Brainscape's Knowledge GenomeTM

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


See full index

270 part 3 > emotional behaviour > Flashcards

emotional behaviour Flashcards

1
Q

limbic system

A
  • includes forebrain area surrounding the thalamus

- critical for emotion

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

aggression: context dependent

A

depends on testing parameters

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

Sympathetic

A

stim organs for fight/flight (i.e. heart) inhibit vegetative activities (i.e. stomach)
- acute

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

Parasympathetic

A

increases digestion – save energy, prep for later events

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

Most situations invoke a combination of sympathetic & parasympathetic ie

A

become alert & inactive, heart rate decrease when danger is present but remote

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

physiological arousal & emotional feelings:

  • spinal cord damage
  • pure autonomic failure
  • BOTOX blocking transmission at synapses (muscle paralyzation)
  • Damaged right somatosensory cortex
  • Partly damaged prefrontal cortex
A
  • After damage to spinal cord – similar emotional experiences to before
  • Pure autonomic failure: almost no output from autonomic nervous system to body
    • No physiological reaction to stressful experience
    • normal emotions reported – but less intense
  • Boltulinum toxin (BOTOX) blocks transmission at synapses & nerve-muscle junctions
    • Muscles paralysed – weaker emotional responses
  • Damaged right somatosensory cortex: normal autonomic response, little subjective experience
  • Partly damaged prefrontal cortex: weak auto response, normal subjective exp
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  • Sudden intense arousal of sympathetic NS without knowing the reason
A

may experience as emotion i.e. panic attack

- Physiological responses increase feelings (increase in HR – increase both pleasant & unpleasant)

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

“anger centre”??

A

doesn’t exist – certain patterns of activation are more closely associated to anger than sadness

  • Much of the cerebral cortex reacts to emotional situations
  • No brain area appears to be specific for experiencing any particular emotion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • Behavioural activation system
A

activity of frontal & temporal lobes of L hemi – low to mod auto arousal & approach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  • Behavioural inhibition system
A

increased activity of frontal & temporal lobes in R hemi – increases attention, inhibits action, stim fear & disgust

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

aggression in hamasters (facing intrusion)

A

Home hamster facing intrusion:
- First attack of intruder: activity builds up in corticomedial area of amygdala (steroid sensitive)
• Increases probability of attacking the next intruder

  • ## stained for an immediate-early gene: c-fos (cell nucleus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

orbital frontal cortex

A

inhibits action in medial amygdala

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

Aggressive, violent, antisocial behaviour depend on both environment & genes

A
  • Env: childhood abuse, witness violent abuse b/w parents, live in violent neighbourhood, lead exposure
  • Heredity : significant for aggressive behaviour but depend on how to measure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Genetic + environment effect on aggression: gene controlling enzyme monoamine oxidase A (MAO A) + bad environment

A

MAO A : an enzyme in synapse that breaks down/metabolize monoamines – some of serotonin/ dope/ norepi after reuptake
• Low activity (short form of gene) – less MAO A enzyme produced + bad childhood – link to aggression, less resilience (greater emotional reactivity?)
• Effect of gene depends on previous experience (increase aggression only in ppl with troubled childhood)
 gene x env interaction

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

low serotonin (5HT) release (indicated by? & associated with?)

A
  • Serotonin levels in neurons: fairly constant (neurons reabsorb most serotonin released & synthesize enough to replace the amt washed away)
    measure instead: - serotonin metabolite levels (serotonin turnover) – concentration of 5-HIAA in extracellular space/ CSF
  • low metabolite levels associated with aggressive behvaiour & impulsiveness
  • mice: social isolate increases aggression & decreases 5-HIAA levels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

twin aggression studies

A

mono twins resemble each other much more than dizygotic twins - violent & criminal behaviour
- adopted children resemble biological parents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

humans – DHEA is inert

A

secreted by adrenals & converted into active sex steroids (T & E2)
- does not have its own receptors, not synthesized directly, antiglucocorticoid effects

hyp: same for T in song sparrows during non-breeding season? since T is not detected in blood plasma & gonads shrink
finding: enzyme 3 beta-HSD is upregulated in non-breeding season (increases capacity for local production of T), low in breeding season

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hormonal effects on aggression

A
  • Same age: those with higher T levels on avg tend to be more aggressive (both M & F)
    • But differences are small
     Hypothesis: aggressive behaviour depends on a sudden burst of T in response to an event (not baseline)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Testosterone, Serotonin & cortisol on agg behv.

A
  • T (esp a burst of T) facilitates aggressive, assertive, dominant behaviour
  • Ser tends to inhibit impulsive behv.
  • Cortisol inhibits aggression (stronger than Ser)
  • Adrenal gland: secretes cort during stress & anxiety – cautious behv  conserves energy
20
Q

anxiety &anger – effect on cortisol

A

 anxiety increases Cortisol levels
- Anger decreases cort levels
- Both M & F: combination of high T & low cort increases aggressive & risky behv.
• Low cort: decreased fear of harmful consequences
• T: increases expected gain

21
Q

Moro reflex in infants

A

sudden loud noise causes newborn arch back & cry

22
Q

Startle reflex

A

loud noise – cochlear nucleus in medulla – area in pons that commands tensing muscles (esp neck) – in less than 2/10 of a second
• More vigorous if already tense
• Enhanced in ppl with PTSD/ more anxiety
 can measure the startle reflex to measure anxiety

23
Q

general adaptation syndrome

A

alarm stage: increased sympathetic nervous system activity (acute)
resistance stage: sympathetic response declines; adrenal cortex continues releasing corticosterone (rats) / cortisol & other hormones to promote alertness
exhaustion stage: occurs after chronic prolonged stress; insufficient energy to sustain responses

24
Q

stressor

A

external stimuli

25
Q

stress

A

internal perception of external stimuli

26
Q

stress response

A

physiological responses to stressor

27
Q

sympathetic NS vs HPA axis

A

SNS: fight/flight responses (acute transient stressors) vs HPA axis: activated under chronic, prolonged stressors

28
Q

acute stress response

A

increased energy availability – blood glucose
increased oxygen intake
increased blood flow to muscles
inhibition of digestion, growth & repair , reproduction, pain perception
altered immune function (move to skin)
enhancement of memory & sensory info
adrenal medulla: secrete catecholamines (epinephrine, norepinephrine, dopamine ) – block receptors = decrease in BP

29
Q

chronic stress response (repeated HPA axis stimulation)

A

can have pathological effects:
energy availability: type 2 diabetes mellitus
inhibition to reproduction: infertility
inhibition of growth & repair : psychosocial dwarfism, slower wound healing
inhibition of immune function: immunosuppression, impaired pathogen resistance
stimulation of CNS: neural degeneration

30
Q

describe the HPA axis

A

responds to signals like elevated norepinephrine levels

hypothalamus secretes corticotropin releasing hormones (CRH) to anterior pituitary – (increases SNS activity) & A pit releases Adrenocorticotropic hormone (ACTH) into blood – reaches adrenal cortex –> releases glucocorticoids like Cortisol and DHEA

Cortisol: increases glucose levels by breaking down more glycogen (more energy available) – negative feedback to hypothalamus & A pit
DHEA: acts in opposition to CORT

31
Q

hippocampus & stress

A

negative feedback to HPA axis
many glucocorticoid receptors (GR) – vs mineralocorticoid receptors (MR) : MR has higher affinity = baseline: lots of GR not bound – only bound when lots of GC present

prolonged high cortisol levels: dendritic atrophy of pyramidal cells & cell loss – vulnerable to overstimulation
hippocampal damage leads to increased cortisol levels (vicious cycle)

32
Q

amygdala & fear

A
  • Amygdala: important for enhancing startle reflex & learned fears
  • Much input from sensory systems (vision, hearing) goes to lateral & basolateral areas of amygdala  relay to central amygdala  combines with pain & stress info received from thalamus
    Mice with stronger connections b/w lateral & central amygdala: more anxious

• Fear learning: strengthens synapses at several connections
- A path through the amygdala for each fear: pain, predator etc
-

33
Q

bed nucleus of the stria terminalis & fear

A

A set of axons that connect the bed nucleus to amygdala

– Long-term, generalized emotional arousal

34
Q

re-appraisal

A

reinterpret a situation as less threatening *effective for coping
 depend on top-down influences from prefrontal cortex to inhibit amygdala activity

35
Q

ind differences in anxiety tendencies

A
  • remain consistent over time for ppl
  • variance: due to genes & epigenetic changes caused by early experiences
  • ind differences correlate strongly with amygdala activity (biological predisposition)
36
Q

Unipolar depression (major depressive disorder)

A

vary b/w normaliy & depression
- Feel sad & helpless most of the day every day for weeks at a time
- Nucleus accumbens becomes less responsive to reward
- Feel worthless, contemplate suicide, sleeping issues
- Cognitive problems: low motivation, impaired attention , memory & sense of smell
- Absence of happiness
- Common to have episodes of depression separated by normal periods
• FALSE: Early eps: longer; later: briefer but more frequent
risk factors: stress & inflammation : increased immune activity (i.e. after injury, highly stressful experiences)
lower levels of a neurotrophin

37
Q
  • Panic disorder
A

frequent periods of anxiety & occasional attacks of rapid breathing, increased HR, sweating, trembling – extreme arousal of Sympathetic NS
• Linked to abnormalities in hypothalamus
 decreased GABA activity, increased orexin (drugs that block orexin receptors block panic responses)

38
Q
  • Post-traumatic stress disorder
A

frequent distressing recollections & nightmares of traumatic event, avoidance of reminders, vigorous reactions to stim
• Cannot be predicted based on severity of trauma / initial reaction intensity
• Most victims have a smaller hippocampus (increases susceptibility)
• Severe stress can impair function in the hippocampus (sometimes shrinkage)
• Recovery from PTSD does not increase size

39
Q

behavioural tests in rats fro depressive-like behaviour

A
  • forced swim test – latency to giving up
  • lever press
  • sucrose preference test : reduction in the sucrose preference ratio = more depressed
40
Q

Relief from anxiety

Pharmalogical

A
  • Anxiolytic (anti-anxiety) drugs: benzodiazepines, diazepam etc.
    • Bind to GABA A receptor  includes a site that binds GABA & sites that modify the sensitivity of GABA site
  • Chloride channel in GABAA receptor:
    • Open: Cl- can enter neuron  hyperpolarize cell/ counteract Na entering the cell through excitatory synapses (GABA synapse is inhibitory)
    benzodiazepines twists the receptor so that the GABA binds more easily *facilitates effects of GABA
41
Q

genetic predisposition to depression

A 
Serotonin transporter (protein regulating axons’ reabsorption of serotonin) gene:
•	Ppl with 2 short forms of gene – stressful events led to major increase in risk of depression 
-- short form magnified reaction to stressful events (NOT Lead to depression) 
& increased emotional reactivity of any type
42
Q

dexamethasone (DEX)

A

artificial steroid: high affinity for glucocorticoid receptors
- mimics GC binding & increase glucose levels
in normal control: result in decreased GC levels
in depressed patients: GC levels are still high
– DEX suppression test can be potentially used for diagnosis

43
Q

non specific (innate) immunity

A

rapid first line of defence monocytes & macrophages

destroy anything “non-self” – but can also damage self

44
Q

specific (adaptive) immunity

A

slower
cell-mediated: T cells (lymphocytes) – mature in thymus: attack pathogens directly (cytotoxic T cells) & help other T & B cells to multiply (helper T cells)
kills specific pathogen upon re exposure

45
Q

cytokines

A

small proteins produced by leukocytes & others

  • combat infection & inform brain
  • stim release of prostaglandins – fever & sleepiness (save energy)
46
Q

antidepressant drugs

A
  • block transporter proteins that reabsorb serotonin, dopamine , norepinephrine into presyn neuron after released (block reuptake)
  • NTs present in synaptic cleft for longer  continue stimulating postsyn cell

increase BDNF levels over course of weeks

270 part 3 (3 decks)

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