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Psych2015 > PSYC2015 Final Exam Content > Flashcards

PSYC2015 Final Exam Content Flashcards

1
Q

What are Tinberg’s 4 questions about the causes of behaviour?

A

Causation - hormones, genes etc.

Development - imprinting, issues of learning etc.

Evolution - e.g parental care in birds but not most reptiles

Function - the contribution of the behaviour to fitness

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2
Q

Describe Darwin’s theory of evolution by natural selection

A
  • Limited resources = competition

- Survival of the fittest

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3
Q

What is meant by fitness?

A

The reproductive success of an animal relative to direct competitors in the population

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4
Q

What are SSDR’s and how do they increase fitness

A

SSDR -> Species-specific defense responses

- Increased survival = increased fitness

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5
Q

Explain how one psychological trait could have been shaped into its present form via natural selection

A

Aggression -> increased competition for resources leading to increased fitness

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6
Q

Explain the differences between adaptations, exaptations, spandrels, by-products & noise

A

Adaptations - An inherited characteristic that emerged through natural selection as it contributed to fitness

Spandrels/By-products - Traits that don’t affect fitness but are linked to other adaptations (e.g. human chins)

Noise - Random variation in a trait that doesn’t affect fitness

Exaptations “Co-adaptations” - A characteristic that didn’t arise as an adaptation, but was later co-opted for its function

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7
Q

How does inclusive fitness and reciprocation solve the problem of altruism and other prosocial instincts

A

Lose something of low value to you by altruism but later gain something of high value to you by reciprocation

  • This increases the collective fitness of the population
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8
Q

What is the social theory of intelligence in evolution

A
  • A socially demanding context
  • Development of general problem-solving skills in order to:
  • Maximise personal fitness in this context

Examples:

  • Remembering personal interactions
  • Deception
  • Planning
  • Arguing and getting your way
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9
Q

What is the theory of sexual selection, what sort of traits are selected for this process

A
  • Selection pressure on traits of health and parental investment

Physical traits - signalling health, determining attractiveness

Behavioural traits - signalling competitiveness & parental investment

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10
Q

Describe how twins and siblings can be compared to estimate the heritability of traits

A

Differences in correlations for some phenotype between siblings/twins -> used to estimate genetic variability (A) & environmental variability (C)

R(MZa)/R(MZt) = A/(A+C)

  • If poor involvement of environment, approaches 1
  • If large involvement of environment, approaches 0.5 or lower
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11
Q

Describe the quantitative genetic analysis approach to studying psychological traits and the problems associated with it

A
  • Quantitatively characterise a behavioural phenotype in a given population
  • Examine the changes in the phenotype distribution in sets of progeny
  • Statistically infer the number of genes responsible for the phenotype
  • If phenotype was due to one gene, it would sort itself into a Mendellian inheritance pattern
  • E.g., rats good at maze and rats bad at maze bred together

Problems:

  • Results do not identify individual genes
  • Necessity for large pedigrees & cross-mating makes human studies unlikely
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12
Q

Describe the single gene approach to studying psychological traits and the problems associated with it

A
  • Some phenotypes have neurobiological bases (e.g., alcohol dehydrogenase for alcoholism)
  • To test -> test people with multiple alleles of the gene
  • E.g., people with “Met/Met” allele had better working memory than those with “Met/Val” & “Val/Val” genotypes

Problems:

  • Ignores epistasis (the background contribution of other genes)
  • Redundancy & Pleiotrophy
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13
Q

Describe the 4 main points at which genetic activity can be modulated by environmental factors

A
  1. Transcriptional control - onset of transciption
  2. Translational control - translation rate & mRNA lifespan
  3. Post-translational control - protein activation, feedback inhibition (protein inhibits transcription of its own gene)
  4. Natural selection of phenotype
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14
Q

Describe the 4 models of gene-environment interactions

A
  1. Genetic and environmental effects might be independent but additive
  2. Some environmental effects might only be seen under certain genetic conditions
  3. Some genetic effects might only be seen in certain environments
  4. Some genetic effects might influence the environment to which an individual is exposed (alcoholics having alcohol in the house)
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15
Q

Describe the epigenetic modification of gene expression

A

Where the environment changes the functional genotype of the cell

  • The DNA is not altered
  • It is chemically modified to be expressed more/less
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16
Q

Describe the non-genetic processes and mechanisms by which maternal care patterns can be inherited from generation to generation

A

E.g., arched-back nursing and licking & grooming in rodent dams produce offspring that are less fearful

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17
Q

How do nerves communicate with each other across synapses

A
  • Action potential travels down the axon
  • Releases vesicles of neurotransmitters into the synaptic gap
  • Neurotransmitters bind to receptors on the post-synaptic neuron
  • Change in form causes membrane to reach threshold
  • Another action potential is caused
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18
Q

What is the rate law and what is spatial & temporal summation

A

Rate law- the strength of a stimulus is represented by the rate of firing of an axon

Temporal summation - sufficiently fast inputs from one neuron

Spatial summation - synchronised inputs from multiple synapses in a small region

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19
Q

What are the different types of neurotransmitters

A

Cholines - Acetylcholine (bind to nicotinic receptors)

Lipids - Anandamides (bind to cannabanoid receptors)

Amino acids - Glutamate & GABA

Monoamines - Dopamine, Noradrenaline, Serotonin

Peptides - Endorphins (bind to opioid receptors)

Nucleosides - Adenosine

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20
Q

What are the different ways in which drugs can act as agonists and antagonists

A

Agonists:

  • Drug that mimics an NT & activates an action potential
  • Enhance the release of NT
  • Blocking the reuptake of NT
  • Blocking enzymes that destroy NT

Antagonists:

  • Blocks the post-synaptic receptors to stop action potentials from occurring
  • Opposite of agonist
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21
Q

What chemical systems do these drugs affect;

nicotine, cocaine, amphetamine, heroin, ecstasy, alcohol

A 
Nicotine - Acetylcholines
Cocaine - Dopamine
Amphetamine - Dopamine
Heroin - Endorphins
Ecstasy - Serotonin
Alcohol - GABA
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22
Q

What neurochemical systems do these drugs affect and what are they mostly used for clinically;
ritalin, antipsychotics, benzodiazepines, SNRIs, SSRIs, beta-blockers, donezipil, morphine, ketamine, cannabidiol

A

Ritalin - dopamine, ADHD

Antipsychotics. - dopamine, schizophrenia

Benzodiazepines - GABA, sedatives

SNRIs - noradrenaline, depression

SSRIs - serotonin, depression

Beta-blockers - noradrenaline, heart problems/anxiety

Donezipil - acetylcholines, dementia

Morphine - endorphins, painkiller

Ketamine - glutamate, sedative

Cannabidiol - anandamides, epilepsy, Parkinson’s

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23
Q

What do these terms mean;

Homeostasis, distress, eustress

A

Homeostasis - the body’s tendency towards a stable equilibrium

Distress - Stress with negative implications

Eustress - Stress that is beneficial to health

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24
Q

Describe the sympathetic and parasympathetic nervous system response to stress and how they are regulated

A

Sympathetic system - stimulates tissues, dilates pupils, elevates heart rate etc.

Parasympathetic system - “calms everything back down”, opposite effects to the sympathetic system

Regulation:
Alpha 2 autoreceptors uptake NA from the synaptic gap

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25
Q

Describe the central noradrenergic response to stress

A

Central noradrenergic = Brain

  • Locus coeruleus (LC) activity is associated with arousal, vigilance and reaction speed
  • LC activity increased when in fear/pain
  • Also important for memory, attention and sensory processing
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26
Q

Describe the HPA axis and how it is regulated

A

Hypothalamus-pituitary-adrenal axis

  1. Hypothalamus releases CRH, which travel to the anterior pituitary
  2. Anterior pituitary releases ACTH, which travels to the adrenal glands
  3. Adrenal glands release glucocorticoids
  • Positive feedback loop (CRH -> noradrenaline -> CRH)

Regulation:
Stimulation of glucocorticoid receptors, inhibiting the HPA axis

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27
Q

Describe the pattern and effects of HPA axis activation in depression

A
  • Depression is associated with chronically elevated levels of glucocorticoids
  • Caused by a loss of negative feedback inhibition over the HPA axis
  • Hippocampus is smaller in people with depression
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28
Q

Describe Schacter and Singer’s two-factor theory of emotion

A
  1. Perception of fearful stimuli
  2. Acitvation of sympathetic nervous system
  3. Awareness of psychological state/arousal
  4. Cognitive appraisal of the situation to determine the most appropriate emotion
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29
Q

How can we distinguish fear from anxiety

A

Duration, focus, effect

Fear - brief, present, specific threat, facilitates escape

Anxiety - prolonged, future focussed, poorly defined threat, promotes avoidance, hypervigilance and caution

30
Q

Describe the limbic system (8 structures)

A
  • A series of structures linking the hypothalamus and the cortex (important for emotion and memory)

Comprised of:

  • Cingulate gyrus
  • Hippocampus
  • Parahippocampal cortices
  • Amygdala (sends outputs to subcortical structures that control emotional arousal)
  • Fornix
  • Septal nuclei
  • Mammilary bodies
  • Anterior thalamus
31
Q

Describe LeDoux’s “low vs high road” model of fear conditioning

A

Low road - fear condition can be a rapid process that doesn’t require conscious appraisal
emotional stimuli -> sensory thalamus -> amygdala -> emotional responses

High road - learning about complex stimuli (e.g. context) requires longer processing time
emotional stimuli -> sensory thalamus -> sensory cortex -> amygdala -> emotional responses

32
Q

What is the neurological basis for the relapse of fear after fear extinction

A

“Competing memory effect”

Following extinction, the CS participates in two different associations
- CS -> US and
- CS -> no US
The meaning of the CS becomes ambiguous

The original CS -> US association is never lost, explaining relapse of fear after fear conditioning

33
Q

Describe the main behavioural and pharmacological treatments for anxiety

A

Behavioural:

  • Exposure therapy
  • CBT

Pharmacological:

  • Benzodiazepines (GABA A inhibitors are sedative)
  • SSRIs
  • Beta blockers (blocks hyperarousal symptoms)
34
Q

What is the evidence that dopamine mediates reinforcement by natural rewards and drugs

A
  1. Dopamine is release by natural rewards
  2. Reinforcing effects are decreased by dopamine antagonists
  3. Reinforcing effects of brain stimulation are modulated by drugs that modulate dopamine
  4. Stimulating dopaminergic neurons is reinforcing
35
Q

What is the evidence that dopamine mediates reinforcement induced by ICSS

A

ICSS - Intercranial self-stimulation

  1. Drugs that increase dopamine (cocaine) increase ICSS
  2. Dopamine antagonists decrease ICSS
36
Q

What is the anhedonia hypothesis

A
  • Dopamine antagonists reduce ICSS responding as they reduce the pleasure of the reward
  • Tested by free-feeding: dopamine had no effect on consumption
37
Q

What is the evidence that dopamine acts as a reward signal, and activates reinforced behaviours

A

Acts as a reward signal:

  • CS (tone) was paired with US (food) for rats
  • Dopamine spiked in response to CS, not the US, even when no food was delivered after the tone

Activates reinforced behaviours:

  • Dopamine depleted rats preferred free-access lab chow as opposed to high-value chocolate which required a lever press (which was a reinforced behaviour)
  • When amphetamine (dopamine agonist) was given to rats, they pressed the lever for much longer than control rats
38
Q

What is the evidence that dopamine is important for the motivation to seek reward

A

Deep brain stimulation to dopamine reward circuitry in depressed patients -> spontaneous “reward-seeking” behaviour

39
Q

What are the differences between pharmacological tolerance and behavioural tolerance

A

Pharmacological tolerance:

  • Acute: active receptors temporarily shut down and are recycled back into the post-synaptic neuron
  • Chronic: repeated receptor stimulation causes the neuron to downregulate receptor production

Behavioural tolerance:

  • Heroin addicts overdose more in unfamiliar environments
  • People feel more drunk if consuming a novel ‘blue’ drink over a familiar drink of equivalent alcoholic content
40
Q

What is the standard pattern of affective dynamics and how does this model explain tolerance and withdrawal

A

Peak A - Initial peak of hedonia when stimulus occurs
Adaptation phase - Gradual decrease of hedonia
Steady level - Contant decreased hedonia while stimulus lasts
Peak B - Initial trough of hedonia when stimulus stops
Decay of B - Return of hedonia back to normal levels

Tolerance - Peak A and feelings of euphoria decrease after many stimulus presentations (pharmacological tolerance)

Withdrawal - Peak B and feelings of withdrawal increase after many stimulus presentations (behavioural tolerance)

41
Q

Which important brain regions for reward and motivation are activated by drug cues

A

Cannabis cues activated the:

  • Ventral striatum (Nacc)
  • Insula cortex
  • Amygdala
42
Q

What is meant by drug use causing hypofrontality

A
  • Loss of grey matter in the frontal regions of the brain in cocaine addicts
  • A higher weekly cocaine consumption was associated with a decrease in prefrontal cortex activation
  • This affects mood, behaviour and motivational impulses
43
Q

Explain Nora Volkow’s model of the addicted brain

A

Non-addicted brain:
- Reward (Nacc), control (mPFC), memory (limbic system), and drive (OFC) all interact to produce an output

Addicted brain:
- Reward, drive and memory signals are stronger, and there is a lack of control contributing to the outcome

44
Q

Describe the main internal hunger and satiety signals from the body

A
  • Medulla is the control centre and compares blood glucose levels against a set point to determine whether to induce hunger or satiety

Leptin - released from fat cells, causes decreased appetite and higher metabolism

Ghrelin - released from the stomach, stimulates appetite and inhibits metabolism

Insulin - released from the pancreas, decreases blood glucose levels by causing tissues to take up glucose from the blood

45
Q

Describe the major actions of hunger and satiety signals in the hypothalamus and how they relate to “orexia” and “anorexia”

A
  • Ghrelin to the ARC stimulates LH and inhibits PVN, which stimulates appetite “orexia”

Leptin/Insulin to ARC stimulates PVN and inhibits LH, which inhibits appetite “anorexia”

ARC = arcuate nucleus of the hypothalamus
LH = lateral hypothalamus
PVN = periventricular nucleus
46
Q

How does the mesolimbic dopamine system contribute to appetite driven by external cues

A

Triggers internal and external cues for appetite

Internal - physiological need for nutrients

External - normative cues (plate size, portions) and sensory cues (smell/sight etc. of food)

47
Q

What role does the OFC play in appetite

A

Important for linking reward to hedonic experience and then to motivation to seek reward

48
Q

What effect does highly palatable food have on eating

A

They mask the effects of satiety (i.e. people eater a larger volume of food if it is highly palatable)

49
Q

What are the principal effects of testosterone on sexual behaviour in males

A

Testosterone within the critical prenatal period causes:

  • enlargement of the SDN
  • changes the synaptic density of neurons

Blocking the action of testosterone in the SDN:

  • blocks male copulatory behaviours
  • reduces sex drive
50
Q

What are the principle effects of oestrogen on sexual behaviour in females

A
  • Controls a females willingness to mate
  • phases of the menstrual cycle and subsequent changes in oestrogen levels affected the percentage of female initiated sex in rat studies
51
Q

What role does the dopaminergic system play in attraction and romantic love

A

Dopamine is released during sex:

  • Causes strong “stimulus salience” effects
  • Rewarding effects of the feeling (even non-sexual encounters)
  • Motivational aspects
  • Psychological aspects
  • Mesolimbic system is activated when shown photos of partners/family/friends… intensity of activation was associated with strength and duration of relationship
52
Q

What are the major psychological effects of oxytocin and vasopressin

A

Both have major effects on:

  • Attachment and trust
  • Social cognition
  • Fear and anxiety

In prarie vole study:

  • Oxytocin was responsible for female attachment
  • Vasopressin was responsible for male attachment
53
Q

What is SCU

A

Sociocognitive understanding

The measure of the development of the:

  • capacity to employ and accept psychological explanations
  • capacity to predict behaviour on psychological grounds
  • Includes emotional understanding (EU), theory of mind (ToM) and false belief (FB) understanding
54
Q

What are two factors that influence the development of SCU

A
  • Linguistic competence

- Conversational environment (mental-state discourse and mind-mindedness)

55
Q

What is mental state discourse and mind-mindedness

A

Mental state discourse - reflects speculation of what others are thinking, implanting thoughts into the child mind
e.g., “The dinosaur wants to play too!”

Mind-mindedness - acknowledges subjective perspective and highlights that the child is their own person
e.g., “What would you do?”

56
Q

What predicts/what are the outcomes of SCU

A

Predictors - emotional, environmental, person-specific and family factors

Outcomes - prosocial behaviours, popularity, aggression, education

57
Q

What is linguistic competence and conversational environment

A

Linguistic competence - the language required to cognitively rationalise what is occurring

Conversational environment - quality and quantity of speech in environments

58
Q

What is false-belief understanding and the habituation paradigm

A

False belief - a milestone of SCU, the distinction between the real state of the world and the represented state of the world (I.e. realisation of the self and other)

Habituation paradigm - a particular action that indicates mental processes (e.g. child sees something surprising so they look at it for longer)

59
Q

What is theory of mind comprehension and its 6 domains

A

ToM - the ability to speculate thoughts, feelings, behaviours and desires of others and realise that they differ from their own

6 domains:

  • Diverse desires
  • Diverse beliefs
  • Knowledge access
  • False belief
  • Belief-base emotion
  • Real vs. apparent emotion (when someone says they’re fine but in reality, they aren’t fine)
60
Q

At what age does false-belief understanding develop? Give experiment example

A

Develops at between ages 3.5-5 years old

Sally-Anne experiment
0-4 years: Sally will look in the box (where the ball is)
4+ years: Sally will look in the basket (where the ball was)

61
Q

Describe the stages of vision and hearing development

A

Vision:
0-4 months - eyes wander, muscles not fully developed, high contrast sensitivity, 15-25cm focal range
5-8 months - Depth perception and colour vision well developed
9-12 months - Ability to judge distance, throwing things

Hearing:
3rd trimester - Inner ear fully developed, fetus responds to mothers voice, EOAE (evoked otoacoustic emmision) tests baby’s hearing

62
Q

What are the stages of grip development

A
  1. Fist grip - 2-5/6 months, holds object
  2. Four finger grip - 7-10 months, grip and release
  3. Pincer grip - can pick up small objects with thumb and forefinger
63
Q

What are the two stages of motor-development

A
  1. Cephalon-caudal (head to toe)
  2. Proximo-distal (midline to extremities)
    Each skill builds upon another
64
Q

What are Piaget’s 4 cross cultural sequences of thought development

A
  1. Sensorimotor - immediate sensory impressions and actions
  2. Preoperational - represent world with images and words
  3. Concrete operational - can manipulate representations and logically reason about concrete events
  4. Formal operational - able to logically reason about concrete + abstract events
65
Q

What is egocentric thinking and object permanence

A

Egocentric thinking - child is unable to see a situation from another perspective from their own, thinks everyone has the same memories as them

Object permanence - the understanding that objects continue to exist even when not directly observed

66
Q

What are the types of language and their ages

A
  1. Expressive - crying in contingent tones
  2. Receptive - receive/understand communication
  3. Vocalisations - saying words
67
Q

Whatis cognitive empathy

A

The understanding that someone might feel a certain way from the situation rather than emotional cues

68
Q

What is Eisenberg’s postulation of empathy and arousal

A

Empathy –> well/poor modulated arousal
Well modulates arousal –> sympathy
Poorly modulated arousal –> personal distress, no sympathy

69
Q

What is emotional contagion and personal distress

A

Emotional contagion - other peoples emotions tiggering the same emotions and behaviours in you
Personal distress - egocentric

70
Q

What are the developmental stages of empathy

A

10-12 months - egocentric
12-24 months - increased interventions/comfort actions
3 years - understand others emotions differ from own
5+ years - understanding of people as continuous

71
Q

What happens at 9 months in terms of anxiety/behaviour

A
  • Babies demonstrate wariness/anxiety
  • Cognitive milestone of object permanence
  • Only want mum and dads care (emblematic of strong relationship development)
72
Q

Outline the differences between empathy and sympathy

A

Empathy - affective response that stems from comprehension of another’s mental state (requires ToM)

Sympathy - affective response for someone else’s feelings

Psych2015 (3 decks)

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