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Brain & behaviour > Lecture 10 - Norepinephrine, 5-HT and epinephrine and emotions > Flashcards

Lecture 10 - Norepinephrine, 5-HT and epinephrine and emotions Flashcards

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1
Q

Outline what Monamine’s are

???????

A 
The collective term for these very important Neurotransmitters in your brain, they include:
•Serotonin (5-HT)
•Melatonin (sleeping)
• Dopamine
•Noradrenaline
•Norepinephrine
•Adrenaline
•Epinephrine
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2
Q

What are the 2 subcategories of Monamines

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A
  1. Tryptamines
    •Serotonin (5-HT)
    •Melatonin (sleeping and can be used as an NT)
2. Catecholamines
•Dopamine
•Noradrenaline
•Norepinephrine
•Adrenaline
•Epinephrine
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3
Q

Which ones are in the periphery

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A

1.
Epinephrine = In the brain
Adrenaline = Periphery

  1. Norepinephrine = in the brain
    Noradrenaline = periphery
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4
Q

What are the precursors for Monamines

A

Amino acids:
•Phenylalanine -> tyrosine -> catecholamines
- including dopamine -> norepinephrine
- L-Tyrosine-> L-dopa-> Dopamine -> NE
•Tryptophan -> Serotonin
- present in bananas and herring
•Thyroid Hormones - can regulate 5-HT, NE and GABA at the level of synapses in this brain

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5
Q

Outline Phenylalanine as a precursor to catecholamines

A

•Phenylalanine (an amino acid) is a precursor to tyrosine
•Tyrosine is a precursor to catecholamines
- i.e. l-tyrosine to l-dopa
• L-tyrosine is metabolised into L-dopa, which is metabolised into NE

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6
Q

Outline Tyrptophan as a precursor to serotonin

A

•Tryptophan (an amino acid) is a precursor to serotonin

  • competes with other amino acids at the brain blood barrier
  • whether or not it goes up depends on what else is at the barrier
  • lots of foods contain tryptophan, i.e. bananas - but its not as easy as just eating tryptophan to increase serotonin, although they will increase serotonin if they go through, they may not go through, it depends on what else is there
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7
Q

Outline the Dopamine metabolising pathways

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A
  1. Phenylalanine, is a precursor to:
  2. Tyrosine
  3. DOPA
  4. Dopamine
  5. Norepinephrine
  6. Epinephrine
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8
Q

Whats the unclear debate about NT’s and mental health

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A

It is unclear, whether:
- Neurotransmitters influence mental health
or
- Mental health, via behaviour, influences neurotransmitter levels
•E.g. not being active, laying in bed all day might influence NT levels

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9
Q

Outline Seligman & Maier (1967) - Learned Helplessness

A

Seligman & Maier (1967) - Learned Helplessness

  • Looked at if you can condition an animal to be helpless
  • Dogs were in a box, with a metal floor, there was a small barrier seperating out two sides
  • Side A was electroctuted after a tone was played but the dog could just jump over to the other side, to side B
  • BUT, if the dog was initially put in the box where there was just the wall was too high to jump over, maybe eve just a wall. when you then subsequently lowered that barrier, they still didnt make an attempt to jump over and escape
  • they were conditioned to expect the tone, and then conditioned to just wait and take it - had learned to be helpless
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10
Q

Outline Seligman’s 3 dogs in a harness study

A

There were 3 dogs, two in a pair, and one control

Dog a: Control, received no shock
Dog b (1st of the pair) This dog got a shock but could stop this shock by putting a paw on a lever
Dog c (2nd of the pair) This dog got the same shocks as those in group, but couldn't stop it with their paws

Dog b was: erratic, unavoidable, un-escapable
Dog c was: meek, subdued and depressed, and when placed in the box, did nothing to escape

  • Showed helplessness can be learned - you can teach people/ animals to be helpless
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11
Q

Outline Peterson, Maier & Seligman (1993) - learned helplessness
***

A

They argued there were 3 levels to this learned helplessness:

  1. Emotional
    - you feel helpless, emotional disruption
  2. Motivational
    - become passive and introverted
  3. Cognitive
    - tell yourself i cannt escape this

This might be a model of chronic stress, not a model of depression

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12
Q

Whats a limitation of generalising this to humans

A

X - learned helplessness doesnt always happen in all humans or all animals, you cant generalise it to everyone

X- doesnt happen in every animal/ every person

X - even in animals, it only stays up to 24-48 hours
- even in animals it doesnt last forever, eventually they will escape when they can

X - Revised this into explanatory style

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13
Q

Outline Explanatory style

A
  • Explanatory style is how a human or an animal attributes what happens to them
  • How we interpret and attribute stressful events

Those who attribute stressors as:

  1. internal (their fault)
  2. Stable
  3. Global (all situations)
    - these humans tend to be more depressed
    - negative explanatory style

Those who attribute stressors as

  1. external - this wasnt my fault
  2. Unstable - this is very unlikely to happen again
  3. Not global - This wont happen in any other situations
    - these are less likely to develop learned helplessness
    - also more likely to be a bit delusional, selectively remembering certain things, only select the positive stuff

Explanatory style is Linked to CBT

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14
Q

What did Weiner (1986) say depression was?

A

Depression is how we attribute causalities of certain events

- as internal, stable and global

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15
Q 
Outline Petty (1994) - Norepinephrine and rats and learned helplessness
???????
A

Looked at Norepenephrine in the Hippocampus of rats

  • in rats with inescapable stress, NE output in the Hippocampus actually increased
  • rats were put in a situation of permanant inescapable stress
  • NE didn’t go down like what was expected, it actually went up, hippocampus became very sensitive to stress (hypersensitivity)
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16
Q

Outline PTSD and coping with stress

**

A

Learned Helplessness might actually be a model of something like PTSD, when you are in constant state of vigiliance/ stress

PTSD = response to uncontrollable traumatic stress leading to instructions, arousal (hypervigiliance) and avoidance (pink bear phenomenon)

  • PTSD involves poor coping in mild stress, hypersensitivity to even slight stressors
  • To qualify as PTSD, it has to be something that is life threatening, something that seriously endagegered the integrity of yourself - or seeing someone in a situation like this (if its a milder situation, it might just be panic disorder)
  • After the event, you try to avoid thinking about it and being in situations that bring up this image - but if you try not to think about it, you will think about it
  • if its constantly popping into your head, you become aroused, hypersensitive, insomnia perhaps (nightmares), become very vigilant
  • being in this state, makes NE increases all the time, making the hippocampus over sensitive to stress
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17
Q

What was the initial idea about learned helplessness, and what is it now?

A

Initial idea: Learned helplessness causes NE and ST to go down
- because you cant do anything, you just sit there and take the punishment

Current idea: Whats actually been found is that if you have recurrent stress, NE and ST actually go up, because you are in a state of always being alert

  • exhaustion of hyper vigiliance that makes these NT’s go up
  • brain is actually working very hard and doing lots of stuff, producing lots of stuff
18
Q

What did Hammack (2012) find about serotonin in the brain

*****

A

They found that also serotonin output also increases during learned helplessness and conditioned defeat (constantly thwarted when trying for a goal directed behaviour)

  • output increases in Dorsal Raphe nuclues (main producer of 5-HT)
  • other areas serotonin also goes up is the basolateral amygdala, bed nuclues of the stria terminalis (associated depression/ fear) and the medial Pre-frontal cortex
19
Q

Whats the debate about how SSRI’s work?

*** email about this

A

Initially after taking them, people may get worse, or maybe something else happens at receptor level after 6 weeks

EITHER:
- Trick the pre-synaptic to make more like we initially thought - by thwarting the reuptaker
OR
- Because initially, there is constantly so much 5-HT in the synapse, there would be less receptors on the post-synpatic. But adding SSRI’s increase receptors We dont need to put much effort in catching it all so dont need many receptors

Not sure which way round the NT’s work in response to anti-depressants
- might be different for depression or anxiety

20
Q

What is evidence against LH

*******

A

X - not all animals develop LH
X - Ronan (2000) Rats that did not develop LH had higher levels of Serotonin metabolites (5-HIAA) in their lateral septum - recyled serotonin quicker - not having it accumulate and stress out the system
X - depressed rats doing exercise

21
Q

Outline the study into depressed rats doing exercise

A

Depressed rats doing exercise - 6 weeks voluntary wheel running
- exercising rats didnt feel LH
- this prevented depressed behavioural consequences of learned helplessness via:
•UP-REGULATED 5-HT1a receptors in dorsal Raphe nuclues went up
- reducing that overactivity of serotonin
•REDUCED BOTH RAPHE NUCLUES AND BED NUCLUES STRIA TERMINALS ACTIVITY (via decrease 5-HT2C excitatory receptors)
- so receptors also went down on top of activity of serotonin

Exercising reduces the impact of 5-HT on depression, and the amount of receptors you have

  • need the optimal amount of Serotonin, not too much or not too little
22
Q

What did Hammack (2012) find - social defeat etc

*****

A

The same stuff happens if you have:
•Chronic social defeat
•Chronic Inescapable shock
- influences the HPA - hypothalamus pituitary axis
- leads to elevated basal levels of Glucocorticosteroids
- seen in MDD

If you handle baby rats (Stressful for them), cortisol levels go up, but then cortisol responses get blunter, get less sensitive, CRH goes up (Cortico-steroid releasing hormone), this is bad for the immune system

23
Q

How is this stuff linked to the immune system

A

Having a pessimistic explanatory style: immune system goes down

  • having chronic elevation of Cortico-steroid releasing hormone (CRH) - higher CRH:
  • associated with responses to stress, but if they stay elevated, it can be bad
  • leads to frequent minor colds and major disease
  • being constantly stressed can be bad for your immune system
24
Q

Outline the summary

???????

A
  1. If you have a situation of unavoidable pain, no control and no escape, many animals will develop LH
    - but those who can metabolise that excess serotonin away might not
    - how quickly you metabolise serotonin is maybe your genetics but also your explanatory style
  2. In these situations we see altered levels of NE/ 5-HT CORT activity
    - resulting in a change of sensitivity
  3. Consequences of a negative generalised cognition (explanatory style), if negative = increased risk of burnout, depression, inactivity, sickness
  4. Exercise can reset this (control/ reward)
    - can down regulate receptors, making them less sensitive
  5. Unclear if depression is just due to low ST and NE
    - if anti-depressants might not work for you, if you are not good at metabolising serotonin away, this might increase to too high a level
    - due to genetic differences. E.g. this treatment may not work for you as you are not a good metaboliser
25
Q

Outline the 4 different theories

A

James-Lange theory
1. Stressor, 2. Hearts pounding, 3. Hearts pounding i must be scared

Canon-bard
1. Stressor, 2. Heart is pounding, 3. you are SIMULTANEOUSLY scared, 4. these two events are independent, they dont effect each other

Schacter & Singer

  1. stressor, 2. arousal, 3. Reason to figure out what it is, 4. experience that emotion
    - ABOUT REASONING

Schacter & Singer Two factor theory

  1. Stressor, 2. arousal IN COMBINATION WITH 3. cognitive labels, 4. experience that emotion
    - More about cognitive labels, which one we know fits the particular situation, e.g. at a funeral, the cognitive label if you are feeling aroused should be sad
    - if your cognitive label doesnt function as well, e.g. in autism, or in Sz, they might not display the correct emotion
26
Q

Outline James theory (1884) USA

???????

A

Previous theories state that it was:
stimulant -> Body response -> emotion
- but james said this was too simple, he said
- stimulus -> sense perception -> brain sensory/ motor areas are activated -> specific visceral (physiological) responses ->specifc emotion

  • Lange (1885) also said this, but said the vasomotor center = basis
    1. Stressor, 2. Hearts pounding, 3. Hearts pounding i must be scared
27
Q

Outline Canon-bard theory (1927) Harvard

???????

A

They argued that these ANS changes are really aspecific, because visceral organs respond too slowly. They said it must be:

Stimulus -> sense perception -> cortex -> conditioned response -> thalamus organises both arousal and emotion SEPERATELY

Canon-bard
1. Stressor, 2. Heart is pounding, 3. you are SIMULTANEOUSLY scared, 4. these two events are independent, they dont effect each other

X - those with spinal cord lesions feel emotions less intensely as they dont have as much bodily feedback
- disproves Canon-Bard as it shows that we do depend on the body

28
Q

Outline Schachter & Singer (1962) theory

???????

A

Specific cognitive labels of stimulus determine general arousal and specific emotion

Context of situation -> GENERAL arousal AND SPECIFIC emotion
- physiological arousal might be the same for happy and for sad, but the emotion will be difference

29
Q

Outline Schachter & Singer 1962 experiment
- Vitamin Injections given to improve vision
????????????????????????????

A

184 men divided into 3 groups:

  1. Informed: of potential side effects
    - e.g. increased heart rate, feeling jittery
  2. ignorant: not told of side effects
  3. Misinformed: given false side effects
    - e.g. blurred vision

Also took 2 difference cognitive circumstances, 20 minute: 1. Happy or 2. Angry stooge

Either given a real adrenaline shot or a placebo

30
Q

Outline Schachter & Singer 1962 experiment FINDINGS

?????????????????????

A

Found that informed and placebo
- scored less high on either happy/ agnry state than those in the misinformed or ignorant

If you have a label or no arousal you are less emotional
- if you are unware for the reasons of your arousal, or there is nothing to be aroused about, you are feeling less emotional

31
Q

How is this implicated in anger management?

A
  • To recognise the physiological precursos to anger, what are your triggers, and how can you physiologically recognise this
32
Q

What were Schachter & singer conclusions?

?????????????????????

A

If there is no causal explanation for arousal,
e.g. no label for the arousal in terms of cognitions: context, experience

If there is a likely explanation: no labelling

under same circumstances; emotional response = degree of physiological arousal

Physiological arousal promotes experiences of emotion

33
Q

What did Dutton & ARon (1974) do?

A

Bridge study
- looking at what happens if we misattribute this physiological arousal, or if we arent sure how to attribute this arousal

Men on high bridge: heart was racing, misattributed arousal into thinking they were attracted

Females received more calls and was perceived more sexually attractive when on a high bridge

34
Q

What are criticisms about emotion theories?

*********

A

X - what about amygdala and fear
- not just cognitions, there is a lot going on in the CNS

X - is it just general arousal, or differences in physiological arousal depending on the type of emotion
- false feedback (heart rate incorrect)

35
Q

What are benefits about emotion theories?

A

√ - Facial feed back can eliecit/ amplify emotions (Strack, Martin & Strepper (1988)

  • pen in your teeth = forced smile, makes you feel happier
  • not always aware of how tense we are, our body is constantly feeding back to us

√- Botox in Corrugator Supercilli muscle

  • decreased activation in amygdala and brainstem (Hennelotter, 2008)
  • dampen emotional understanding language (Haves, 2010)
  • wont be attributed empathy as much, wont feel empathic yourself
  • but do feel less depression

Understanding each other and experiening emotions depends on the body feeding back to us

36
Q

What did Lisa Feldman Barrett do?

  • Conceptual Act model of emotion
  • Solving the emotional paradox

IMPORTANT FOR THE EXAM
?????????????????????

A

Solving the emotional paradox (2006)
- tried to bring everything together, as it seemed like a bit of mess, wanted to unify theories on emotion

  • We use the context of where we are and why we are being aroused

Said we have a core affect: Neurophysiological state, which we need to look at from 2 angles:
•Pleasure vs displeasure
- is it a good emotion or a bad emotion

• How intense this emotion is - high arousal vs low arousal
- reflected by the physiological stuff

We then take this information and categorise the emotion based on our knowledge of emotions

  • can maybe have multiple emotions at once
  • usually the cognitive label helps you figure it out (CBT)
37
Q

Outline how CBT is relevant here

******

A

Stimulus -> Cognitive appraisal -> Autonomic arousal (indicating what the intensity is) (can be manipulated) -> behaviour - > emotional experience

If we change either one of the 3, e.g. changing our explanatory style, this will change our physiological arousal. Can change physiological arousal to change cognitive appraisal

By changing our cognition or arousal (relax) or behaviour (exposure)
- emotional experience (fear, anger, depression) changes

Might need a good therapist to help you figure out what you are experiencing

38
Q

What does internal, stable, global explanatory style cause?

A

A situation that is appraised as internal, stable, global, a threat/ no control causes:
•Autonomic arousal
•Avoidant behaviour - never going to help us

39
Q

Outline the Amino Acid cocktail thing they did

A

Tried to give people an amino acid cocktail, including Tryptophan, it was disgusting

  • in those who were vulnerable to depression it helped a bit, but for those who weren’t it didnt do much
  • because it’s not as simple as taking it, as it competes in the Blood brain barrier
40
Q

What are the types of dperessions we are kind of discussing here

A

• Depressions with anxiety
•Depressions with PTSD
- as in hyper vigilance etc
•Major Depression Disorder
•Mid-week blues, after taking MDMA, lack of serotonin after expulding it
•Learned Helplessness not linked to all types of depression
X - not the best to compare animals to humans

41
Q

How does caffeine work in this stuff
??????? what are adensonises
******

A

Caffeine is an adenosine inhibitor and this will release all the catecholamines

  • can make you feel quite anxious, can interpret your physiological responses as anxiety
  • if you dont know why you are feeling phsyioligcal symptoms, can lead to panic attacks - but as soon as you know why you are experiencing this, you can kind of stop it

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