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Year 1 Biological Psychology > Prof Balgrove > Flashcards

Prof Balgrove Flashcards

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1
Q

Gene manipulation: Monoamine oxidase type a knockout mice

A
  • Gene codes for an enzyme in mitochondria of cells
  • Enzyme breaks down dopamine, norepinephrine and serotonin
  • Enzyme is not produced in knockout mice, who have increased aggression, but no change in motor activity or sexual activity
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2
Q

Hormone manipulation: Lab controlled experiments

A
  • Testosterone gel can cause men to make intuitive decisions (n=2430
  • 100 mg T in a topical gel spread onto upper arms and chest (or placebo)
  • T administered @9am, tested from 2pm onwards
  • Took the cognitive reflection test which estimates the capacity to override incorrect intuitive judgements with deliberate correct responses
  • Testosterone administered reduced CRT scores
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3
Q

Prenatal development stages

A

Germinal period:

  • 0-2 weeks
  • Time from conception to implantation

Embryonic period:

  • 2-8 weeks
  • heartbeat begins
  • Recognisable body periods
  • Sexual differentiation begins

Fetal period:

  • 9th week-birth
  • Last 3 months
  • Rapid growth of body and brain
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4
Q

Mechanisms of neural development

A
  • Neural proliferation
  • Neural differentiation
  • Neural selection and migration
  • Synaptogenesis and synaptic maintenance
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5
Q

What is synaptogenesis/

A
  • Creation of large numbers of synapses

- Number of synapses increases 10 times in the first year

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6
Q

Infancy brain growth

A
  • 75% of adult size
  • Most growth is in size/complexity of neurons
  • Not addition of new neurons
  • Environment affects brain development
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7
Q

Infancy brain plasticity

A

2 years - double synaptic connections than adult brain

3 years - triple synaptic connections than adult brain

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8
Q

Childhood brain deevelopment

A

First 10 years - brain twice as active as adult’s

2nd decade - growth levels off and pruning begins apart from visual cortex (less synaptic connections)

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9
Q

What is pruning of synapses?

A
  • Elimination of synapses
  • Number of connections between neurons are reduced
  • Begins around 1 years old
  • Pruning complete at 10 years of age in visual cortex
  • Continues in pre-frontal cortex
  • Number of synapses in adulthood 40% less than in peak during childhood
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10
Q

Myelination of the brain

A
  • Baby’s brain is relatively unmyelinated
  • Myelination happens in 4th week of pregnancy
  • at birth spinal chord and medulla is myelinated: support basic life functions so need to be quick
  • During first year there is an increase in myelination of the basic sensory and motor systems
  • Later on tge connections between cortical, subcortical areas and corticortical connection are myelinated
  • Increase in white matter until teens
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11
Q

What is grey matter

A
  • Neuron cell bodies
  • Dendrites
  • myelinated and non-myelinated axons
  • Glial cells
  • Synapses
  • Capillaries
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12
Q

What is white matter

A
  • Deeper in the brain
  • Fewer cell bodies
  • Mainly long-range myelinated axons
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13
Q

What is necrosis?

A
  • Unplanned cell death

- Assassination

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14
Q

What is apoptosis?

A
  • Planned cell death

- Suicide

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15
Q

What is neurodegeneration?

A
  • Related to apoptosis and necrosis
  • E.g. dementias
  • Can be from physical trauma e.g. stroke
  • Can also be when mental go untreated e.g. depression
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16
Q

Atrophy of the brain due to ageing

A
  • Neurons die with age due to irreversible damage
  • No neurotransmission
  • Can continue to still be alive and increase in complexity
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17
Q

Structural changes: Dendritic length and complexity

A
  • Age-related regression in dendritic branches and spines of pyramidal neurons of the prefrontal superior temporal and precentral cortices
  • Dendrites can continue to increase in length with age (up until a certain point), but they lose complexity
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18
Q

Structural changes: White matter loss

A
  • Age effects

Diffusion tensor imaging:

  • Allows for in vivo examination of white matter microstructure
  • Greater difference between young and old in anterior as opposed to posterior corpus collosum
  • Greater difference in frontal white matteer than in temporal, parietal or occipital suggests anterior to posterior gradient of ageing
  • Greatest reduction of blood flow and loss of neural tissue in frontal region
  • Decline in memory
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19
Q

Functional changes: Different brain activity

A

Reductions of activity in some brain regions and networks:

  • Old may have less ability to recruit
  • Old may fail to engage adequate strategies
  • Dedifferentiation

Increases of activity:

  • Non-specific recruitment that may have nothing to do with task performance
  • Reduced inhibition due to loss of white matter?
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20
Q

Mechanisms of cognitive ageing: Inhibitory deficit hypothesis

A
  • Decreased ability to suppress irrelevant information that interferes with ongoing processes
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21
Q

Mechanisms of cognitive ageing: Compensation hypothesis

A
  • Increased neural activity or recruitment of additional brain regions to counteract dysfunction
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22
Q

What are Circadian rhythms

A
  • Based on biological rhythms
  • Biological activities that rise and fall along a 24-hour cycle
  • Triggered at appropriate times by brain structures that act as biological clocks e.g. suprachiasmatic nucleus
  • Set by factors in the environment, particularly light
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23
Q

What are ultradian rhythms?

A
  • Biological rhythms that are less than 24 hours

- E.g. sleep cycles are ultradian and last 90 mins

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24
Q

Role of endogenous pacemakers and exogenous zeitgebers

A
  • Main pacemaker for endogenous circadian rhythms is the suprachiasmatic nucleus (SCN)
  • Small group of cells located in the hypothalamus
  • Called SCN because it lies just above the optic chiasm, therefore it can receive info directly from the eye and the rhythm can be rest by the amount of light entering the eye.
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25
Q

Sleep-Wake circuitry

A
  • Suprachiasmatic nucleus is the master clock
  • If damaged the circadian rhythm is abolished
  • Retina –> SCN –> pineal gland
  • Pineal gland produces melatonin
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26
Q

What is cortisol

A
  • Increases under conditions of stress
  • Increases endogenously near the end of each night
  • Increase might be related to memory consolidation
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27
Q

How is temp related to a circadian rhythm

A
  • Temp follows a circadian rhythm

- Influences alertness rhythm and falling asleep and waking up

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28
Q

What is a zeitgeber?

A
  • A stimulus that resets the biological clock (e.g. bright light, exercise, temperature)
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29
Q

How do we set our biological clock?

A
  • Without time cues resetting the the clock each day sleep occurs a little later each day
  • Natural rhythm is a little above 24 hours
  • Rhythm is controlled by internal zeitgebers
  • If time cues remain absent, free-running occurs
  • Sleep and wake periods change greatly with each successive day
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30
Q

What is melatonin?

A
  • Hormone secreted by the pineal gland that controls sleep and wake cycles
  • Secreted during darkness
  • Signals night time
  • Leads to drowsiness and decrease in body temperature
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31
Q

How do we assess the circadian pacemaker

A
  • Onset of melatonin secretion under dim light condition s( dim light melatonin onset or DLMO) is the single most accurate marker for assessing the circadian pacemaker
  • DLMO is useful for determining whether an individual is entrained (synchronised) to a 24 hour light/dark cycle or is in a free-running state
  • DLMO is also useful for assessing phase delays or advances of rhythms in entrained individuals
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32
Q

Atkinson and Shiffrin’s multi-store memory model (1968)

A
  • Memory is a series of information that moves through different stores
  • Info is detected by sensory organs and if attended to is moved to short term memory
  • Info is moved to long-term memory if rehearsed
  • If not rehearsed the info is lost due to decay or displacement
  • Simplistic model
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33
Q

What is sensory memory?

A
  • Info not immediately attended to is held briefly in a temporary ‘buffer’, making it possible to attend too some of it a bit later
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34
Q

What is sensory memory for vision called?

A

Iconic memory

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35
Q

What is sensory memory for audition called?

A

Echoic memory

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36
Q

What is sensory memory for touch called?

A

Haptic memory

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37
Q

Iconic memory: Capacity

A

That of the visual system

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38
Q

Iconic memory: Duration

A

0.3 to 1.0 seconds

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39
Q

Iconic memory: Processing

A

No additional beyond raw perceptual processing

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40
Q

Echoic memory: Capacity

A

Unknown

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41
Q

Echoic memory: Duration

A

3-4 seconds

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42
Q

Echoic memory: Processing

A

None additional beyond raw perceptual processing

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43
Q

Short-term memory: Capacity

A

7 plus or minus 2 ‘chunks’ (of information) of information

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44
Q

Short-term memory: Duration

A

18-20 seconds (average)

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45
Q

Short-term memory: Processing

A
  • To hold info in STM it is often encoded verbally
  • Strategies such as visualisation may also be used
  • Strategies make it possible to ‘rehearse’ the info
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46
Q

What is a ‘chunk’ of information?

A

Single letters such as “GJK” are each a chunk, but recognisable words like “CAR” are a single chunk

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47
Q

How can information be held in short-term memory?

A
  • Maintenance rehearsal
  • Repeating the information silently or aloud so that it is recalled immediately when needed
  • Does not add meaning to info
  • Unlikely to be remembered when it is no longer being repeated
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48
Q

How is information in long-term memory represented?

A
  • Represented as changes in brain wiring

- In the ‘conductivity’ of existing synapses, and in the formation of new synapses and destruction of old ones

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49
Q

Long-term memory: Capacity

A

Virtually unlimited

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50
Q

Long-term memory: Duration

A

Up to a lifetime

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51
Q

Long-term memory: Proocessing

A

Information is organised according to meaning and is associatively linked

52
Q

Type of rehearsal in LTM

A
  • Elaborative rehearsal
  • Involves the process of expanding upon new info by adding to it or linking it to what one knows
  • Makes it more meaningful (for encoding and retrieval)
53
Q

Craik and Lockhart’s (1972) levels of processing model

A
  • Deeper levels of analysis produce more elaborate, longer-lasting, and stronger memory traces than shallow levels of analysis
54
Q

What is working memory?

A
  • System for actively maintaining and manipulating information
  • Fundamental to the performance on cognitive tasks and day-to-day activities
  • Conceptualised as an active workspace because it is closely linked with the voluntary allocation of attention
  • Engages two anatomically and functionally distinct attention systems in the human brain (dorsal frontoparietal system and ventral frontoparietal system)
55
Q

What is the dorsal frontoparietal system?

A

Mediates the top-down guided voluntary allocation of attention to locations or features

56
Q

What is the ventral frontoparietal system?

A

Detects unattended or unexpected stimuli, and triggers shifts of attention

57
Q

What is the fibrous tunic of the eye?

A
  • Outer layer
  • Provides protection
  • Comprised of the sclera and cornea
58
Q

What is the vascular tunic of the eye?

A
  • Middle layer
  • Provides nutrition
  • Comprised of the iris, the choroid, and the ciliary body
59
Q

What is the retina of the eye?

A
  • Inner layer
  • Provides transduction
  • Dark spot is the macula and fovea
  • Light spot is the optic nerve
  • Area of the retina is the optic disc (blind spot) - has no photoreceptors
60
Q

What is the choroid of the eye?

A
  • Highly vascular
  • Very thin
  • Lines entire surface of the sclera
  • Brown
  • Designed to prevent light rays from bouncing back out of the eyeball
  • Opens up at the rear of the eyeball permitting the passage of the optic nerve
  • Anterior part of the choroid is thicker which creates an internal muscular ring toward the front of the eyeball –> ciliary body
61
Q

What is the macula of the eye?

A
  • At its centre is the fovea
  • Is responsible for our sharp central vision
  • Humans and primates have one fovea
  • Certain bird species (e.g. hawks) are bifoviate
  • Dogs and cats have no fovea but a central band known as the visual streak
62
Q

What is Astigmatism?

A
  • Cornea is improperly shaped
  • Light entering the eye in not properly refracted
  • Inability of cornea to properly focus image onto the retina
  • Test for this by using a chart which has lines of different darknesses
63
Q

What is glaucoma?

A
  • When ciliary bodies in the eye clog up
  • Either by. improper drainage of waste or by excess of aqueous humour
  • Creates intraocular pressure
  • Peripheral vision is impaired
64
Q

What is iris albinism?

A
  • Lack of pigment in the iris

- Pinkish hue of the eye

65
Q

What is presbyopia?

A
  • Lens’ are old
  • “Old sight”
  • Inability of the lens to accommodate properly
  • Loss of elasticity in lens with age
66
Q

Anatomy of eye movement

A
  • 6 extraocular muscles attached to each eye and arranged in three pairs
  • Controlled by an extensive network of structures in the brain
67
Q

What are fixational eye movements?

A

-Small involuntary movements that occur during visual fixation

3 categories:

  • Microsaccade
  • Ocular microtremor
  • Ocular drift
  • Contribute to maintain visibility by continuously stimulating neurons in the early visual areas of the brain
  • In the absence of retinal jitter the visual percept rapidly fades out and may even completely disappear under certain conditions
68
Q

Fixational eye movements: Microsaccade

A

Miniature versions of voluntary saccades

69
Q

Fixational eye movements: Ocular microtremor

A

A constant, physiological, high frequency (peak 80Hz), low amplitude (estimated circa 150-2500nm) eye tremor

70
Q

Fixational eye movements: Ocular drift

A

Random movement of eyes through a visual angle of up to 5 minutes of arc

71
Q

What are saccadic eye movements?

A
  • Quick, simultaneous movements of both eyes in the same direction
  • The fastest movement of an external part of the human body; lasts from about 20 to 200 milliseconds
72
Q

What is smooth pursuit (eye movements)

A
  • Ability of the eyes to smoothly follow a moving objects
  • Visual animals can voluntarily shift gaze
  • Differs from the vestibulo-ocular reflex, which only occurs during movements of the head and serves to stabilise gaze on a stationary object
  • Most people find pursuit extremely difficult to initiate without a moving visual signal
73
Q

What are vergence eye movements?

A
  • Simultaneous movement of both eyes in opposite directions to obtain or maintain single binocular vision
  • The two eyes converge to point to the same object
  • Eye must rotate around a vertical axis so that the projection of the image is in the centre of the retina in both eyes
  • To look at an object closer by the eyes rotate towards each other –> convergence
  • To look at an object farther away they rotate away from each other –> divergence
  • Closely connected to accommodation of the eye = changing the focus of the eyes to look at an object at a different distance
74
Q

What is the vestibulo-ocular reflex?

A
  • Reflex eye movement that stabilises images on the retina during head movement
  • Produces an eye movement in the opposite direction to the head movement
  • Preserves the image on the centre of the visual field
  • Does not depend on visual input and works in total darkness or when eyes are closed
75
Q

What are the 3 semicircular canals?

A
  • Anterior
  • Posterior
  • Horizontal
  • In each vestibular organ
  • Function is to detect angular accelerations of the head
  • Canals are bi-directionally sensitive and approx mutually perpendicular to detect angular head movement in any direction
  • Signals from these cause relevant eye muscles to move
76
Q

What is the optokinetic reflex?

A

Allows the eye to follow objects in motion whilst the head remains stationary

77
Q

Outer segment of the retina

A

Houses molecular components for light absorption and generation of electrical signals

78
Q

Inner segment of the retina

A

Harbours machinery for protein synthesis and energy production

79
Q

What is the pigment in the outer segment of the retina?

A
  • Retinal
  • Light-sensitive derivative of vitamin A
  • Absorbs light photons and a cell membrane protein molecule (Opsin)
  • Opsin determines which wavelength will be absorbed
80
Q

Sequence of phototransduction

A
  1. Light strikes the retina
  2. The retinal molecule absorbs a photon
  3. The retinal is transformed (undergoes isomerisation), opsin is also transformed
  4. Generation of an electrical impulse which is transmitted through the optic nerve to the brain for processing

Takes a minimum of 5 photons to trigger a nerve impulse

81
Q

What are midget ganglion cells?

A
  • Receive input from midget bipolar cells

- Called midget because of the small sizes of their dendritic trees and cell bodies (either on or off centre)

82
Q

What are parasol ganglion cells?

A
  • Receive input from diffuse bipolar cells
  • Look like little umbrellas
  • Large size of dendritic trees and cell bodies
  • Larger receptive fields than midget ganglion cells
83
Q

What are photosensitive ganglion cells?

A
  • Contain their own photopigment (melanopsin)
  • Respond directly to light even in the absence of rods and cones
  • Project to the suprachiasmatic nucleus via the retinohypothalamic tract –> setting and maintaining circadian rhythms
84
Q

What is language?

A

The method of human communication, either spoken or written, consisting of the use of words in a structured and conventional way

85
Q

What is visual modalit?

A

Seeing words

86
Q

Where does visual modality occur?

A

Circuitry for seeing the statistical regularities of words forms develops within the ventral occipitotemporal cortex

87
Q

Where is the visual word form area situated?

A
  • Part of the left fusiform gyrus and surrounding cortex

- Right hand side of VWFA is part of the fusiform face area

88
Q

What is the visual word form area

A
  • Hypothesised to be involved in recognising lower-level shape images
89
Q

What is auditory modality and where is it performed?

A
  • Hearing words
  • In the primary auditory cortex
  • Primary and association auditory cortices process all sounds instead of just speech sounds
90
Q

What is the superior temporal sulcus?

A
  • Part of the temporal lobe
  • Has multi-sensory processing capabilities especially for social perception e.g. voices versus sounds, biological motion, moving faces versus moving objects, stories versus nonsense speech, gaze of others.
  • It is activated significantly more during human speech in comparison to other sounds
91
Q

What is phonology (language)

A

Sounds

92
Q

What is morphology (language)

A

forms of words

93
Q

What is semantics (language)

A

Meaning

94
Q

What is syntax

A

Grammer

95
Q

What is pragmatics?

A

Social use of speech

96
Q

What areas of the brain are involved in speech production?

A

Pars opercularis (Brod 44) and pars triangularis (Brod 45) of the inferior frontal gyrus (Broca’s area):

  • Production and articulation of language
  • Control of spoken/written/sign language production

Primary motor cortex - M1 (mouth area):

  • Controlling the physical movements of the mouth and articulators
  • Near the Broca’s area
97
Q

Historical models of brain language organisation: Modular/sequential processing

A
  • Proposed by Carl Wernicke in the 1870s
  • Expanded by Norman Geschwind in the 1960s
  • Based on language having two basic functions: comprehension (sensory/perceptual function), and speaking (motor function)
  • Localisation of speech is one of the weakest points of this models as Broca’s area is involved in comprehension
98
Q

What is Broca’s (non-fluent) aphasia?

A
  • Deficit in speech production but motor function intact
  • Aggrammatism (telegraphic speech, error in tense, number and gender)
  • Deficit in programming and initiating speech
  • Deficit in intonation and stress patterns
  • Comprehension relatively spared
99
Q

What is telegraphic speech?

A

Content words retained, function words and word endings used sparingly

100
Q

What is agrammatism?

A
  • Form of excessive aphasia

- Refers to the inability to speak in a grammatically correct fashion

101
Q

What is Wernicke’s (fluent) aphasia

A
  • Deficit in semantic processing, word salad output
  • Not deaf but might be related to hearing
  • Normal rate and rhythm of speech
  • Can also result in failure to understand non-speech sounds, such. as sounds of machinery

Paraphasias

  • Phonemic paraphasia: house for mouse
  • Semantic paraphasia: house for barn
  • Neologism: zaffle, fontrap (not in lexicon but follows correct syntax)
102
Q

What is conduction aphasia?

A
  • No info is processed from Wernicke’s region to the Broca’s region
  • fluent speech and intact comprehension
  • Deficits: oral reading, word repetition
  • Phonemic paraphasias
  • Transpositions of sound within a word e.g. velitision for television
103
Q

What us transcortical motor aphasia?

A
  • Similar to Broca’s aphasia (non-fluent speech but good comprehension)
  • echolalia = compulsive repetition but delays in initiation
  • Severely impaired writing ability
104
Q

What is transcortical sensory aphasia?

A
  • Similar to Wernicke’s aphasia (fluent speech and poor comprehension)
  • Echolalia and semantic paraphasia (production of unintended syllables, words, or phrases during the effort to speak)
105
Q

What is the lexical route?

A

The process whereby skilled readers can recognise known words by sight alone, through a ‘dictionary’ lookup procedure

106
Q

What is the nonlexical or sublexical route?

A

The process whereby the reader can ‘sound out’ a written word

107
Q

What is dual route theory

A
  • Different lesions in the nonlexical or lexical routes can cause different types of dyslexia
  • Different rates of occurrence between different languages
108
Q

What is EEG (electroencephalograph)

A
  • Measures average electrical activity of local set of cortical neurons
  • Measured as electrical potential differences across the scalp (also called brain waves)

Alpha: medium fq and amplitude
Beta: high fq and low amplitude
Theta: low fq and high amplitude
Delta: very low fq and high amplitude

109
Q

Stages of sleep

A

Awake: beta waves
Drowsy: alpha waves
Stage 1: theta waves appear (light sleep)
Stage 2: Sleep spindles and K complexes (asleep but may respond to some events such as noise)
Stages 3 and 4 (slow wave sleep): delta activity (very deep sleep, non-responsive to most stimuli and slow to wake)

110
Q

What is REM sleep?

A
  • Rapid eye movement sleep
  • Begins 70-90 minutes into the sleep cycle
  • Increased heat rate, darting eyes, twitching hands, fee and face, erection and clitoral enlargement
  • On EEG: resembles waking state, irregular, low amplitude and high fq, sawtooth waves, and theta waves
  • Dreaming: mostly in this stage of sleep
  • No muscle tone –> paralysed
111
Q

Hypothalamic and brain stem sleep regulation: wakefulness

A
  • Activation of the ascending reticular activating stem
  • This arousal system projects to the limbic system and cortex by two routes (ventral and dorsal)
  • Active during wakefulness but inactive during sleep, especially during REM
112
Q

Hypothalamic and brain stem sleep regulation: Wake-promoting pathways (neurotransmitter)

A

Serotonin - raphe nuclei
Dopamine - periaqueductal grey and VTA
Norepinephrine - locus coeruleus
Acetylcholine - pons and basal forebrain
GABA - also in basal forebrain, reducing activity in inhibitory neurons in the cortex –> increased cortical activity

113
Q

Hypothalamic and brain stem sleep regulation: Sleep

A
  • GABAergic neurons in the hypothalamus inhibit all the wake-promoting brain regions ensuring that all arousal systems are inhibited in a coordinated fashion
  • Inhibition of the arousal system causes sleep
114
Q

Why do we sleep hypothesis: Restoration

A
  • Sleep helps repair normal wear and tear on body and brain
  • Restores homeostasis
  • REM = brain growth, repair and reorganisation
  • SWS = bodily growth and repair, flushing out neurotoxins
  • Restoration also occurs outside of sleep and the degree of physical exertion is not proportionate to the amount of additional sleep
115
Q

Why do we sleep hypothesis: Survival value

A
  • Stops people from going out when low light puts them at risk for predators
  • Outdated and limited scope
116
Q

Why do we sleep hypothesis: Consolidation

A
  • Processing of information acquired during the day (i.e. strengthening the neural connections, combining relevant info into a coherent whole).
117
Q

What does sleep deprivation affect?

A
  • Severe sleep deprivation hurts virtually all aspects of functioning
  • Increases stress hormone cortisol
  • Can lead to death in animal studies
  • Ill health (diabetes, heart disease, cancer)
  • Complex tasks are least affected, and long boring tasks are most affected
118
Q

Why do we dream hypotheses: Activation-synthesis hypothesis

A
  • Dreams are the brain’s attempt to make sense of random patterns of neutral activity generated during sleep
  • Explains physiological basis for bizarre dream imagery
  • An example of an epiphenomenal view, in contrast to functional views
119
Q

Why do we dream hypotheses: Virtual reality problem-solving

A
  • Practice responses to threats from the environment
120
Q

Why do we dream hypotheses: Reflecting or part of memory consolidation

A
  • Dreams being related to memory consolidation, possibly for emotional and social memory
121
Q

What is the epiphenomenal view?

A

Dreams have no function and no adaptive effects. Dreams are decorative ‘spandrels’

122
Q

Dyssomnias: Insomnia

A
  • Difficulty initiating or maintaining sleep lasting for at least one month
  • Can be caused by many factors (stress, alcohol use, learned abnormal sleep patterns)
123
Q

Dyssomnias: Hypersomnia

A
  • Chronic condition marked by excessive sleepiness
124
Q

Dyssomnias: Apnoea

A
  • Repeated stopping of breathing during sleep
  • Severe apnoea had >30 times per hour
  • May be due to physical reasons in the trachea or due to signals not being sent by the brain
125
Q

Dyssomnias: Narcolepsy

A
  • Rare disorder characterised by sudden extreme sleepiness
  • Person suddenly falls into sound sleep –> usually REM
  • May be due to orexin/hypocretin deficiencies
  • May be genetic

Year 1 Biological Psychology (3 decks)

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