in?

A

sensory thalamus

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16
Q

When do we respond very quickly to a stimulus?

A

When the stimulus evokes fear and bypasses the cortex

Engage in fear without thinking, simply start feeling very agitated

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17
Q

what are the main circuits involved in fear conditioning?

A
  1. sensory areas - process the conditioned and unconditioned stimuli
  2. certain regions of the amygdala that undergo plasticity
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18
Q

Where does fear reponse start in the brain?

A

Amygdala

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19
Q

What is amygdala dedicated to detecting?

A

Emotional salience of the stimuli

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20
Q

What does amygdala activate?

A

Areas involved in preparation for motor function involved in fight or flight

Triggers the release of stress hormone and sympathetic nervous system

leads to bodily changes that prepare us to be more efficient in a danger

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21
Q

What brain regions is closely connected to amygdala and what are their roles?

A
  1. Hippocampus
  2. Prefrontal cortex

Help brain interpret the perceived threat

Involved in higher processing of context

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22
Q

Where does the conditioned stimulus flow from?

A

The lateral amygdala to the central nucleus of the amygdala

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23
Q

What controls defensive behaviour i.e. freezing?

A

Pathways from central nucleus of amygdala to downstream areas

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24
Q

what does the hypothalamus ochestrate?

A
  1. Freezing or fleeing response and all the physical manifestation
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25
Q

where is amygdala located in?

A

Medial temporal lobe

composed of number of different nuclei

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26
Q

What is lateral nucleus?

A

primary nucleus input of the amygdala

It receives input from the thalamus and the cortex which provide it with information of the sensory stimuli the animal is experiencing

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27
Q

What is the primary output nuclei of the amygdala?

A

Central medial nucleus

Projects to a number of different structures

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28
Q

Where does the central medial nucleus project to?

A
  1. Paraventricular nucleus of the hypothalamus and triggers release of stress hormone cortisol
  2. Lateral hypothalamus - stimulating the autonomic nervous system
  3. Periaqueductal grey matter - which in mice causes fear behaviours such as freezing
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29
Q

What happens when the downstream targets are coordinated?

A

The amygdala is able to produce many of the physiological changes associated with feeling of fear:

  1. Increased heart rate
  2. Sweating
  3. Dilation of the pupils
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30
Q

What is fear conditioning?

A

When an animal learns to fear something

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31
Q

What happens in a typical fear conditioning experiment?

A
  1. A mouse is given an unconditioned stimulus which is inherently negative such as a painful foot shock
  2. causes a natural unconditioned response - the expression of fear
  3. Also uses a neutral stimulus e.g. a sound which on its own produces no fear
  4. When the neutral and unconditioned stimuli are presented , the animal learns the association between the sound and the shock
  5. A neutral stimulus of the sound is then able to cause the fear behaviour itself without the shock
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32
Q

What is related to fear conditioning?

A

The concept of fear extinction

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33
Q

When does extinction occur?

A

When the conditioned stimulus of the tone is presented repeatedly without the unconditioned stimulus of the foot shock

The animal gradually learns that the sound no longer predicts a shock

The association is broken and the fear behaviour is no longer displayed

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34
Q

What is amygdala thought to be?

A

Primary area of the brain responsible for fear conditioning

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35
Q

How does amygdala participate in fear conditioning?

A
  • The unconditioned stimulus of the foot shock travels to the spinal cord to the thalamus and cortex
  • Which both project to the lateral nucleus of the amygdala
  • The synaptic input from the unconditioned stimulus of the shock is strong enough to excite lateral amygdala neurons
  • Activation of neurons in the central medial nucleus and produces a fear response
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36
Q

What happens when the neuron encoding the shock and the neuron encoding the sound fire together?

A

Synaptic plasticity occurs

This strengthens the synapse between the incoming neuron carrying information about the neutral stimulus of the sound and the lateral amygdala neurons

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37
Q

What does the lateral amygdala neuron do?

A

Excite central medial nucleus and produces feeling and fear

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38
Q

What are the neuroanatomical regions involved in anxiety disorders?

A
  1. Amygdala: the central fear centre
  2. Locus Coeruleus: Norepinphrine secretion - stimulated by active HPA axis
  3. Septohippocampal GABAERGIC system
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39
Q

Amygdala: The central fear centre

A
  1. Crucial for fear conditioning

2. Lesion in humans demonstrated pivotal for storage and processing of emotional memories

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40
Q

Locus coeruleus: Norephinephrine secretion

A

LC stimulation generates panic attack

LC blockade decreases panic attacks

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41
Q

Septohippocampal GABAERGIC system

A
  1. Mediate anxiety and vigilance
  2. High concentration of GABAergic neurons and receptors
  3. Directly connected to LC
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42
Q

What does the stimulation of the stress response engage?

A

Locus Coeruleus

Generating excessive response to a fear stimulus

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43
Q

Within a non-clinical population, where will there be differences in?

A

presentation of certain phenotypes

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44
Q

Who tends to have a larger amygdala?

A

Healthy children and adults with higher anxiety levels

45
Q

What exhibits anxiety-related changes across the human adult lifespan?

A

Intrinsic functional connectivity between amygdala and multiple cortical networks

46
Q

What is high-level trait anxiety predicted by?

A

Low-level global amygdala connectivity

47
Q

What demonstrated anxiety-related changes of connectivity with left amygdala?

A

Somatomotor and dorsal attention networks

48
Q

What had changes of connectivity with the right amygdala?

A

Frontoparietal control and ventral attention networks

49
Q

What contributes to individual differences in anxiety behaviours?

A

Both low-level sensory networks and high-level associative network

50
Q

What varies with individual’s level of anxiety?

A

Amygdala response to threat-related stimuli located outside the current focus of spatial attention

51
Q

What leads to differential activation of amygdala?

A

stimuli with different objective levels of threat

52
Q

What is consistent with the most previous fMRI studies of conscious perception of threatening stimuli?

A

consciously processed fearful faces selectively activate the dorsal but not the basolateral amygdala.

53
Q

Where is the activation of amygdala altered in?

A

Abnormal anxiety

54
Q

What is the consequence of people with anxiety?

A

The amygdala will be much more rapidly reactive to fearful stimuli

55
Q

What is associated with lifespan anxiety?

A

The number of synaptic connection of amygdala with neurons in the cortex

56
Q

When is it more likely that an individual will experience anxiety?

A

The more connection that exist between amygdala neurons and cortical neurons

57
Q

What showed a positive correlation between ipsilateral amygdala iFC and anxiety?

A

An area adjacent to left lateral occipital, parietal, and superior temporal cortex

58
Q

Who had stronger iFC of the left amygdala correlated with higher level of trait anxiety

A

The right posterior central area

Whereas an inverse correlational profile existed for the left dorsal lateral prefrontal cortex

59
Q

What are the neurotransmitter thereoies of anxiety?

A
  1. Norepinephrine
  2. Serotonin
  3. GABA
60
Q

What is norepinephrine?

A

Excess leads to excessive activation of cortex

NE reuptake inhibitors such as tricyclic antidepressant that block NE are effective anti-anxiety treatments

61
Q

What is NRI associated with?

A

down-regulation of beta adrenergic receptors

62
Q

What are beta adrenergic agonist and antagonist?

A

Agonist - Anxiogenic

Antagonist - Anxiolytic

63
Q

What does stress paradigms generate?

A

Hypersecretion of NE

64
Q

What is serotonin role?

A
  1. Complex

2. 5-HT can be anxiolytic and anxiogenic

65
Q

For serotonin, what is effective anti-anxiety treatment across disorders?

A

SSRI

66
Q

What are effective in some anxiety disorders?

A

Serotonin tricyclic antidepressant

67
Q

What does Benzodiazepine (BZ) bind to?

A

GABA-A receptor
enhance GABA activity
potent anxiolytic

68
Q

What does other GABA-receptor modulators (alcohol) have?

A

Anxiolytic effects

69
Q

What is observed in brains of anxious disorders?

A

Reduction of BZ receptor

70
Q

What enhanced anxious behaviours?

A

GABA-A/BZ receptor

71
Q

What does benzodiazepine act as?

A

GABA-A allosteric modulator

72
Q

What does BZ potentiate when it binds to its site?

A

Inhibitory action of GABA and produce:

  1. Sedation
  2. Sleep
  3. Anxiolysis
  4. Anticonvulsant activity
73
Q

How is anxiety treated?

A

Anxiolytics

74
Q

What are the drugs used to treat various anxiety disorder?

A
  1. Benzodiazepine
  2. Tricylic antidepressant
  3. Monoamine oxidase inhibitors
  4. Selective serotonin reuptake inhibitors
  5. Buspirone
75
Q

What are examples of benzodiazepine, what disorders?

A
  1. Valium
  2. Xanax
  3. GAD
  4. PTSD
  5. Panic disorder
76
Q

What are examples of tricyclic antidepressant?

A
  1. Tofranil
  2. Aventil
  3. Panic disorder
  4. GAD
  5. OCD
  6. PTSD
77
Q

What are examples of monoamine oxidase inhibitors?

A
  1. Nardil
  2. Parnate
  3. Social phobia
  4. Panic disorder
78
Q

What are examples of SSRI?

A
  1. Prozac
  2. Zoloft
  3. Paxil
  4. Social phobia
  5. Panic disorder
  6. OCD
  7. PTSD
79
Q

What are examples of Buspirone

A
  1. BuSpar
  2. GAD
  3. Panic disorder
  4. OCD
80
Q

What does anxiety disorders have?

A

Heterogenous origin

81
Q

Where did most of the abundant research on PTSD actually come from?

A

Vietnam veterans

30% of veterans that came back from war experienced PTSD

82
Q

What does PTSD have?

A

one of the highest incidence of suicide among all of the mental illness

83
Q

What is PTSD?

A

A form of anxiety occurring after exposure to a traumatic event

84
Q

What are examples of traumatic events?

A
  1. War
  2. Natural disaster
  3. Terrorist attacks
  4. Physical assault
  5. Rape
  6. Child abise
  7. Car accidents
85
Q

What is PTSD characterised by?

A
  1. Increased physiological reactivity to reminders of trauma
  2. Sleep disturbances/nightmares
  3. Flashback to the traumatic event
  4. Avoidance of cues associated with trauma
  5. Numbing of emotional responses/detachment
86
Q

What does imaging studies show?

A

High levels of responsiveness of amygdala to trauma cues

  1. Less activity in anterior cingulate and medial prefrontal cortices
87
Q

What does PTSD cause?

A
  1. Dysregulation of HPA axis
  2. Low cortisol
  3. High CRH
  4. High catecholamine
88
Q

What are the current pharmacological approaches for PTSD therapy?

A
  1. Use of benzodiazepine

2. Beta-adrenoceptor blockers

89
Q

What does behavioural therapy include (PTSD)?

A
  1. Exposure based therapy in which an individual is exposed to a reimagining of the original trauma/ a cue associated with the original trauma in the absence of an aversive outcome
90
Q

What is the therapeutic benefit in targeting epigenetic mechanism for PTSD therapy?

A
  1. Infralimbic medial prefrontal cortex to improve strength and persistence of extinction
91
Q

What is a region linked specifically with memory extinction?

A

Infralimbic medial prefrontal cortex

92
Q

What does histone acetyltransferase add?

A

Acetyl groups of histones, generally associated with relaxing wound DNA

93
Q

What does HDAC do?

A

Remove these acetyl groups

94
Q

What histone methyltransferase (HMT) do?

A

Add methyl groups to histone, generally associated with tightening wound DNA

95
Q

What does HDM do?

A

Remove those methyl groups

96
Q

What does DNA methyltransferase (DNMT) do?

A

Add methyl groups to DNA, sometimes associated with DNA silencing

97
Q

How does the animal learn to stop responding feafully to stimulus via sounds?

A

Accumulation of new memories

98
Q

What can help PTSD sounds?

A

Extinction which is new learning

99
Q

What can accelerates the process of new learning or extinction?

A
  1. Ketamine

2. Hallucinogenic

100
Q

What requires de novo transcription?

A

Consolidation of emotional memories

101
Q

What is required to convert transient short term memory into persistent long-term fear memory (CREB activation)?

A

New gene transcription in the amygdala

102
Q

What does memory consolidation also require?

A

Epigenetic changes (acetylation)

103
Q

What promotes memory consolidation?

A

Enhancing acetylation

104
Q

What are the consequence of PTSD?

A
  1. Lack of extinction of fear memories
  2. Reduced size amygdala in PTSD sufferers
  3. Hippocampus size predicts PTSD risk
105
Q

What are the physiological reactions to PTSD?

A
  1. Flashbacks - reliving trauma
  2. Racing heart or sweating
  3. Bad dreams
  4. Having difficulty sleeping
  5. Frightening thoughts
  6. Feeling tense
  7. Having angry outburst
106
Q

What does virtual reality run on ?

A

Commodity-level personal computers and provide interactive, immersive experiences and scenarios that open many doors for psychological research and behavioural health applications

107
Q

What can VR provide?

A

a way to immerse users in stimulations of the traumatic experience

the clinician can precisely control the scene’s emotional intensity and customize the pace and relevance of the exposure for the individual patient

108
Q

What is the main role of virtual reality?

A

Re-learning to ‘‘extinguish’’ emotional memory as therapeutic strategy to treat PTSD

109
Q

What mediates the formation of new memories?

A

The use of histone de-acetylase inhibitors (HDAC) such as:

  1. Valproic acid
  2. Lithium

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