Biopsychology Flashcards

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1
Q

what is the nervous system?

A

the primary internal communication system, it is made up of the central nervous system (CNS) and the peripheral nervous system (PNS).

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2
Q

what is the central nervous system?

A

it is made up of the brain and the spinal chord.

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3
Q

what is the role of the brain?

A

the central control centre, it processes sensory information and controls motor and cognitive functions.

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4
Q

what is the role of the spinal chord?

A

an extension of the brain, it passes messages to and from the brain and connects nerves to the PNS, also responsible for reflex actions.

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5
Q

what is the peripheral nervous system?

A

it transmits messages via neurons to and from the CNS and is subdivided into the somatic nervous system (SNS) and the autonomic nervous system (ANS).

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6
Q

what is the role of the somatic nervous system?

A

controls muscle movement and receives information from sensory receptors.

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7
Q

what is the role of the autonomic nervous system?

A

regulates vital functions of the body e.g. breathing, heart rate, digestion etc. it has two main divisions: the sympathetic nervous system and the parasympathetic nervous system.

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8
Q

what does the sympathetic nervous system do?

A

prepares the body for a ‘fight or flight’ response in stressful situations, e.g. increased heart rate / breathing rate, dilates pupils, inhibits digestion / saliva production.

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9
Q

what does the parasympathetic nervous system do?

A

regulates the body back to its normal state after the stressor is gone e.g. decreases heart rate / breathing rate, constricts pupils, stimulates digestion / saliva production.

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10
Q

describe the divisions of the nervous system.

A
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11
Q

what is the endocrine system?

A

one of the body’s major information systems and in charge of slower bodily processes such as cell growth, it is made up of hormones and glands.

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12
Q

what is the role of hormones?

A

chemical messengers - transferring information and instructions from one set of cells to another.

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13
Q

what is the role of glands?

A

produces the hormones e.g. hypothalamus, pituitary gland, adrenal gland, thyroid gland etc.

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14
Q

what does the hypothalamus do?

A

the part of the brain that controls the endocrine system, it is connected to the pituitary gland and tells it to release hormones.

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15
Q

what does the pituitary gland do?

A

it is the ‘master gland’ in the brain that controls release of hormones around the rest of the body.
- in posterior, releases oxytocin for contractions in childbirth.
- in anterior, releases adrenocortical trophic hormone (ACTH) for stimulation of adrenal cortex and releases cortisol during stress.

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16
Q

what does the adrenal gland do?

A
  • in the adrenal medulla, releases adrenaline and noradrenaline which are the key hormones for the ‘fight or flight’ response.
  • in the adrenal cortex, releases cortisol to stimulate the release of glucose to provide the body with energy.
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17
Q

what does the thyroid gland do?

A

releases thyroxine for regulating metabolism.

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18
Q

what do the endocrine system and autonomic nervous system work together for?

A

to produce certain effects in the body e.g. the fight of flight response.

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19
Q

how do the endocrine system and the ANS work together for the ‘fight or flight’ response?

A

when a person perceives a situation as stressful, the sympathetic branch of the ANS is triggered and the stress hormone adrenaline is released in response, leading to physiological changes (increased heart rate, sweating, and so on), this state of arousal in the system is known as the ‘sympathetic’ state. Once the perceived stressor passes, the ‘parasympathetic’ branch of the ANS returns the body to normal, reducing the effects and activity of the sympathetic branch.

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20
Q

what are neurons?

A

nerve cells which transmit messages chemically and electrically (vary in size but they have the same structure).

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21
Q

what are the three types of neurons?

A

motor, sensory and relay

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22
Q

what is the role of the motor neuron?

A

connects the CNS to muscles and glands.

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23
Q

what is the role of the sensory neuron?

A

carries messages from the PNS to the CNS.

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24
Q

what is the role of the relay neuron?

A

connects sensory neurons to motor and other relay neurons.

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25
Q

what is the structure of neurons?

A

they vary in size, but all have the same structure; a cell body (soma), nucleus branches (dendrites), the axon, myelin sheath, nodes of ranvier, axon terminals.

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26
Q

what does the cell body (soma) do?

A

contains the nucleus.

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27
Q

what does the nucleus do?

A

contains the genetic material of the cell.

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28
Q

what do dendrites do?

A

carry nerve impulses from neurons to the cell body. (away from synapse)

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29
Q

what does the axon do?

A

carries the impulses away from the cell body down the length of the neuron. (towards synpase)

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30
Q

what does the mylein sheath do?

A

it protects the axon and speeds up electrical transmission of the impulse.

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31
Q

what do the nodes of ranvier do?

A

speed up transmission by forcing it to ‘jump’ across gaps along the axon.

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32
Q

what do the axon terminals do?

A

communicate with the next neuron in the chain across the synapse.

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33
Q

desrcibe the structure and function of a neuron.

A

neurons transmit messages chemically and electrically, they vary in size but all have the same structure. They have a cell body (soma), containing genetic material, of the cell (the nucleus) and branches (dendrites) which carry nerve impulses from neurons and carry functional information to the cell body. The axon carries impulses away from the soma, down the length of the neuron. The axon is covered in a protective layer known as the myelin sheath, which speeds up electrical transmission of the impulse. This effect is achieved by making the impulse ‘jump’ between gaps in the myelin sheath - these gaps are known as the nodes of ranvier. At the end of the neuron are axon terminals which allow for communication with adjacent neurons in the chains across the synapse.

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34
Q

what is a synapse?

A

the gap between neurons (chemical transmissions via neurotransmitters).

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35
Q

what are neurotransmitters?

A

chemicals that diffuse across the synapse to the next neuron in the chain.

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36
Q

what is synaptic transmission?

A

the process where neighbouring neurons communicate with each other by sending chemical messages across the synapse that separates them: signals with neurons are transmitted electrically while signals between neurons are transmitted chemically.
an electrical impulse reaches the end of a neuron (pre-synaptic cell) and triggers the release of neurotransmitters from tiny sacs called synaptic vesicles, which crosses the synapse and enters the receptor sites on the dendrites of the next neuron (the post-synaptic cell), where the chemical message is converted back into an electrical impulse and the process of transmission begins again in another neuron.

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37
Q

what are two types of neurotransmitters?

A

excitatory and inhibitory

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38
Q

what do excitatory neurotransmitters do?

A

stimulate the brain e.g. adrenaline.

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39
Q

what do inhibitory neurotransmitters do?

A

calm the brain and help create balance e.g. serotonin.

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40
Q

what is excitation?

A

the neurotransmitters excite the next neuron which produces an action potential e.g. adrenaline causes excitation of post-synaptic neuron which increases positive change and more likely to fire.

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41
Q

what is inhibition?

A

these neurotransmitters stop an action potential e.g. serotonin cause inhibition in the receiving neuron which makes it more negatively charged and less likely to fire.

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42
Q

what is summation?

A

the firing of post-synaptic neurons are decided by summation, a nerve cell can receive both excitatory post-synaptic potentials (EPSPs) and inhibitory post-synaptic potentials (IPSPs) simultaneously; the EPSPs and IPSPs are summed and if the net effect on the post-synaptic neuron is inhibitory then the neuron will be less likely to fire (negatively charged) and if the net effect is excitatory then the neuron will be more likely to fire (positively charged).

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43
Q

what is localisation of function?

A

the theory that different areas of the brain are responsible for different behaviours, processes or activities.

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44
Q

what are the four lobes of the brain?

A

frontal lobe, parietal lobe, occipital lobe and temporal lobe.

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45
Q

what areas are located in the frontal lobe?

A

motor area and broca’s area

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46
Q

what is the function of the motor area and what will happen if it gets damaged?

A

it is in the back of the frontal lobe and controls voluntary movement in the opposite side of the body (left controls right, right controls left), damage to this area of the brain may result in a loss of control over fine movement.

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47
Q

what is the function of broca’s area and what will happen if it gets damaged?

A

it is in the left hemisphere of the frontal lobe and it is responsible for speech production, damage to this area causes broca’s aphasia - characterised by speech that is slow, laborious and lacking influency.

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48
Q

what area is located in the parietal lobe?

A

somatosensory area

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49
Q

what is the function of the somatosensory area and what will happen if it gets damaged?

A

it is at the front of the parietal lobe and it is where sensory information from the skin (heat, pressure and so on) is processed, damage to this area can affect the sensitivity of certain parts of the body.

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50
Q

what area is located in the occipital lobe?

A

visual area

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51
Q

what is the function of the visual area and what will happen if it gets damaged?

A

each eye sends information from the right visual field to the left visual cortex and from the left visual field to the right visual cortex, damage to the left hemisphere can produce blindness in part of the right visual field of both eyes and vice versa.

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52
Q

what areas are located in the temporal lobe?

A

wernicke’s area and the auditory area

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53
Q

what is the function of the auditory area and what will happen if it gets damaged?

A

it analyses speech based information and damage to this area may produce partial hearing loss - the more extensive the damage, the more extensive the loss.

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54
Q

what is the function of wernicke’s area and what will happen if it gets damaged?

A

it is in the left temporal lobe and it is responsible for language comprehension, damage to this area leads to wernicke’s aphasia and people who have this will often produce nonsense words (neologisms) as part of the content of their speech.

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55
Q

what are the strengths of the localisation of the brain theory?

A

there is research evidence: neurosurgery - damage to areas of the brain has been linked to mental disorders and neurosurgery is a last resort method, dougherty et al (2002) found that a third of OCD sufferers who had part of the cingulate gyrus removed from their brain showed improvement in symptoms following the procedure, which suggests that behaviours associated with serious mental disorders may be localised.

there is research support:
- petersen et al (1988) found that Wernicke’s area was active when performing listening tasks, and Broca’s area was active when undertaking reading tasks which supports the idea that different areas of the brain have specific functions.
- buckner and peterson (1996) revealed semantic and episodic memories reside in different parts of the prefrontal cortex.

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56
Q

what is a weakness of the localisation of the brain theory?

A

dick and tremblay (2016) found that only 2% of modern researchers think that language in brain is completely controlled by broca’s and wernicke’s area, advances in the brain imaging techniques mean that neural processes in the brain can be studied with more clarity so it seems that language function is distributed more holistically which contradicts localisation theory.

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57
Q

what is brain plasticity?

A

the brain’s capacity to reorganise its structure and function throughout life, due to experience (environmental).

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58
Q

what is functional plasticity?

A

the brain’s ability to move functions from a damaged area of the brain to other undamaged areas.

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59
Q

what is structural plasticity?

A

the brain’s ability to actually change its physical structure as a result of learning.

60
Q

who conducted research on brain plasticity and when?

A

maguire et al (2000) and draganski et al (2006)

61
Q

what was maguire et al’s aims and procedures?

A

they aimed to examine whether structural changes could be detected in the brain of people with extensive experience of spatial navigation (london taxi drivers.

their procedure included a matched-pairs design and used MRI scans on 16 male right-handed lonon taxi drivers and a control group (50 male, right handed non-taxi drivers).

62
Q

what did maguire et al find and conclude?

A

they found increased grey matter in the brains of taxi drivers compared with control group in 2 brain regions, the right and left hippocampi (posterior hippocampus) and a correlation was found between amount of time spent as a taxi driver and volume in the right posterior hippocampus.
they concluded that the findings provide evidence for structural differences between the hippocampi of london taxi drivers and control ppts, therefore suggesting that extensive practice with spatial navigation affects the hippocampus.

63
Q

what did draganski et al do in their study and what did they find?

A

they imaged the brains of medical students 3 months before and after their final exams and found that learning-induced changes were seen to have occurred in the posterior hippocampus and the parietal cortex presumably as a result of learning.

64
Q

what are the strengths of brain plasticity?

A

there is research support: maguire et al (2000) and draganski et al (2006), they show how the brain has the ability to change and adapt due to experiences / learning, which increases the reliability of it.

bezzola et al (2012) demonstrated how golf training produced neural changes in participants aged 40-60, shows that brain plasticity can continue throughout the lifespan.

65
Q

what are the weaknesses of brain plasticity?

A

medina et al (2007) showed that drug use leads to poorer cognitive functioning in later life and increased risk of dementia.

60-80% of amputees have been known to develop phantom limb syndrome (continued experience of sensations in missing limb as if it was still there) due to reorganisation in the somatosensory cortex which suggests that the brain’s ability to adapt to damage is not always beneficial.

66
Q

what is functional recovery?

A

the transfer of functions from a damaged area of the brain after trauma to other undamaged areas.

67
Q

what is neuronal unmasking?

A

the process for functional recovery where ‘dormant’ synapses (which have not received enough input to be active) open connections to compensate for a nearby damaged area of the brain, this allows new connections in the brain to be activated, thus recovering any damage occurring in specific regions.

68
Q

what structural changes in the brain is this process supported by?

A

axonal sprouting, denervation super-sensitivity and recruitment of homologous

69
Q

what is axonal sprouting?

A

the growth of new nerve endings which connect with other undamaged nerve cells to form new neuronal pathways.

70
Q

what is denervation super-sensitivity?

A

this occurs when axons that do a similar job become aroused to a higher level to compensate for the ones that are lost, it can have oversensitivity e.g. pain.

71
Q

what is recruitment of homologous?

A

it is similar areas on the opposite side of the brain where specific tasks can still be performed e.g. if broca’s area was damaged on left side of brain, right sided equivalent would carry out function and functionality may shift back to left side.

72
Q

what are the strengths of functional recovery?

A

there is real-world application: it contributed to field or neuro-rehabilitation - knowledge of axonal growth has led to new therapies e.g. constraint movement therapy used with stroke patients which shows that research into functional recovery is useful as it helps medical professionals known when interventions need to be made.

there is research support:
- taijiri et al (2013) found that stem cells provided to rats after brain trauma showed a clear development of neuron like cells in injured area which demonstrates ability of brain to make new connections using neurons manufactured by stem cells.
- banerjee et al (2014) treated TACS people, found 100% recovery using stem cells.
(COUNTERPOINT) - small sample of 5 people used.

73
Q

what are the weaknesses of functional recovery?

A

there is conflicting evidence:
- elbert et al found neural regeneration is less effective in older brains so explains why adults find change more demanding, individual differences must be considered when assessing the likelihood of functional recovery.
- schneider et al (2014) found 40% recovery for people with 16 years+ education, 10% for those with less than 12 years of education which implies that people with brain damage are less likely to achieve full recovery.

74
Q

what is hemispheric lateralisation?

A

the idea that two halves of the brain are functionally different and certain processes or behaviours are controlled by the hemisphere rather than the other (the right side of the brain processes info from the left half of the body and the left side of the brain processes info from the right half of the body).

75
Q

what is the left hemisphere mainly for?

A

language production

76
Q

what is the right hemisphere mainly for?

A

visual motor tasks

77
Q

what is split-brain research?

A

a series of studies involving epileptic patients who had experiences commissurotomy surgery - where the corpus callosum is severed so that the two hemispheres are separated and do not communicate with each other to reduce the severity of their epilepsy and reduce them to just one half of the brain.

78
Q

what is the corpus callosum?

A

a thick brand of nerve fibres that divided the brain into left and right hemispheres, it connects left and right sides of the brain allowing for communication between both sides.

79
Q

who conducted a study for split-brain research and when?

A

sperry (1968)

80
Q

what was sperry’s aim in his study?

A

to examine the extent to which the two hemispheres are specialised for certain functions.

81
Q

what was sperry’s method in his study?

A

performed a quasi experiment in a lab enviroment (opportunity sample) where he studied 11 participants who had experienced surgeries for severe epilepsy and they were given different tasks: describe what you see task, tactile test and drawing task.

82
Q

what did the participants have to do in the describe what you see task?

A

to describe the picture presented to either the left or the right visual field.

83
Q

what did the participants have to do in the tactile test?

A

an object was placed in the participant’s left or right hand and they had to describe what they felt or choose a similar object from a series of alternate objects.

84
Q

what did the participants have to do in the drawing task?

A

to draw the picture presented to either the left or right visual field.

85
Q

what were the findings in sperry’s study?

A

in the describe what you see task, when the picture was presented to the right visual field, the patient could describe what they saw (demonstrating superiority of LH) but when presented to left visual field, they could not and often reported that there was nothing present.

in the tactile tests, when the object was placed in the patient’s right hand, they could describe verbally what they felt or could identify the test object in a series of objects but when placed in left hand, they could not describe what they felt but they could identify a test object by selecting similar appropriate object.

in the drawing tasks, when the picture was presented to the right visual field, while the right hand would attempt to draw a picture, it was never as clear as the left hand but when presented to the left visual field, the left hand would consistently draw clearer and better pictures than right hand.

86
Q

what were the conclusions in sperry’s study?

A

he concluded that certain function are lateralised in the brain and the severing of the corpus callosum resulted in limited communication between the hemispheres which explains the distinct responses, which supports the view that the left hemisphere is verbal (for language production) and the right hemisphere is ‘silent’ but emotional (for verbal motor tasks).

87
Q

what are the strengths of split-brain research into hemispheric lateralisation?

A

brain lateralisation is believed to be the advantage of increasing neural procession capacity as this leaves one hemisphere free to engage in another task e.g. LH on language and RH on visual tasks at the same time, however, there is little empirical evidence to show lateralisation infers an advantage or functioning of brain.

fink et al (1996) used PET scans to identify which brain areas were active during a visual processing task, finding both RH and LH were as far as visual processing is concerned.

turk et al (2002) discovered a patient who after receiving damage to LH was able to develop the capacity to speak in the RH, suggesting the adaptability of the brain and that language is not necessarily restricted to LH.

88
Q

what are the weaknesses of split-brain research into hemispheric lateralisation?

A

the idea that LH and RH are analysers or synthesisers may be wrong, people do not have a dominant hemisphere which impacts their personality, just LH and RH may have different functions, no artistic - analytical brain.

split-brain procedures are rarely carried out so finding patients who have had this procedure done is difficult, which has made it difficult to find sufficient numbers of participants for research into split-brain research and draw useful conclusions.

generalisation issues - in sperry’s research, his control group were neurotypical, not eplieptic, which is a confounding variable - the differences may be a result of epilepsy rather than split-brain.

89
Q

what are the two different types of ways of studying the brain?

A

scanning techniques and traditional methods

90
Q

what are the scanning techniques?

A

fMRIs (functional magnetic resonance imaging), EEGs (electroencephalogram) and ERPs (event-related potentials).

91
Q

what are the traditional methods?

A

post-mortem examinations

92
Q

what do fMRIs do?

A

it measures blood flow during a task and it shows the neurons in the brain that are the most active (during a task) use the most energy, it creates a 3D map of the brain, highlighting localisation of function.

93
Q

what are the strengths of fMRIs?

A

it is low risk and doesn’t rely on the use of radiation.

it is virtually risk-free, non-invasive and straightforward to use.

high spatial resolution, strong detail and provides clear picture of brain activity and how it is localised.

94
Q

what are the weaknesses of fMRIs?

A

it is expensive.

poor temporal resolution due to 5-second time-lag behind image on screen and initial firing of neuronal activity (individual neurons activity cannot be seen) so may not truly represent moment-to-moment brain activity.

95
Q

what do EEGs do?

A

measures electrical activity through the action potential or nerve impulses, transmitted along neurons, EEG scanners measure this through electrodes attached to the scalp which indicate level of activity in the brain.

96
Q

what are the strengths of EEGs?

A

they are relatively low cost and non-invasive.

very useful in diagnosing conditions such as epilepsy and the processes involved in activities such as sleep.

high temporal resolution so can accurately detect brain activity which shows the real-world usefulness of this technique.

97
Q

what are the weaknesses of EEGs?

A

poor spatial resolution due to superficial, general regions only - electrical activity often detected in several regions so it can be difficult to pinpoint the exact region of activity.

information gained is very generalised so technique cannot be used to isolate exact neuronal activity.

can be uncomfortable due to being non-invasive.

98
Q

what do ERPs do?

A

measures brain activity through electrodes attached to the scalp, as in EEGs, but while a stimulus is presented to the participant.

99
Q

what are the strengths of ERPs?

A

they bring much more specificity to the measurements of neuronal processes than EEGs.

high temporal resolution, which means they are frequently used to measure cognitive functions and deficits such as maintenance of working memory.

non-invasive and enables determination of how processing is affected by specific environmental manipulation.

100
Q

what are the weaknesses of ERPs?

A

there is a lack of standardisation in the methodology, meaning that the findings are in question and elimination all extraneous variables in order to isolate an ERP can be difficult.

there is poor spatial resolution due to superficial, general regions only.

101
Q

what do post-mortem examinations do?

A

study the physical brain of a person who has died and displayed particular behaviours while they were alive that suggested brain damage.

102
Q

what are the strengths of post-mortem examinations?

A

post-mortem evidence was vital in providing a foundation for early understanding of key processes in the brain e.g. broca’s area, wernicke’s area, also used to study patient HM’s brain to identify the areas of damage which could be associated with his memory deficits, this means that post-mortems continue to provide useful information.

103
Q

what are the weaknesses of post-mortem examinations?

A

they raise ethical issues of consent from the individual before death, participants may not be able to provide informed consent e.g. patient HM, which challenges the usefulness of post-mortem studies in psychological research.

it is hard to establish a cause-effect link as changes in brain structure may not be related to the disorder that the patient had, but due to another issue.

104
Q

what are biological rhythms?

A

cyclical patterns in biological systems which respond to environmental influences, 2 key factors that govern them are endogenous pacemakers (internal) and exogenous zeitgebers (external).

105
Q

what three rhythms do the biological rhythms include?

A

circadian rhythms, infradian rhythms and ultradian rhythms

106
Q

what are circadian rhythms?

A

lasts a 24 hour cycle e.g. sleep / wake cycle, body temperature.

107
Q

what is the sleep / wake cycle and how does it work?

A

it dictates when humans / animals should be asleep and awake, daylight (an exogenous zeitgeber) effects when we feel drowsy (ready to sleep) and when we feel alert (ready to wake) - it is the external cue for sleeping.

light is first detected by the eye, which then sends messages connecting the level of brightness to the suprachiasmatic nuclei (SCN), the SCN then uses this information to coordinate the activity of the entire circadian system e.g. hormones, body temperature etc which controls wakefulness / sleepiness.

108
Q

what is the suprachiasmatic nuclei (SCN)?

A

a group of cells in the hypothalamus that respond to light and dark signals.

109
Q

how does body temperature work in regards to circadian rhythms?

A

human body temperature is at its lowest in the early hours of the morning and at its highest in the early evening, sleep typically occurs when the core temperature starts to drop, and the body temperature starts to rise towards the end of a sleep cycle promoting feelings of alertness first thing in the morning.

110
Q

who conducted research into circadian rhythms?

A

siffre (1962/1975), aschoff & wever (1976) and folkard et al (1985).

111
Q

what did siffre do in his study and what did he find?

A

he studied the effect of a complete lack of daylight on his own sleep / wake cycle, by living in a cave for several months at a time, after 2 months he came out and he thought it was mid-august but it was actually mid-september and he found that his 24-hour sleep / wake cycle was increased (25 hour cycle) by the lack of external cues, making him believe one day was longer than it was and leading him to thinking that fewer days passed.

112
Q

what did aschoff & wever do in their study and what did they find?

A

they found that participants who spent 4 weeks in a bunker without natural light showed circadian rhythms of 24-25 hours, except for 1 participant = 29 hours, this suggests that the natural circadian rhythms is slightly shortened by the effects of exogenous zeitgebers (daylight).

113
Q

what did folkard et al do in their study and what did they find?

A

they found that when participants were deprived of sunlight for 3 weeks and the length of day was manipulated by the researcher to 22 hours rather than 24, only one participant easily adjusted to the shortened day, this suggests the strength of the body’s sleep / wake cycle, as it resisted environmental changes.

114
Q

what are the strengths of research into circadian rhythms?

A

research into circadian rhythms has useful practical apllications, e.g. how to manage the shift patterns of night workers so that they are more productive and make fewer mistakes as research has shown that shift workers are 3 times more likely to develop heart diseases than people who work more typical patterns, this shows that this kind of research is useful in the real world, however, studies investigating effects of shift work tend to use correlational methods which means it is difficult to establish whether desynchronisation of the sleep / wake cycle is actually a cause of negative effects as there may be other factors.

research has also led to the improvement of medical treatments, circadian rhythms co-ordinate a number of the body’s basic processes and the levels of these throughout the course of a day has led to how medical treatments can be administered in a way that corresponds to a person’s biological rhythms so this research can help increase the effectiveness of drug treatments.

115
Q

what are the weaknesses of research into circadian rhythms?

A

research into circadian rhythms often use small sample sizes (only one, in the case of siffre) so generalisation may be difficulty also, participants had access to artificial light which could be considered as a confounding variable e.g. turning off a light to go to sleep may have similar effects as the end of natural light at the end of a day, so the internal validity is therefore in question.

116
Q

what are infradian rhythms?

A

lasts longer than 24 hours (weekly, monthly, yearly) e.g. menstrual cycle.

117
Q

what is the menstrual cycle?

A

it a monthly infradian rhythm and it is governed by monthly changes in hormone levels which regulate ovulation, lasts approximately 28 days from first day of period to day before next period, it is regulated by hormones (endogenous) - oestrogen which rises to make and release egg = ovulation and progesterone which thickens the womb lining, ready for pregnancy.

if there is no pregnancy, following ovulation, then the lining is shed and menstruation occurs.

118
Q

what are some exogenous factors that might affect the menstrual cycle?

A

lifestyle factors e.g. smoking, alcohol, caffeine and drugs etc, contraceptive pill / drugs, diet, stress, menstrual cycle synchronisation.

119
Q

who conducted research for menstrual cycle synchronisation and when?

A

stern and mcclintock (1998)

120
Q

what did stern and mcclintock do in their study and what did they find?

A

they studied 29 women with a history of irregular periods, samples of pheromones were gathered from 9 women at different stages of their cycles via a cotton pad placed in their armpit (which were worn for at least 8 hours to ensure than the pheromones were picked up), the pads were then treated and frozen to be rubbed on the upper lip of the other women.

on each day of the women’s menstrual cycles, the pads were applied to 20 women and the researchers found that 68% of women experienced changes to their cycle which brought them closer to the cycle of their ‘odour donor’.

121
Q

what is seasonal affective disorder (SAD)?

A

it is a yearly infradian rhythm and it is a depressive disorder which has a seasonal pattern, a form of depression (yearly cycle - circannual rhythm), symptoms are triggered during winter months when there are reduced daylight hours which is an exogenous factor.

during the night the pineal gland secretes melatonin (which induces sleep) until dawn when there is an increase in light and in the winter, the lack of light means the secretion process continues for longer which is an endogenous pacemaker and thought to have an effect on the production of serotonin in the brain.

this can also be classed as a circadian rhythms as experience of SAD may be due to the disruption of sleep / wake cycle and can be attributed to prolonged periods of daily darkness during winter.

122
Q

what are the strengths of infradian rhythms?

A

synchronisation of the menstrual cycle has evolutionary value as it may have been advantageous for females to menstruate and fall pregnant together so their babies are cared for collectively in a social group to increase chances of survival, suggesting that synchronisation is an adaptive strategy.

an effective treatment for SAD has been develop due to research, sufferers are given a light box to stimulate effects of sunlights during winter months which led to a relief of symptoms in 60% of sufferers which increases the practical usefulness of the research.

123
Q

what are the weaknesses of infradian rhythms?

A

research into the menstrual cycle is likely to be affected by many variables e.g. diet, exercise etc. which means findings of studies may not be valid as they may act as confounding variables, which may also explain why other studies have failed to replicate findings and have found no evidence of menstrual synchrony.

124
Q

what are ultradian rhythms?

A

lasts less than 24 hours e.g. stages of sleep.

125
Q

what is the sleep cycle?

A

the cycle continues throughout the night and each of the stages are characterised by a different level of brain activity which is monitored using an EEG, there are two types of sleep: NREM (non-rapid eye movement) and REM (rapid eye movement).

it lasts around 90 minutes and has 5 stages:
stages 1 and 2 - light sleep where the person may be easily woken, where there is a decrease in heart rate and body temperate and brainwave patterns start to become slower (alpha waves) which then become slower as sleep progresses (theta waves), stages 3 and 4 - deep sleep where it is difficult to wake the person up and brain activity becomes delta waves (slower and greater amplitude), the body is recharged for the immune system, memories are consolidated and the cardiovascular system is overhauled.
stage 5 - REM sleep where the body is paralysed yet brain activity speeds up to resemble the awake brain (theta waves), there is a boost for creativity and dreaming occurs.

126
Q

what are the strengths of ultradian rhythms?

A

dement and kleitman (1957) found that REM activity was highly correlated with dreaming, participants woken during REM sleep were able to describe dreams in vivid detail, which supports effect of biological rhythms on the brain and body, however, the sample size (9 participants) was criticised.

research has improved understanding of age, related changes in sleep and it has been observed that deep sleep reduces with age, van cauter et al (2000) found that sleep deficit may explain issues in old age, so in order to increase deep sleep relaxation and medication is useful which suggests that knowledge of ultradian rhythms has practical value.

lab studies of sleep leads to control of extraneous variables which means the researchers can exclude temporary variables e.g. noise, temperature etc, however, lab studies are not representative due to complicated machinery attached to participants so it is invasive as their ordinary sleep patterns are not represented.

127
Q

what are the weaknesses of ultradian rhythms?

A

tucker et al (2007) found large differences between participants in terms of duration of each sleep stage and suggested that these differences are likely to be biologically determined which makes it difficult to describe ‘normal sleep’ in a meaningful way.

128
Q

what are endogenous pacemakers?

A

internal mechanisms that govern biological rhythms e.g. sleep/wake cycle, although internal they can be altered by the environment e.g. siffre’s study.

129
Q

what is an example of an endogenous pacemaker?

A

SCN (suprachiasmatic nucleus)

130
Q

what is the SCN and what is its function?

A

a group of cells in the hypothalamus that respond to light and dark signals, light travels through the optic nerve of the eye to the SCN - signalling that it is time to be awake and it also signals to other parts of the brain that control hormones e.g. pineal gland, body temperature etc.

131
Q

what happens when we are exposed to light (e.g. the sun)?

A

the SCN increases body temperature, delays melatonin production and releases cortisol.

132
Q

what happens when we are exposed to darkness (e.g. when it turns night)?

A

the SCN increases melatonin production, which stays elevated throughout the night to promote sleep.

133
Q

who conducted animal studies to support the role of the SCN?

A

decoursey et al (2000) and ralph et al (1990)

134
Q

what did decoursey et al (2000) find in their study?

A

they found that the sleep/wake cycle disappeared when the SCN was destroyed.

135
Q

what did ralph et al (1990) find in their study?

A

they found that when the SCN transplanted from mutant hamsters to normal hamsters, their cycles went to 20 hours.

136
Q

what is the significance of the pineal gland melatonin to support the role of the SCN?

A

the SCN passes information to the pineal gland (behind the hypothalamus), during the night the pineal gland increases production of melatonin.

137
Q

what is melatonin?

A

a chemical that induces sleep and is inhibited during periods of wakefulness.

138
Q

what are the weaknesses of endogenous pacemakers?

A

research has revealed that there are numerous circadian rhythms in many organs and cells in the body, such as peripheral oscillators are found in organs where they are influenced by actions of the SCN but also act independently, an example of this would be where damiola et al (2000) demonstrated how changing feeding patterns could alter circadian rhythms of cells in the liver by up to 12 hours, whilst leaving the rhythm of the SCN unaffected which suggests other complex influences on the sleep/wake cycle.

total isolation studies such as siffre’s case study are extremely rare (he used artifical light), in everyday life pacemakers and zeitgebers interact and it doesn’t make sense to separate the two for the purpose of research which isolates influence of internal pacemakers, lowering the validity of the research.

139
Q

what are exogenous zeitgebers?

A

external cues from the environment that reset biological clocks through entrainment (synchronisation of biological clocks to 24 hours).

140
Q

what are examples of an exogenous zeitgebers?

A

light and social cues

141
Q

what is light and its function?

A

it can reset the SCN, thus playing a role in the maintenance of the sleep/wake cycle, and has an indirect influence on key processes in the body that control such functions (hormone secretion and blood circulation).

142
Q

who conducted research on light to support it as an exogenous zeitgeber?

A

campbell and murphy (1998)

143
Q

what did campbell and murphy (1998) find in their study?

A

they found that when light was detected by skin receptor sites (by shining light on the back of the knees) rhythms changed by up to 3 hours.

144
Q

what are examples of social cues?

A

babies’ rhythms and jet lag are entrained by bedtimes and mealtimes.

145
Q

what are the weaknesses of exogenous zeitgebers?

A

exogenous zeitgebers do not have the same effect in all environments as the experience of people who live in places where there is very little darkness in summer and very little light in winter tell a different story e.g. people who live within the arctic circle have similar sleep patterns all year round, despite spending around 6 months in almost total darkness which suggests that the sleep/wake cycle is primarily controlled by endogenous pacemakers that can override environmental changes in light.

miles et al (1977) recount the study of a young man, blind from birth, who had an abnormal circadian rhythm of 24.9 hours, despite exposure to social cues, such as regular mealtimes, his sleep/wake cycle could not be adjusted which suggests that social cues are not effective in resetting the biological rhythm.