Biopsych 2 Flashcards

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1
Q

What is localisation of function?

A

The principle that specific functions have specific locations within the brain

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2
Q

What is Franz galls theory of phrenology?
What did Pierre flourens do?

A

The study of the structure of the skull to determine a persons character and capacity
Used animal experiments to demonstrate main divisions of the brain were responsible for different functions.
Since the 19th cent, techniques have grown considerably

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3
Q

What is the motor cortex:
Role
Location

A

Responsible for generation of voluntary movements
Located in frontal lobe along pre central gyrus
Motor cortex on each side of brain- left responsible for muscles on right vice versa
Diff parts of motor cortex control diff body parts and they are logically offered (eg part that control foot is next to part that controls leg)

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4
Q

What is the somatosensory cortex?
Located?

A

Detects sensory events in diff parts of the body
Located in parietal lobe along the post central gyrus
Uses sensory info from skin to produce sensations of touch pressure pain temp and localises it to specific regions of body
Like motor cortex, one on each side and cross wired

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5
Q

What is the post central gyrus?

A

Area of cortex dedicated to processing of sensory info related to touch

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6
Q

where is the primary visual center of the brain?
where does visual processing actually begin? then where does it go?

A

in the visual cortex in the occipital lobe. visual cortex spans both hemispheres (left receives info from right vf vice versa)
begins in retina where light strikes photoreceptors. nerve impulses are then transmitted to brain by optic nerve
some nerve impulses then travel to parts of brain to be involved in coordination of circadian rhythms but most terminate in thalamus which passes info onto visual cortex

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7
Q

what is the auditory center? where is it? describe the auditory pathway

A

concerned with hearing
mostly lies within temporal lobes on both sides in the auditory cortex.
pathway starts in cochlea where sound waves are converted to nerve impulses which travel to auditory cortex by auditory nerve
first stop is brain stem where basic decoding happens, then thalamus where further processing occurs. ends at auditory cortex which recognises sound and generates response

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8
Q

what are the 2 language centers?

A

broca’s area and wernicke’s area

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9
Q

what is broca’s area?

A

posterior portion of left frontal lobe
critical for speech production
discovered by paul broca due to patient who could only say ‘tan’ but could understand speech. also studied others with similar problems and lesions in left frontal hemisphere

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10
Q

what is wernicke’s area?

A

posterior portion of the left temporal lobe???
critical in speech understanding
his patients could speak but not understand

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11
Q

what did wernicke propose?

A

language involves separate motor and sensory regions.
motor region in brocas is close to area that control mouth, tongue, vocal cords.
sensory region in wernicke’s is close to part of brain responsible for auditory/visual input
there is a neural loop between brocas and wernickes

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12
Q

evaluation of localisation of function and language centres

A

-
not everyone agrees functions are localised eg equipotentiality theory (lashley 1930) suggests basic motor and sensory functions are localised but more complex arent. says intact areas of cortex can takeover responsibilities following injury. says effect of damage is determined by extent not location

research suggests how areas communicate is more important that which region controls specific process. wernicke claimed areas are interdependent. eg french neurologist described case where loss of ability to read led to damage to connection between visual cortex and wernickes area. suggests complex behaviours move through diff structures before response produced. damage to connection between any 2 points in this process leads to impairments similar to damage to localised brain region for that specific function

individual diff- eg bavelier et al 1997 did silent reading study and found variability in patterns of activity between people. found activity in right temp lobe, left front, temp, occip lobes. gender differences- harasty et al 1997 found larger brocas and wernickes in women due to greater use of language

language may not be confined to brocas- bronkers et al 2007 examined lesions using MRI and found other areas may have contributed to reduced speech. significant as lesions in brocas usually cause temporary disruption- suggests speech is complex and network not localised

+
support for language centres from aphasia studies eg brocas and wernickes. expressive aphasia- cant produce language shows brocas is important for speech. receptive aphasia- cant understand language shows wernickes is important in comprehensive

case study evidence- Gage, Tan, HM

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13
Q

what is hemispheric lateralisation?

A

the fact that 2 halves of the brain arent entirely alike and each hemisphere has functional specialisms

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14
Q

how are the 2 hemispheres attached? what does this mean?

A

the corpus collosum ( a bundle of nerve fibers that connect the 2 halves)
means info can be sent from one half to other and we can for example, talk about things experienced in right hemisphere despite left for language

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15
Q

what is a commisurotamy?

A

cutting through the corpus collosum as treatment for severe epilepsy.
prevents violent electrical activity from crossing from one hemisphere to another. known as split-brain patients

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16
Q

describe Sperry and Gazinga’s research 1967

A

studied capabilities of split-brain patients. sent info to one hemisphere to study hemispheric lateralisation as corpus collosum is cut so info cant travel to other spot
-ppt stares at dot (so info only goes to 1 visual field)
- picture shown to 1 visual field for 1/10 second (so cant move eyes)
-found that picture shown in rvf could be described but not drawn (info goes to left hemisphere-left for language)
- picture shown to lvf could draw with left hand (controlled by right hemisphere). can only describe when theyve drawn it
- same concept with holding something in left/ right hand

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17
Q

what have we learnt from split brain reserach?

A

differences between hemispheres (left for language and right for visual-spatial processing and facial recognition)
but hasnt shown that brain is organsied into discrete regions w specific tasks and instead suggests connectivity between diff regions is as important as operation of diff parts

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18
Q

evaluate lateralisation

A

assumed that it leads to increased neural processing capacity- using only one hemisphere to engage in task means other is free to engage in another function but little evidence for this. rogers et al 2004 found that (in chickens), lateralisation is associated w ability to perform 2 tasks simultaneously- does provide some evidence that lateralisation increases efficiency

lateralisation changes w age- lateralised patterns in younger people seem to become bilateral when older. szaflarski et al 2006 found language is more lateralised to left when getting older but at 25, lateralisation decreases each decade. may be cuz using other hemisphere may compensate for age related decline in functions

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19
Q

evaluate split brain reserach

A

gazzinga 1998 suggests some early discoveries have been disconfirmed. eg originally suggested right cant handle any language but case studies have opposed this (JW learnt to speak out of right)

limitations of the actual research- many studies only have around 3 ppts. conclusions drawn from individuals w confounding physical disorder.

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20
Q

evaluate Sperry and Gazzinga’s study

A

+
scientific - consistent results, same task, shown for 1/10s
applications- develop treatments, understand roles of hemispheres
high internal validity- presentation of stimulus to one hemisphere means most likely measuring what each hemisphere does
good ethics- corpus collosum already cut-no manipulation of IV, all consented, could withdraw, fully informed

-
small, atypical sample so not generalisable
gazzinga- discoveries disproved
lack of controls- no valid control group, some on medication, some had more disconnection than others
low ecological validity- irl people have unrestricted view so info not selectively delivered to one hemisphere

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21
Q

what is brain plasticity?

A

the brain’s ability to change and adapt as a result of experience.

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22
Q

what is functional recovery?

A

moving functions from damaged area of the brain after trauma to another area

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23
Q

what types of experience can change neural organisation?

A

plasticity as a result of life experience- gain new experiences means nerve pathways that are frequently used develop stronger connections and ones barely used die. this pruning allows brain to adapt. natural decline with age so ways of reversing this have been found eg Boyke et al 2008 found evidence of brain plasticity in 60 year olds (increased grey matter in visual cortex when learnt to juggle)

playing video games- complex cognitive and motor demands. Kuhn et al 2014 compared control w group that was trained for 2 months 30 mins a day at video game and found increased grey matter in various brain areas that wasnt found in control

meditation- davidson et al 2004 compared 8 monks with 10 volunteers with no meditation experience. both fitted with electrical sensors and asked to meditate. more gamma wave (coordinate neuron activity) activity in monks. students showed slight increase in gamma. so makes short term changes as well as long term (monks had more before experiment

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24
Q

what are the mechanisms for functional recovery?

A

regenerative developments in brain due to its plasticity
neural masking and stem cells

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25
Q

what is neural unmasking?

A

wall 1977 discovered dormant synapses (blocked)
normally would be ineffective because rate of neural input is too low for them to be activated
increased rate of input that occurs when surrounding area is damaged can unmask them
this gives way to the development of new structures over time.

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26
Q

how can stem cells lead to recovery of a stroke?

A

unspecialised cells that can take on characteristics of nerve cells
diff views of how this works:
cells implanted into the brain can directly replace dead cells
or
transplanted stem cells can secrete growth factors that rescue injured cells
or
transplanted cells form a neural network which links uninjured brain site where stem cells are made with the damaged region of the brain

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27
Q

evaluation of plasticity

A

research support from animal studies- kempermann et al 1998 found increased no of neurons in hippocampus of rats in complex environments compared to in lab cages

research support from human studies- maguire et al 2000 studied london taxi drivers to discover whether changes in brain could be detected as a result of extensive navigation experience. used MRI to calculate amount of grey matter in taxi drivers brains and control. posterior hippocampus of taxi drivers were significantly larger. volume was positively correlated with time theyd been driving

28
Q

evaluation of functional recovery

A

Tajiri et al 2013 assigned rats w brain injury to 2 groups. 1 received transplants of stem cells into affected region. control had injection into brain that contained no stem cells. 3 months later, brain stem of rats w stem cells showed development of neuronlike cells in injured area. also, stream of stem cells migrating into brains injured site. not case for control
age diff- plasticity reduces with age. so would think could not recover after brain injury but studies have suggested that even abilities thought to be fixed in childhood can be modified w intense training. elbert et al 2001 concluded capacity for neural reogranisation is greater in kids than adults as adults need more practice (+ or -?)

29
Q

what is a post mortem examination?

A

see underlying neurobiology of particular behaviour. when a person dies, you can examine brain to look for abnormalities not found in control that may explain behaviour in life. eg used on Tan and HM- identified language and memory areas) can also see depression from post mortem (reduced no of glial cells(provide support and insulation in neurons) in frontal cortex)

30
Q

what is an fMRI?

A

measure changes in brain activity whilst performing task. measures blood flow to areas of brain indicating neural activity. more active= more oxygen demand= increased blood flow
can be used to produce maps of brain areas involved in particular activity
ppt asked to do task for 30s then control state for 30s to see which areas are activated due to stimulus

31
Q

what is an EEG? electroencephalogram

A

measures electrical activity in the brain
electrodes placed on scalp detect small electrical charges due to brain activity. electrical signals graphed over period of time produces an EEG
can detect brain disorders eg epilepsy (spikes of activity)
4 basic patterns- alpha, beta, delta, theta. awake but relaxed- alpha, physiologically aroused- beta, REM sleep- beta, sleep- delta and theta

32
Q

what is an ERP?

A

small voltage changes triggered by events or stimuli.
difficult to pick out due to all other electrical activity happening
show stimuli repeatedly then avg responses together- any extraneous activity will not appear repeatedly
ERPs can be divided into 2 categories: waves occurring in first 100millisecs after stimuli presented are called sensory (reflect initial response to physical characteristics of stimulus)
ERPs after 100millisecs reflect how subject evaluates stimulus and are called cognitive (demonstrate info processing)

33
Q

evaluate post mortem examination

A

+
provides foundation for early understanding of key brain processes
broca and wernicke used it to find links between language and brain
improve medical knowledge and help create hypotheses for research
deeper regions such as hippocampus can be seen
high spatial resolution

-
damage found may not be linked to deficits in behaviour
ethical issues of consent eg HM couldnt
people die in varying circumstances and stages of disease
length of time between death and post mortem (poor temp resolution), age of death and drug treatment are confounding variables

34
Q

evaluate fMRI

A

+
no radiation- risk free, non invasive, straight forward
high spatial resolution- clear pic of localisation

-
expensive
person has to stay very still for clear image
poor temporal resolution- 5s delay between image and neuronal activity

35
Q

evaluate EEG

A

+
invaluable in diagnosis eg of epilepsy- spikes of electrical activity
contributed to understanding of stages of sleep
high temporal resolution- takes readings every millisecond
cheaper than other techniques so more accessible

-
generalised nature of info received- 1000s of neurons
isnt useful for pinpointing exact source of neural activity as electrical activity is detected in diff regions of brain at same time
poor spatial resolution
superficial data- doesnt penetrate into brain

36
Q

evaluate ERP

A

+
more specific than EEG
high temporal resolution
researchers can identify diff ERPs and describe role of them in cognitive functioning
cheap
non-invasive

-
lack of standardisation- difficult to confirm findings
background noise and extraneous material must be completely eliminated to establish pure data which isnt easy to achieve
superficial data- cant penetrate into brain
poor spatial resolution

37
Q

what is a biological rhythm?

A

a cyclical change in the way biological systems have evolved because the environment in which the organism lives has cyclic changes eg seasons/ day-night

38
Q

what is a circadian rhythm?
how long is it?
examples?

A

circadian rhythms (body clock) optimize organisms physiology and behaviour to best meet varying demands of day/night cycle
24 hours
sleep-wake cycle, core body temp, hormone production

39
Q

what is the master pace maker?
how is it reset?

A

synchronises circadian rhythm in all body cells
superchiasmatic nuclei (SCN)
light resets body clock through photoentrainment- light-sensitive cells in the eyes act as brightness detectors sending info about environmental light levels to SCN which uses info to coordinate activity of circadian system

40
Q

what is the sleep-wake cycle?

A

light/darkness are external signs to wake up but circadian rhythm dips and rises through day
strongest sleep drive occurs between 2-4am and 1-3pm dips
sleepiness felt in dips is greater if we’ve had lack of sleep

sleep also determined by homeostatic control- drive for sleep increases over day as we use up energy

41
Q

what is free-running?

A

internal clock is free running so will keep cycle of 24-25 hrs despite lack of external cues
but, it is intolerant of major alterations in sleep eg jet lag because body clock out of balance

42
Q

what is core body temp rhythm?

A

lowest (36c) at 4.30am and highest (38c) at 6pm
sleep occurs when temp begins to drop and temp rises at last few hrs of sleep prompting alertness in morning
small drop between 2-4pm explaining sleepiness in afternoon

43
Q

what is hormone production rhythm?

A

production and release of melatonin from pineal gland peaks during hours of darkness. by activating chemical receptors in brain, melatonin encourages feelings of sleep
dark-more melatonin produced, light- melatonin production drops and person wakes

44
Q

what are individual diffs in circadian rhythms?

A

babies- no circadian rhythm
children- stable rhythms
teenagers- sleep phase delay- not tired in evening (perhaps due to more hormone release)
adulthood- rhythm matures- stable

45
Q

describe michel siffre’s study

A

subjected himself to long periods of time underground to study his circadian rhythms
no external cues (clocks, daylight, radio) other than lamp
slept, ate, woke when he felt was appropriate- influenced by internal body clock
1) 61 days in southern alps 1962, resurfaced 17th sept thinking it was 20th aug
2) 6 months in cave in texas, rhythm settled to just over 24hrs but some dramatic changes
3) 1999 looked at effects of ageing- clock ticked more slowly compared to before- 48hrs

46
Q

describe aschoff and wever’s (1976) study

A

ppts in underground bunker w/o environmental and social cues
found most people displayed rhythm between 24-25 hrs but some 29hrs
shows circadian rhythm persists despite isolation from natural light which demonstrates existence of endogenous clock- supports siffre’s research of free running
but shows external cues are important as body clock wasnt perfectly accurate

47
Q

describe folkard’s study

A

see if external cues can override internal clock
12 ppts lived in cave for 3 weeks, isolated from time cues
went to bed at 11:45 and woke at 7:45
clock ran normally but gradually quickened to 22 hours
at start, rhythms matched clock but as it quickened, it no longer matched as they still followed 24hr cycle other than 1 person who settled to 22hrs
suggests circadian rhythms can be guided slightly but internal body clock is most important

48
Q

evaluate circadian rhythms

A

research support for importance of light- hughes tested circadian hormone release in 4 ppt at British Antarctic station and found in summer, cortisol levels followed usual pattern of high when wake low when sleep but after 3m of darkness, peak changed to noon- but similar study didnt find this

individ diff- cycle length varies from 13-65 hours (Czeisler 1999) and cycle onset is diff eg duffy 2001 found diff between morning and evening people and peak of rhythm

research methodology- in early studies, ppts not isolated from artificial light as it wasnt though to affect but research shows this isnt true

prac aps- chronotherapeutics- study of how timing affects drug treatments. right conc should be released at right time eg highest risk of heart attack in morning. slow release drugs, take and then not released until hours later

temp may be more important than light (buhr et al 2010)- SCN transfers light info into neural messages that set body temp. small fluctuations send powerful signal

49
Q

what are ultradian rhythms? eg?

A

less than 24hrs eg sleep stages and BRAC

50
Q

what are the sleep stages?

A

90 minute cycle of diff stages of REM and NREM.
discovered through EEG patterns- deep sleep shows slowed brain waves, REM resembles someone awake

51
Q

what is BRAC?

A

basic rest activity
90 ultradian rhythms during the day
instead of moving through sleep stages, we move from stages of alertness to psychological fatigue
research suggests we can focus for 90 min then body begins to run out of resources resulting in lack of concentration ad hunger
shown through 10:30 coffe break (splits 9-12) and afternoon naps

52
Q

what are infradian rhythms? eg?

A

more than 24hrs eg menstrual cycle and annual rhythms

53
Q

what is the human menstrual cycle?

A

23-36 day long cycle
regulated by hormones which promote ovulation/ stimulate uterus for fertilisation
ovulation occurs half way through cycle when oestrogen levels peak
after ovulation, progesterone levels increase in preparation for possible implantation of embryo

54
Q

what are annual rhythms?

A

often related to seasons eg migrate at lower temps
human calendar year influences behaviour regardless of temp
research suggests seasonal variation in mood especially in women (SAD) winter also associated w increased heart attacks

55
Q

evaluate ultradian and infradian rhythms

A

individ diff in sleep stages- tucker et al 2007 suggested differences are biologically determined maybe even genetic. ppts studied over 11 nights in strictly controlled labs measuring time asleep, in each stage and time to get to sleep. deep sleep was particularly different so not circumstances as they were highly controlled

research supports BRAC- ericsson et al 2006- elite violinists, found practice was 90 mins and distributed through day. found most successful napped to recover from practice. found same in athletes, writers

exogenous cues on menstrual cycle- can synchronise w other women not on oral contraceptives. study- sweat taken and rubbed onto upper lip of other ppt who was kept separate- cycle synchronised - pheromones

menstrual cycle influences mate choice- prefer slightly feminised for long term but in ovulatory phase, more masculine- prefer kindness and cooperation for long term but males w good genes for short term

lunar rhythms- midwives believe more babies born on full moon but stats show this is subjective association. mental health professions believe moon alters behaviour but no real evidence

56
Q

what are endogenous pacemakers? examples?

A

mechanisms within body that govern internal, biological bodily rhythms
SCN, pineal gland

57
Q

what are exogenous zeitgebers? examples?

A

environmental cues such as light that help regulate biological clock in an organism
light, social cues

58
Q

what do endogenous pacemakers and exogenous zeitgebers do?

A

reset biological rhythms to stay in tune with external world

59
Q

superchiasmatic nucleus as an ep

A

main ep in mammals
tiny cluster of nerve cells in the hypothalamus
acts as master clock which links to other brain regions that control sleep and arousal
neurons in scn spontaneously synchronise so target neurons receive correctly timed signals
scn has built in circadian rhythm which olny needs resetting when light levels change
also regulates manufacture and secretion of melatonin in pineal gland

60
Q

what is the flow diagram from light levels- melatonin production?

A

low light (ez)
retina
optic nerve
scn (ep)
pineal gland
produces melatonin
(high light leads to stopped production of melatonin)

61
Q

pineal gland and melatonin as eps

A

scn sends signals to pineal gland telling it to increase or decrease production of melatonin depending on light levels
melatonin induces sleep by inhibiting brain mechanisms that promote wakefulness
despite endogenous nature, scn and pineal gland must be sychronised to light levels outside

62
Q

light as an ez

A

receptors in SCN are sensitive to light level change
light resets body clock each day
rods and cones in retina detect light to form visual images
3rd type of light detecting cell that gauges overall brightness to help reset internal body clock
melanopsin protein is sensitive to natural light
some retinal cells contain melanopsin and carry signals to SCN to set daily body clock

63
Q

social cues as ez

A

mealtimes and social activities
ascoff et al 1971 showed individuals are able to compensate for lack of light by responding to social cues
klein and wegmann 1974 studies jet lag and found circadian rhythms of travelers adjusted quicker if they went outside- exposed to social cues of new time zone
circadian rhythm of blind people is no different
but
both studies can be better explained by light (blind people may still have some light perception

64
Q

evaluate endogenous pacemakers

A

role of SCN- animal studies eg Morgan 1995- bred hamsters w abnormal rhythm of 20hr. SCN of these hamsters transplanted into brains of normal hamsters who began to show abnormal rhythm. same in reverse

normally SCN coordinates all rhythms but sometimes out of step w each other eg ppt spent 25 days in lab w no access to ezs. at end, core body temp still 24 hrs but sleep-wake was 16

65
Q

evaluate exogenous zeitgebers

A

support for role of melanopsin in setting rhythm from blind people. skene and ardent 2007- most blind people still have some light perception and normal rhythms suggesting pathway from retinal cells containing melanopsin to SCN still intact. people wo light perception show abnormal circadian entrainment

burgess et al 2003- exposure to bright light prior to E->W flight decreased adjustment time on arrival. 3 groups- bright light(1), intermittent bright light(2), dim light(3). 1 shifted rhythm 2.1 hrs, 2 1.5 hrs and 3 0.6 hours. 1 felt sleepier and woke 2 hours earlier (closer to home time zone)

vetter et al 2011- investigated importance of light in regulation of sleep-wake and activity-rest pattenrs of 2 groups over 5 weeks. 1 group- normal light, other- blue enriched (closer to daylight). all kept sleep log and wore measuring devices. over study, sunrise advanced 42 mins- normal light group adjusted circadian rhythm with this, other group didnt- adjusted to office hours- shows light is important and that blue light competes w natural light as dominant zeitgeber