Biological Psychology Flashcards
(118 cards)
1
Q
Describe the different ways to administer drugs
A
All aim to affect the CNS
- Oral Ingestion - Easy and safe method, but unpredictable. Can damage digestive system
- Injection - Strong, fast and predictable effects. Higher infection risk and hard to reduce the effects of.
- Inhalation - Absorbed into the bloodstream through capillaries in lungs. Difficult to regulate, can damage lungs.
- Absorption through mucous membranes - Nose, mouth, rectum.
2
Q
How do drugs penetrate the CNS?
A
Blood brain barrier makes it difficult for dangerous chemicals to pass from blood vessels of CNS into neurons.
Affect the nervous system differently. Bind to synaptic receptors by influencing neurotransmitters or influence chain of chemical reactions elicited in postsynaptic neurons by activation of their receptors.
Drug metabolism mediated by liver enzymes. Eliminates drugs ability to pass through lipid membranes so can no longer penetrate blood-brain barrier.
3
Q
What is drug tolerance?
A
State of decreased sensitivity to a drug that develops as a result of exposure to it
Two categories
- Metabolic intolerance - tolerance due to changes reducing the amount of drug getting to action site
- Functional tolerance - Tolerance due to changes that reduce the reactivity of action sites.
4
Q
What is drug withdrawal?
A
Adverse effects of discontinuing drug use. Opposite effects to drug. Suggests that effects may be produced by same neural changes that produce drug tolerance. Exposure changes the nervous system, when no longer present, neural changes create a symptom.
5
Q
Is there a genetic component to drug addiction?
A
Has a higher genetic predisposition than some diseases.
Sons of alcohol dependent fathers have increased alcohol tolerance and reduced hangovers.
Enzyme aldehyde dehydrogenase involved in metabolism of alcohol. Those deficient experience skin flushing when alcohol is less effectively metabolised.
6
Q
Pinel, Mana & Kim (1989)
A
- Looking at contingent tolerance to the anticonvulsant effect of alcohol.
- Rats that received alcohol before convulsive stimulation became tolerance to its anticonvulsant effect
- Rats that received the same injections after a convulsive stimulation did not become tolerant.
7
Q
Crowell, Hinson & Siegel (1981)
A
- 2 groups of rats receiving 20 alcohol and 20 saline injections
- One group received all 20 alcohol injections in a distinctive test room and the 20 saline injections in their colony room, while other group of rats received alcohol in colony room and saline in distinctive.
- Assessed the hypothermic - temperature-reducing effects of alcohol.
- Only found tolerance in rats who were injected in the environment that had been paired with alcohol administration. Tolerance has a phycological component. The body predicts it, so makes adjustments.
- Drug addicts may overdose when receive drug in new context. Tolerance in same environment.
8
Q
Siegel et al. (1982)
A
More heroin tolerant rats died from a large dose in a novel environment compared in familiar.
Shows that drug administration in novel contexts can be deadly.
9
Q
Describe the physical dependence approach to drug addiction
A
Stats that addicts are trapped in a circle of drug taking and withdrawal syndromes.
Early treatment programs were based on this. Tried to break the cycle. Failed bc some drugs do not produce withdrawal distress and drug taking patterns differ.
Led to positive incentive theories of addiction - addicts take drugs to obtain the pleasure of the drug.
10
Q
Describe intracranial self-stimulation
A
Self-administered shock to pleasure centers of the brain
Olds and Milner (1954) discovered this, stating that brain sites that mediate self-stimulation are those that normally mediate the pleasurable effects of natural rewards.
The mesocortical pathway plays an important role for reward processing and drug self-administration.
Evidence is that
- Lesions to path disrupt self-stimulation
- Hernandez et al. (2006) - Self-stimulation led to increased DA in pathway.
11
Q
Mesocortical Pathway
A
Path through which dopaminergic projections travel to reach the neocortex.
Important for reward processing and drug self-administration
12
Q
Nigrostriatal pathway
A
The dopaminergic tract from the substantia nigra to the striatum.
Associated with motor control.
Degeneration associated with parkinsons.
13
Q
Dopamine and drug addiction
A
DA antagonists are drugs which interfere or inhbibt the physiological action of DA. They mainly abloish self-administration and conditioned place preference effects.
Dopamine is important in the rewarding effects of drugs.
14
Q
Nucleus accumbens and drug addiction
A
Part of the mescocortical DA pathway which receives inputs from the ventral tegmental area. Seems to be related to reward and pleasure.
Findings
- Animals self-administered drugs into area
- Injections produced a conditioned place preference for compartment of administration
- Lesions blocked self-administration and development of place preferences.
- Self-administration shows increased levels of extracellular dopamine in area.
15
Q
Habitual Drug Use
A
Positive incentive theory says ppl motivated to take drugs by the anticipated pleasure. There is a decreased hedonic value (liking) of drug.
Mesotelencephalic DA system plays a role in drug anticipation as neutral stimuli that predict drug administration predict increased firing of DA activity in rats (Weiss et al., 2000).
Childress et al. (1999) - Cues associated with drug use led to increased activation in drug-associated brain regions.
16
Q
Explain the reasons for drug relapse
A
- Stress
- Drug-priming - exposure to formerly abused drug.
- Exposure to cues associated with drug taking e.g. US soldiers addicted to heroin in Vietnam war got rid of addiction once returned home.
Pickens et al. (2011) - After cocaine withdrawal there was a gradual increase in lever pressing for cocaine in response to cue. Explains why people relapse after years of absence. Suggested that improving the surroundings of drug addicts is useful.
17
Q
What is comparative cognition?
A
Comparative cognition is the aim of understanding cognition across the animal kingdom, looking at how it works, what is good nature and how it evolved (Shettleworth, 2010).
Important to investigate both humans and other species. Comparisons can help us be informed of the origins of our own cognition.
Best way to do this is to look at functional similarities. When investigating a non-verbal species, need to accept a part of the animals behaviour as the same as a persons verbal account. Means you never know if it is correct or not.
18
Q
Wittlinger, Wehner, & Wolf (2006) Ants
A
Saharan desert ants are able to return home in a straight line. Suggested that they measure distance between stops and know distance home.
Manipulated ant’s legs. Shortened, normal, stilts.
Stump and stilt = overshot
Normal = Found way home.
Suggested that they have some form of pedometer, counting their steps to guide them home. Have specialised navigation skills.
19
Q
Describe the importance of the cortex in investigating brain size
A
Humans have a large pre-frontal cortex compared to other species.
Dunbar (2009) - investigated relationship between size of social group and neocortex ratio. Found that social group size is the best predictor of neocortex size. In humans, it is suggested that pre-frontal cortex necessary for formation of complex social groups. Evidence against the foraging hypothesis. Sociality is the main selection pressure on primate brain size.
Barton (2006) - Primates have large neocortex, but no known cognitive processes mediated mainly by it. Instead, they are mediated by networks that link neocortex with other structures. Suggesting that it process info from all senses. Primate have complex visual systems, reason for large brains in humans as visual specilisaion important and a central part of human evolution.
Some studies also suggest visual specialisation linked to sociality, links with Dunbar.
20
Q
Explain the role of the Hippocampus on brain size within comparative cognition
A
Foraging hypothesis - Proposed that there are correlations between brain size and foraging behaviour. This was an early idea which lead to the idea that large brains reflect selection on cognitive abilities.
Jerison (1973) - Principle of proper mass, the more important a function is, the more brain area is devoted to it.
E.g. of elephants - Hippocampus where mental maps stored. Elephants have large hippocampus, behaviour of walking long distances to watering holes.
Garamszegi and Eens (2004) - birds who store a lot of food usually have larger brains than expected for brain size, perhaps reflecting sensory and motor specialisations in storing and retrieving food behaviour. Idea of mental maps.
Healy and Clayton (1994) - brains of food storing birds. Brain develops quickly within the first few weeks of life. Marsh tits who are food stores, show a continual increase in the hippocampus which is also influenced by experience in using spatial memory.
21
Q
What are the limitations in looking at intelligence within comparative cognition?
A
Shettleworth (2010) - Claims that it is not a useful term for describing animal behaviour. It describes a global ability in humans, whereas cognitive abilities of animals mainly modular.
Needs to be defined formally in respect to a specific goal. Biological intelligence should be defined in terms of fitness or goals e.g. choosing a good mate.
Vickery & Neuringer (2000) - Different intelligences are employed in different situations by different species.
22
Q
What is evidence for behavioural evolution within comparative cognition?
A
Tinbergen et al. (1963) - Eggshell removal in gulls. Bird leaves chicks to drop off egg shells. Removing them protects offspring by predators.
Looked at other gull species unaccessible to predators - they did not remove eggs from nest.
Fullard et al. (2004) - Bat avoidance behaviour in moths. Bats search for moths by using ultrasonic cries. On island of Tahiti, Bats not present yet auditory nerves of moths still fire to bat cries, but did not drop to the ground. In the absence of selection, the sensory input has been decoupled from the motor avoidance response.
This is an example of natural selection shaping cognition.
23
Q
Describe the process of mate bonding within comparative cogniton
A
Evolutionary psychologists understand human behaviour through considering the pressures that led to their evolution.
Most mammals form mating bonds.
Polyandry - Matting arrangement where 1 female bonds with more than 1 male. Only in species where reproductive contributions of males are greater than those of females. Males need better ability to process and remember spatial info than females.
Monogamy - Bonds formed between 1 male and female. In species where each female could raise more young if had more help. Need similar abilities to find way around.
When comparing species differences in cognition, it must be based on more than 1 test.
24
Q
Describe neuronal density within comparative cogniton
A
Herculano-Houzel (2009, 2011) - Neuronal density scales are different across mammals. Number of neurons is correlated in cerebral cortex & cerebellum. Coordinated scaling. In primates, cerebral cortex increases in mass as gains neurons to a greater degree than the cerebellum therefore its relative mass increases
Cognition depends on an absolute feature of the brain e.g. total number of corticial neurons and conduction velocity of fibres.
25
What are the limitations in comparing brain sizes across species?
Much research has questioned why some have larger brains relative to body weight.
The **foraging hypothesis** explores the connection between brain and cognitive abilities. Says that fruit eating species need good spatial and temporal learning abilities for tracking scattered locations.
Led to the question of exploring how parts of the brain evolve in association with specific behaviours. Whether it is concerted or mosaic.
Same brain parts in many veretebrates, but sizes are structures characteristics of each group.
26
What are the two divisions of the peripheral nervous system?
Division outside the skull and spine.
**_Somatic Nervous System_**
Interacts with external environment. Composed of afferent nerves which carry sensory signals to the CNS and efferent nerves which carry motor signals from the CNS to muscles.
**_Autonomic NS_**
Regulates the body's internal environment. Afferent nerves carry signals from the internal organs to the CNS. Efferent nerves carry motor signals from the CNS to internal organs.
Has 2 kinds of efferent nerves - sympathetic - autonomic motor nerves that project from the CNS and spinal cord. Parasympathetic nerves project from brain and part of spinal cord.
27
Which division of the brain is this?
Hindbrain
28
Describe the cerebrum
Controls abstract thought and learning.
Central and lateral fissure divide each hemisphere into 4 lobes - frontal, parietal, temporal, occipital.
29
Which area of the cortex is this?
Frontal lobe
Motor activity, speech, planning, impulse control
30
Which area of the cortex is this?
Parietal Lobe
Integrates sensory information by sensing body position and integrating visual information.
Spatial tasks.
31
Which area of the cortex is this?
Temporal lobe.
Contains the primary auditory cortex involved in processing auditory information. Left temporal lobe contains Wernicke's area - involved in language comprehension.
32
Which area of the cortex is this?
Occipital lobe
Contains the primary visual cortex which handles visual information.
33
What are the different classes of neuron?
Multipolar: 2+ processes extending from cell body
Unipolar: 1 process extending
Bipolar: 2 processes extending
Interneurons: Neurons with a short/no axon. Integrate the neural activity within a single brain structure.
34
What do glial cells do and what kinds are there?
- Surround neurons and provide support and insulation.
- Exchange chemical signals with neurons to control establishment and maintenance of synpases between neurons
- Moderate neural activity
- Control blood-brain barrier
**Oligodendrocytes** - Extensions, help information move faster along axons.
**Schwann Cells** - Form spirals around axon. Guide axonal regrowth after damage.
**Astrocytes** - Star-shaped. Allow passage of chemicals from blood to CNS. Regulate blood flow to brain. Form the blood brain barrier.
**Microglia**: Respond to injury and disease by triggering inflamatory reponses.
35
Describe how the spinal cord is made up?
Two different areas
- Gray matter: Cell bodies and unmyelinated interneurons
- White mattter: Myelinated axons
Axons join via the dorsal root or ventral root.
Dorsal root axons form the dorsal root ganglia.
36
Evaluate the use of MRI
- High res images
- High spatial resolution
- 3D images
37
Evaluate the use of fMRI
- Images of oxygen flow in the blood to active areas of brain. Active areas use more oxygenated blood. Oxygenated blood has magnetic properties that influenced the waves.
- Poor temporal resolution
- Nothing injected
- Better spatial resolution
38
Introduction to memory
Memory - process of storing and retrieving information.Important process to human life.
The importance of memory means that damage to the brain can have a detrimental effect, producing memory disorders. Study of memory disorders has contributed to understanding of memory.
One of the most influential models of memory is the multi-store model proposed by **Atkinson & Shiffrin (1968)**.
3 stores are proposed,
- sensory stores
- short-term stores
- long-term store.
The model proposes that information is lost because it decays and that long-term memories are lost through the process of retrieval.
39
Describe the case of HM
Epileptic who had temporal lobes removed which reduced LTM. Suffered from mild retrograde amnesia - inability to remember the past. Could still recall from childhood, why it is mild. Also, severe anterograde amnesia - no longer form new memories. Most STM intact.
**_Tests of measurment_**
- Block-tapping memory test - STM good for spatial info
- Digit-span test - Recall digits provided the time between learning and recall was within the duriation of STM.
- Incomplete Pictures & Mirror Tracing - Ev of new memory. He improved performance over time, but could not refer back to the first time when he performed the task.
**_Findings_**
- Led to distinction between STM and LTM. Separate.
- He had problems with memory consolidation. Could not move memories from STM to LTM.
- 2 categories of LTM, explicit and implicit memory.
- Shown that medial temporal lobe important within memory. Challenging view at the time that memory functions were diffused throughout the brain.
40
What is the difference between retrograde and anterograde amnesia?
**Retrograde**: Inability to recall past memories
**Anterograde:** Inability to create new memories
41
Describe the case of Clive Wearing
Herpes simplex encephalistis, inflammation in left temporal lobe, severe damage to hippocampus. Extremely short memory span.
- Able to remember he was married = spared semantic memory
- Could not remember wedding = impaired episodic memory
- Could not remember divorce = Impaired semantic memory
- Asked if remembered PM John Major, but earlier on seen car with plate 'JMV' and instantly said 'John Major vehicle' showing he had implicit memory for his name.
42
Describe the case of K.C.
Damage to brain, both hippocampi. Suffered from anterograde amnesia and gradual retrograde amnesia. Could not store new memories and recall past just before accident, but could recall far back memories. Intact semantic memory, but lacked episodic memory of past.
It was suggested that hippocampus important for episodic memory, however damage left semantic intact, leading to the suggestion that episodic and semantic memory could be formed and stored separtely, processed by different brain regions.
Visual imagery, emotion centres in the brain and fontal areas invovled in self-referential processing important for autobiographical memories.
43
Describe the case of Jon and his memory problems
Examined by **Baddeley, Vargha-Khadem and Mishikin (2001**).
Had developmental amnesia due to premature birth and anoxia, resulted in severe hippocampal damage. From age of 5, memory problems apparent. However, had good intelligence and semantic memory, impaired recall, but intact recognition. Led to suggestion that episodic memory not necessary for recognition or acquisition of semantic knowledge.
44
Describe the case of Patient R.B. (Memory)
Suffered damage to one part of hippocampus (CA1 pyramidal cell layer) and developed amnesia. Suggests that hippocampal damage alone can produce amnesia.
Transient global amnesia the strongest evidence that selective hippocampal damage can cauase medial temporal lobe amnesia. Shorter, lasts 4-6 hours, happens suddenly in normal adults.
This also related to abnormalities in the CA1 subfield of the hippocampus.
45
What is memory consolidation and is there any evidence for it happening?
Common form of amnesia is post-traumatic amnesia - usually due to concussion. May cause retrograde amnesia for time before injury and anterograde for time after.
Period of anterograde amnesia suggests a temporary failure of memory consolidation. Concussions disrupt recent memories, suggesting that older ones have been stregthened = evidence of memory consolidation.
46
Describe Hebb's (1949) theory of memory consolidation
Argued that memories of experiences are stored in the short-term by neural activity. These memories at risk of disription, but eventually structural changes in synapses provide them with stable long-term storage. Suggests that it is a brief process.
Usually studied by using electroconvulsive shock (ECS) - intense, seizure-inducing current to the brain through electrodes on scalp.
47
Squire, Slater and Chace (1975) in response to Hebb (1949)
Found a long-gradient of ECS-produced retrograde amensia when measuring memory for TV shows prior to ECS therapy.
Found that lasting memories become more reistant to disruption throughout life. It is not a brief process like Hebb suggests.
48
What does standard consolidation theory propose?
Proposes that the hippocampus stores memories temporarily.
Also suggested that the hippocampus involved in establishing memories, but that they become stronger and less dependent on the hippocampus over time.
49
What is global cerebral ischemai?
Interuption of blood supply to the brain.
Often suffer from medial temporal lobe amnesia e.g. patient R.B.
50
What did Selye (1950) propose about stress?
Stress response has a **dual nature**. Two main effects.
1. Short-term produce adaptive changes which help the animal respond to the stressor.
2. Long-term - Changes which negatively impact health.
51
Describe the first system of the stress reponse
**Hypothalamic pituitary adrenal (HPA) system**
- Stressor activates the hypothalamic pituitary axis which produces corticotrophin-releasing factor.
- CRF from hypothalamus stimulates the anterior pituitary gland to release adrenocorticotropic hormone (ACTH).
- ACTH stimulates adrenal glands to produce the hormone corticosteroid - hormone releases stored glucose from the liver for energy + controls swelling after injury.
Measure stress by looking at glucocorticoids.
E.g. trier social stress test **Kirschbaum et al. (1993).**
- Baseline
- Give 5-minute speech as job application and spend 5 minutes counting back from 1,022.
- Saliva and blood samples collected. Increased levels of substances known to indicate the activation of HPAA
- Salivary cortisol peaks 10 minutes later, hGH peaks 40 minutes later. Serum cortisol, prolactin and ACTH peak immediately after test
Success - Gives objective measure of stress
52
Describe the second system of the stress response
**Sympathetic Nervous System**
- System important because it becomes activated by stressors.
- When activated, epinephrine and norepinephrine are released from the adrenal medulla which prepares the body for a flight or fight response.
- As a result, there is increased blood flow to muscles, pupil dilation and glycogenesis. Need more energy, so provides us with this.
- After threat is gone, can take 20-60 minutes for body to return to normal. Good for evolution.
- Priming body for action means that you can effectively cope with threat. Critical role in surival, more likely to survive.
53
Describe the case of gastric ulcers in response to stress
Lesions to lining of the stomach which happen to those who encounter stress often.
Are psychosomatic - psychological factors play a role.
However, changed when discovered that they caused by baceria.
**Blaster (1996)** - Stress mediates the susceptibility of the stomach wlal to be damaged by H.pylori causing ulcers.
Other research suggests that it is not enough to produce the disorder as some health subjects have signs of it (75%). Psychological treatments reduce the signs of the infection. Stress increases susceptibility.
54
How does the immune system respond to stress?
**_Innate Immune System_**
- First to react
- Triggered when toll-like recpetors bind to molecules on the surface of the pathogens.
- Inflammation one of the first respinses to invasion of pathogens. Triggered by release of chemicals from damaged cells. Inflammation increases blood flow to sute carrying important cells called phagocytes.
- Cytokines important - attract lecukocytes and other phagocytes to infected area. Promote healing of damaged tissue.
**_Adapative Immune System_**
- Evolved more recently
- Slower
- Reacts against specific antigens
- Has a memory - once reacted against pathogen, reacts effecitvely against same in the future. Gives vaccinations preventative effect.
- Main cells are specialised leukocytes called lymphocytes which are produced in bone narrow.
- Two major classes
_B-Cells_ - Anti-body mediated immunity happening in body fluids, outside cells.
_T-Cells_ - Cell mediated immunity to attack cells that are compromised, inside cells.
55
What are the effects of stress on the immune system?
Seen as disruptive, however this is not consistent with evolution as every organism encounter stress, important.
During acute stres, increased chance of skin-lesion interacting with pathogens. Why the immune system boosts during acute episodes of stress, cytokines released.
**Segerstrom & Miller (2004)** - Effects of stress on immune function depend on the kind of stress.
Acute stress can improve immune function to innate immune system.
Chronic stress negatively impacts adaptive immune system, no idea when will end. Suppression of the immune system, functional.
56
How can exercise help to combat stress?
**Exercise** is an acute stressor which produces free-radicals that contriubute to oxidative stress.
**Steptoe and Butler (1996)**
- Habitual vigorous exercise associated with reduced emotional distress and positive emotional wellbeing.
**Stewart et al. (1994)** - Self-reported time exercising predicated range of positive health outcomes 2 years later. Reduced anxiety, depression and subjective wellbeing.
**Cramer et al. (1990)** - Effects of exercise over 15 weeks. Increased wellbeing, however anxiety decreased then began to increase again.
57
How can socialising help to combat stress?
"**Cohen and Willis (1985)** - **Stress buffering hypothesis**. The presence of a social support system helps shield an individual from the negative impact of stressful events.
Alternative is **social baseline theory** proposed by **Coan (2008)**. Suggests that social proximity and connection is a baseline condition for adaptive and healthy human functioning. Humans expect to live in groups. Out-sourcing some of our regulatory needs to close others is our expected state of being.
**Beckes & Coan (2011)** - Support theory. Human brain designed to assume it is embedded in a social network characterised by familiarity, joint attention, shared goals. Social proximity inhibits release of stress hormones and promotes good health. Social rejection a source of stress.
**Jakubiak & Feeney (2016)** - Social proxmity studied by looking at interpersonal touch. Two mechanisms suggested. Relational-cognitive pathway = feelings of security, support, trust. Neurobiological pathway = increase in oxytocin, reduced hormonal and phyiological reactivity to stressors.
**Coan et al. (2016)** - Handholding reduced neural response to a stressor. Spouse handholding associated with least unpleasantness.
**Masters et al. (2009)** - Reduced pain when looking at partner compared to stranger and when holding hand.
"
58
What are the effects of loneliness on stress?
Social proximity is important for survival and stress reduction. Suggested that loneliness is an aversive state that motivates us to seek social interaction to promote our survival and health. Stigmatised.
**Doane & Adam (2010)** - Loneliness associated with increased cortisol awakening response next morning.
**Cacioppo et al. (2015)** - Socially isolated have increased activity of the HPA axis.
Don't have access to stress-buffering influences of social interaction.
**Holt-Lunstad, Smith and Layton (2010)** - Increased numbs of social relationships led to decrease in risk of mortality.
59
Wolf et al. (2007) Stress and Immune Function
Stress in mothers can aggregate asthamtic symptoms in children.
Asthma in children increases measures of stress in mothers.
60
Does stress increase the susceptibility to disease?
No because..
- Immune system has many redudant components, disruption to one of them may have little effect.
- Stress produced effects may be short-lived
- Declines in some aspects of immune function may induce compensatory increases in others.
- Difficult to study, only correlational studies.
**Cohen et al. (1991)** - Stress questionaires then injection of virus or saline. Those who scored higher on stress scales developed colds.
61
Introduction - Sleep
**Siegel (2008)** defines sleep as a rapidly reversible state of immobility and greatly reduced sensory responsiveness. Essential part of life. Large portions of life spent sleeping. Assume that it fulfils a critical biological function. Sleep deprivation has an impact on both REM and slow-wave sleep
62
Describe REM sleep
Rapid eye movement (REM) accounts for 20-25% of the sleep cycle Low amplitude and high frequency EEG activity. Pattern similar to when the brain is awake. Fast eye movements, eyes move rapidly beneath closed eyes. Core muscles relaxed, increased variability in physiological function e.g. HR, blood pressure and breath rate.
63
Describe slow-wave sleep
Stages 3 and 4 of sleep cycle. Stage 3 = Body enters deeper stage of sleep. Occasional delta wave, stage 4 mostly delta waves. Stage 4 = Deepest form of sleep with lowest ability to generate arousal. Reduction in HR
64
Compare both REM and slow-wave sleep
**Stage of sleep affects activity in the brain and body**
* - REM = Less body relaxation. Increase in HR compared to reduction in HR in slow-wave.
* - EEG activity similar to when the brain is awake whereas slow-eave shows different.
**Early evidence suggests REM responsible for dreaming.**
* **Dement and Wolper (1958)** - Did things whilst participant slept e.g. throw water. Objects incorporated ended up being in dream.
* Large amount of evidence against this now e.g. anti-depressants suppress REM sleep, but ppl do not report reduced rates of dreaming.
65
What happens if you deprive an individual of REM sleep?
Default theory = Dangerous to stay in slow-wave for a long time which is why the body has stages.
**Nykamp et al. (1998)** - Studied effects of sleep deprivation in REM stage. Participants were awakened every time they entered REM sleep and had to stay awake for a further 15 minutes. Participants did not report feelings of tiredness despite having 5 hours sleep. No REM rebound. Suggests REM sleep not required.
**Webb & Agnew (1967)** - Participants had to be awakened 17 times in first night of REM sleep deprivation and 67 times during the 70th night. Suggests that the amount of REM sleep is regulated separately from amount of slow-wave sleep. REM sleep serves a special function. Suggested it is important for memory consolidation - leads acquired memory traces to stabilise.
**Rasch et al. (2004)** - SSRIs reduce REM but no effect on finger tapping performance. Perform better on memory tasks even though have no REM sleep.
66
Describe what happens if you deprive an individual of slow-wave sleep
* Short sleepers tend to get as much slow-wave sleep as people who sleep for longer periods
* Reducing sleep time results in reduction in stages 1 and 2, but not slow-wave.
* Sleep deprivation leads to an increase in sleep efficiency where slow-wave sleep is prioritised.
* Suggests that slow-wave sleep is important/has a restorative capability.
67
Describe the different theories of sleep
**_Recuperation theory_**
* Being awake depletes energy resources by disrupting homeostasis.
* Sleep is the act of returning us to baseline levels.
* Slow-wave activates the rest and digest systems.
* Explains why we need to have a lot more sleep after not having much for a while.
* E.g. **Xie et al. (2013)** - Theory that sleep removes neurotoxic waste products which arise in the awake brain. Neurotoxic waste is a range of proteins linked to neurodegenerative disease.
**_Adaptation Theory_**
* Argues that sleep is a reaction to the internal 24-hour timing system that evolution has primed us for. Programmed to sleep at night regardless of what happens during the day.
* Focuses on when we sleep. - Humans not well adapted to life in dark, sleep at night to conserve resources.
* Motivated to sleep, but don't need it to survive and don't need a certain amount of sleep.
* Sleep related to how vulnerable a species is whilst sleeping and how much time it needs to spend to feed itself and take care of survival characteristics e.g. Zebras sleep for 2 hours a day and must continuously graze to eat enough.
68
What effect dies sleep deprivation have on decision making?
**Iowa gambling task**
* Test of risky decision making
* Those with frontal damage drawn to bad decks.
* Led to suggestion that sleep deprivation reduces activity in the vmPFC and patients with damage here show increased anger, less empathy.
**Killgore et al. (2006)**
* Looking at if sleep deprivation has negative impact on decision making in iowa task.
* Perform at baseline and then awake for 49 hours.
* Need an extreme amount of sleep deprivation in order to see results
69
Describe what animal studies show about sleep deprivation
Carousel apparatus to deprive rats of sleep. Hooked up to an EEG and each time it detects they are sleeping, they are thrown into water.
Sleep deprived rats die after 12 days. Died from stress, not due to lack of sleep. Difficult to study in animals.
70
Describe Insomnia
Report that it takes hours to sleep, but when tested they sleep for longer than described.
Sleep apnoea often misdiagnosed as insomnia. Unaware that often awake.
Periodic limb syndrome - Involuntary and unaware limb movements associated with feelings of having slept poorly. Report poor sleep, but unaware of problem.
71
Describe Hypersomnia
Most commonly studied form is **narcolepsy** = severe daytime sleepiness and daytime sleep episodes. Only spend an hour more sleeping. Sleep at inappropriate times.
* Gene found to contribute **Orexin**. Reduced levels in cerebrospinal fluid and brain.
* Synthesised in brain by neurons in hypothalamus. Region linked to promotion of wakefulness.
**Cataplexy** - Recurring losses of muscle tone during wakefulness triggered by emotional experiences. Results in daytime sleepiness, sleep paralysis and hypnagogic hallucinations.
72
What are the effects of long-term sleep reducing and what are the differences between short and long-term sleepers?
Long-term sleep reducing = High plasticity. People can adjust to some degree of sleep deprivation. Sleep becomes more efficient after prolonged burst of sleep deprivation.
**Fichten et al. (2004) -** Compared sleepers. Long sleepers sleep more and short sleep less. No evidence that short sleepers were suffering.
**Friedman et al. (1997)** - Reduced sleep over 9 weeks and then reduced duration over a year. Sleep efficiency increased. Consistent with plasticity of sleep. However, small sample size.
73
Tamakoshi & Ohno (2004) Sleep and health
Sleeping 8 hours not as healthy as proposed Fewest deaths between 5-7 hours. However, correlational data. Doesn't prove that sleeping 8+ hours causes health problems.
74
Describe the stage of wakefullness
Beta activity is rapid and low voltage. Alpha activity occurs just before sleep. There is higher voltage and lower frequency.
75
Describe stage 1 of sleep
- Low voltage - High frequency - Similar but slower to alert wakefulness - Lower HR and reduction of muscle tension
76
Describe stage 2 of sleep
- Slightly higher amplitude - Lower frequency - Two wave forms. K complexes = Single large negative wave followed by single large positive wave. Sleep spindle = 1-2 seconf waxing and waning burt of 12- to 14-Hz waves.
77
What has comparative analysis of sleep shown
* Mammal and bird sleeping suggests that sleep servers a physiological function rather than protecting and saving energy.
* Dolphins sleep with half of brain as against logic of natural selection to risk predation while sleeping.
* Not a higher-order human function as many mammals sleep
* Lots of sleep not required e.g. horses sleep 2hrs
* No relation between sleep time, level of activity and body size
78
Describe the 4 brain areas involved in sleep
**Posterior hypothalamus**
* Promote wakefulness
**Anterior hypothalamus**
* Promote Sleep Reticular Formation
* Suggested that there is a wakefulness producing area. Electrical stimulation to area in sleeping cats awakened them from a lengthy period of EEG desynchchronization.
* Low levels of activity in this area produce sleep
* High levels in area produce wakefulness
* Referred to as the reticular activating system
**Reticular REM-Sleep Nuclei**
* Part of the caudal reticular formation
* Involved in wakefulness and production of REM sleep.
* REM sleep controlled by nuclei scattered throughout caudal reticular formation
* Each site responsible for controlling one of the major indices of REM sleep e.g. a site for reduction of core-muscle tone.
* REM sleep only occurs when a network of independent structures are active together.
79
Introduction - Development of the Nervous System
The brain undergoes considerable development through its lifetime. Process starts with a single fertilised egg, ends with a functional adult brain. The brain is plastic, continuously changing in response to its genetic programs and environment. It is altered both by experience and as the brain develops throughout time. Neurodevelopment refers to the development of the brain and is influenced by many factors. Developing neurons undergo 5 different phases in order to become the human brain we know of. Some of these happen in order, whereas others are more long-term or overlap.
1. Induction of the neural plate
2. Neural proliferation
3. Migration and aggregation
4. Axon growth and synapse formation
5. Neuron death and synapse rearrangement
A fertilised egg is **totipotent**, meaning that is has the ability to become any type of body cell. However, 4 days after embryological development, newly created cells lose their totipotency and begin to specialise. At this stage, developing cells are **pluripotent**, they can give rise to many different types of body cell and have unlimited capacity for self-renewal and become any type of mature cell. As the embryo develops, new cells become increasingly specialised. New cells are **multipotent**, can only develop into one class of cells e.g. blood cells. Most developing cells eventually become **unipotent**, they can only develop into one type.
80
Describe the process of Induction of the Neural Plate (First stage in dev of NS)
* 3 weeks after conception, patch of tissue on dorsal surface of embyro becomes neural plate.
* NP = Tissue going to develop into nervous system
* Development induced by chemical signals from mesoderm layer
* As pulled together, broader areas fuse. Neural tube forms basis of CNS. Neural crest forms basis of PNS.
* Cells of neural plate often refered to as stem cells which are pluripotent and have unlimited capacity for self-renewal.
* Growing neural plate folds to form neural groove. Lips of this form the neural tube which becomes the cerebral ventricles and spinal canal.
81
Describe the process of neural proliferation (2nd stage in neural development)
* Tissue which develops into neural tube. recognisble as fluid filled tube. Cells of this increase in species specific ways which results in characteristics.
* 3 swellings appear at end of neural tube - become the forebrain, midbrain and hindbrain.
* Pattern controlled by chemical signals from organiser areas of the neural tube - floor plate and roof plate.
82
Describe the process of migration (Third stage of neurodevelopment)
* Cells migrate to the target location by moving through cells already formed.
* Two types of neural tube migration
1. **Radial Migration** = Moving out by moving along radial glial cells in straight line to outer wall of tube
2. **Tangenetial Migration** - Moving up, occurs at righ angle ro radial.
* Two types of migration for developing cells
* **Somal transolation** - Growth of extension in direction of migration
* **Glia-mediated migration** - Temporary network of radial glia cells appear in developing neural tube and move along radial glia network.
* Movement guided by environment
**Neural crest migration**
* Travels along further distance
* Guided by chemical signals
* Glial cellls involved in release of chemical signals
83
Describe the process of aggregation (third stage in neurodevelopment)
After migration, cells need to align themselves with other cells and form structures.
Both processes mediated by cell-adhesion molecules.
No synpases or dendrite yet, so have narrow gap junctions.
84
Describe the process of axon growth (fourth stage of neurodevelopment)
Once migration complete and structures formed, axons and dendrites begin to grow.
**Sperry (1963)** tested the **chemoaffinity hypothesis** which is the hypothesis that postsynaptic surfaces release specific chemical labels which attract target axons in both dev and regeneration.
Found out that axons capable of precise growth by rotating eyes of frogs.
- When rotated 180 without cutting optic nerve, frog misdirects tongue strikes by 180.
- Optic nerve cut and eye rotated 180 = first blind, once nerve regen frog misdirects strike by 180. Axons grow back to original synaptic sites.
* Series of chemical signals attract and repel axonal growth
* Pioneer growth cones = First travel to route and interact with guidance molecules
* Fasiculation - Tendency of developing axons to grow along paths established by preding neurons
**_Topographic Gradient Hypothesis of Axonal Migration_**
* Axon targets arrange same way on terminal surface as original
* Growing axons guided to their target by 2 intersecting chemical gradients
* Axons maintain spatial relationships with neighbours due to chemical gradients on target cell body
85
Describe the process of synapse formation (4th stage in neurodevelopment)
* Once reached site, need to establish pattern of synapses
* Need coordinated activity of 2 neurons to create synapse between
* Depends on prescence of glial cells
* High levels of cholestrol needed
86
Describe the process of neuron death & synapse rearrangement (5th stage in neurodevelopment)
More neurons are produced than required.
**Necrosis** - Passive cell death
**Apoptosis** - Active cell death
* Safer than necrosis
* Structures pulled apart carefully
* Inflammation prevented
* Consequence of cancer
Triggered by..
* Some genetically programmed for early death
* Failure to obtain chemicals, competition
Promoted by neurotrophins which promote growth and survival.
**_Synapse Rearrangement_**
* Space is left when neurons die. Filled by axon terminals.
* Rearrangement of synaptic connections leading to increased selectivity of transmission
87
Explain how the human brain is not fully developed at birth
* Find out from animal models. Develops slowly which is unique.
**Focus on the Prefrontal cortex**
* Age-related changes in cog function.
* Role in _working memory_ - Keeping releavnt info accesible for short periods of time while completing task.
* Planning and carrying out sequences of actions
* Inhibiting responses inappropriate for current context
* Following rules of social behaviour
* Infants don't display certain cog functions e.g. Piaget.
* Diamond (1991) says because neural circuity of prefrontal cortex not developed yet. Synaptogenesis not maximal until early in 2nd year.
The brain increases in **size** due to
* Synaptogenesis. Differs between regions.
* Myelination of sensory and motor areas - Increases speed of axonal conduction.
* Increased dendritic branches - Pattern progresses from deeper to more superficial layers.
88
Explain how experience affects early development
Two _types_ of _experience_
1. P**ermissive** = Necessary for info in genetic program to be manifiested
2. **Instructive** = Contribute to direction of development
Development is _time-dependent_
* **Critical period** - If occur without, have no effect
* **Sensitive period** - Period when most sensitive
**_Bolhuis, Okanoya & Scharff (2010)_**
* Songbirds produce 2 classifications of vocalisations, calls and songs.
* If reared in isolation with no tutor, birds sing abnormal songs in subsong period.
* Defeanded birds after critical period: Abnormal song
* Defended birds after crysallised song: Normal singing
**_Deprivation on ocular dominance columns in PVC_**
* Depriving one eye of input for early days of life has lasting adverse effect, but doesn't happen if other eye also blindfolded
* - 1 Blindfolded = Ability of eye to activate VC reduced, ability of other eye increased. Early deprivation changes pattern of synpatic input into layer IV of PMC. Reorganises the system.
* Width of clums of input from deprived eye is decreased and width from non-deprived increased
**_Topgraphic Sensory Cortex Maps_**
* **Knudsen & Brainard (1991)** - Owls with vision deplacing prisms on eyes. Led to change in auditory spatial map in tectum. Owl with prisms that shifted visual world to 23 degrees to right had auditory map which shifted 23 to right.
89
Explain how experience affects neuroplasticity in adults
The mature brain can still change and adapt. Changing the way humans think about selves and those with brain damage.
**Hertzog et al. (2008)** - Exercise may reduce or delay memory problems.
**Muhlnickel et al. (1998)** - Tinnitus produces reorganisation of primary auditory cortex.
**Elbert et al. (1995)** - Musicians who played with left hand have enlarged hand rep area in right somatosensory cortex.
90
Describe autism and attempts to identify its neural mechanisms
* Apparent before age of 3, hetereogenous disorder (impaired in some things, superior in others) with genetic basis
* Neural mechansims - Damage to some neural structures. Fusiform face area shows less fMRI activity in response to faces. Mirror neurons - role in understanding intentions of others.
91
Describe Williams Syndrome and attempts to identify its neural mechanisms
* People sociable and empathetic, Good language skills, low iq
* Serious cognitive deficits such as attentional problems and spatial abilities.
* Missing one of the copies of chromosome 7
* Thinner cortex and white matter. Thinning in orbiotofrontal cortex and boundary of pariertal and occipital cortex.
92
Discuss brain tumors as a cause of brain damage and the different types
**Meningiomas Tumours –** Grow between the meninges and 3 membranes covering the CNS.
* Are also encapsulated tumours – Grow within own membrane, but usually benign.
**Infiltrating Tumours –** Grow through surrounding tissue.
* Usually malignant – difficult to remove
**Gliomas Tumours –** Develop from glial cells and rapidly infiltrate.
**Metastatic Tumours** – Grow from being transported to the brain through the bloodstream.
93
Discuss strokes as a disorder of brain damage
Produce dead tissue area called infarct. Surrounded by dysfunctional area called penumba which is the goal of stroke treatment.
Two types
* **Cerebral Hamemorrhage:** Cerebral blood vessel ruptures and blood seeps in and destroys surrounding tissue
* Cerebral Ischemia: Disruption of blood supply to brain. 3 causes, thrombosis - plug blocks blood, embolism, plug carried and ecomes lodged, Arteriosclerosis, walls of blood vessels thicken and create blockage.
**_Glutamate_** important
* NDMA most involved
* NA+ and CA2 enter postsynaptic triggering release of glutatame, spreading toxin
94
Discuss closed-head injury as a cause of brain damage
Brain injury which does not penetrate skill.
Contustions - Damage to cerebral circulatory system. Brain bashes against skill. Blood collects in sudural space
95
Discuss infections as a cause of brain damage
Invasion of the brain by microorgansisms resulting in infalmmation called encephalitis.
Two types of viral infections
1. Affinity for neural tissue e.g. rabies
2. Attack neural tissue, but no special affinity e.g. herpes
96
Discuss neurotoxins as a cause of brain damage
E.g. mercury led
Produce toxic psychosis
Some produced by body
97
Discuss and provide examples of neurological diseases associated with brain damage
Epilepsy - Faults at inhibit synapses causing many neurons to fire in bursts.
Parkinson's Disease - Movement disorder of old age. Associated with degenration in substantia nigra and little dopamine
Huntington's Disease - Motor disorder associated with severe dementia.
MS - Attacks myelin of axons in CNS
98
Explain the process of neural degeneration in response to nervous system damage
**_Antereograde degeneration_**
* Degeneration of distal segment between cut and synpatic terminals. Swells and breaks off due to being cut off from metabolic centre
**_Retrograde Degeneration_**
* Degeneration of proximal segment between cut and cell body.
* Slower as regenerating axon makes new synaptic contact
99
Explain the process of neural regeneration in response to nervous system damage
* Non-existent in CNS, but possible in PNS
* If original Schwann cell myelin sheath intact, regenerating axons may grow through to reach orginal target
* If nerve severed, may grow into incorrect sheaths
* If ends widely separated - no meaningful regeneration
* Schwann cells promote regeneration by producing neurotopic factors which stimulate growth cones, axons and cell adhesion molecules.
Collateral Sprouting = Axon degenerates, axon branches grow out from healthy neurons and synapse at sides vacted by degenerating axon.
100
Explain the process of neural reorganisation in response to nervous system damage-
* **Pons et al. (1991)** - Mapped primary somatosensory cortex of monkeys whose contralateral arm sensory neurons cut 10 yrs before. Cortical face rep had expanded into orginal arm area.
Investigated in humans using the blind.
Mechanisms of Neural Reorganisation
* Strengthening of existing connections
* New connections established by collateral sprouting.
101
Explain how to promote recovery of function after brain damage
Difficult to compenstate between true recovery and compenstatory changes as things such as brain swellings can make it look as if there has been an improvement.
**_Neurotransplantation_**
* Transporting foetal tissue, but has limited success in humans
* Transporting stem cells e.g. embyronic stem cells into damaged rat spinal cord. Those with damage showed improved mobility.
**_Rehabilitative Training_**
* **Weiller et al. (1999)** - Constaint-induced therapy. Tied down arm for 2 weeks while affected one got training. Increase in performance.
* Cognitive and physical exercise - Active individuals less likely to get neurlogical disorders. However, problems in measurement.
**_Promoting Regeneration_**
* Induce in the CNS but directing growth of axons by Schwann cells.
* Also by neuroprotective molecules
102
Describe Phantom Limb syndrome and adult plasticity
* Claims that it is due to reorgnaisation of the somatosensory cortex
* Feels touch on face and phantom limb due to proximity on somatosensory cortex
* 20% of those born without limbs report this
* 50% of ppl experience severe pain in limbs
103
Describe the nonmatching-to-sample model of explicit memory in Monkeys
* Experiment showed that monkeys with bilateral medial temporal lobectomies have problems forming long-term memories for objects in delayed non-matching-to-sample test.
* Monkey shown distint object under which it finds food
* After a delay, monkey presented with 2 object, sample and unfamilar.
* Must remember the sample object so it can select the unfamilar object and find food under it.
* Well trained monkeys performed well
* Those with bilateral medial temporal lobe lesions performed poorly.
* Similar to those of HM.
* Shows that amnesia from medial temporal lobe damage is due to hippocampal damage
*
104
Describe the nonmatching-to-sample model of explicit memory in rats
* Better at lesioning hippocampus than monkeys as little damage to other areas. Using aspiration in monkeys.
* Tested using Mumby box.
* Hippocampus large role in object-recognition memory
105
What evidence is there to suggest that damage to the medial temporal cortex is responsible for object-recognition deficits after medial temporal lobectomy?
3 major structures of medial temporal lobe are the
- Rhinal cortex
- Amydala
- Hippocampus
Removal of rhinal cortex produces severe and permnanent deficits. Removal of the hippocampus produces only moderate deficits. Amydala has no effect.
106
How does the hippocampus play a special role in memory for location?
Rodent spatial memory tested using
* **Morris water maze test** - Rats learn to swim to hidden platform. Difficult for those with hippocampal lesions. Shows hippocampus important for spatial learning
* **Radial arm maze test** - Arms radiate from chamber. Those intact learn to visit only rhose with food. Measure of reference and working memory. As rat becomes familar with envornment, hippocampal neurons only fire when rat in particular part. Each place cell has a difference place field.
107
What role does the inferotemporal cortex play in storing memories?
Bussey and Saksida (2005) - Says it stores memories of visual input. Retrieve visual memories here.
108
What role does the amydgala play in storing memories?
* Little evidence of storing memories
* Strengthens emotionally significant memories stored in other structures
* Explains why emotion provoking events are remembered more
109
What role does the prefrontal cortex play in storing memories?
* Damage doesn't result in amnesia
* Different parts of it play different roles in memory
* Those with lesions lose some episodic abilities. Antereograde and retrograde deficits for temporal order of events. Deficits in working memory.
* Difficulity performing tasks involving series of responses
110
What role does the cerebellum play in storing memories?
* Storage of learned senorimotor skills
* Role in Pavlovian conditioning
111
What role does the striatum play in storing memories?
* Memories for consistent relationships between stimuli and responses
* Learning referred to as habit formation
112
Explain LTP and its involvement in memory
* When synpases are made stronger by repeated stimulation
* Only occurs if presynaptic firing is followed by postsynaptic firing.
* Lasts for a long time
* Effects seen in structures implicated in learning and memory e.g. drugs that influence learning and memory have parallel effects on LTP, induction blocks learning of Morris water maze until subsided.
**_Three part process_**
* Induction (learning)
* Maintenance (memory)
* Expression (recall)
113
Explain the induction of LTP in learning
* Studied where NDMA glutamate receptors prominent which do not respond unless glutamate binds and neuron partially polarized.
* Ca2+ channels don't open unless conditions of excitation and depolarisation met.
* If postsynaptic neuron is depoalrised when gluatamate binds to recepotes, NDMA receptors permit entry of calcium ions which induce LTP by activating protein kinases
114
Compare Alzheimer's Amnesia with medial temporal lobe amnesia
* Alzheimer's is a cause of amensia
* Characterised by short-term memory deficits.
* Deficits in implicit memory for verbal and perceptual material, but not for sensorimotor learning
* Low levels of **acetlycholine** due to degeneration of the basal forebrain
115
Explain the difference between convergent and divergent evolution
**Convergent -** Evolution in unreleated species of similar solutions to some environmental demands. Evolve an **analgous** structure which is similarity of function and characteristics, not necessairly similar in apperance.
**Divergent** - Groups from the same common ancestor evolve and accumulate differences resulting in the formation of a new species. have a homologous structure - similar structure but different functions.
116
Is collaboration unique to humans? Provide evidence for this.
**_Cooperation_**
* **Melis, Hare and Tomasello (2006)** - Chimps recongise when a collaborater is needed. Only cooperate with effective helpers, those who have been fair collaboraters before. Evidence for social constraints - ability to solve cooperative problems.
* **Bullinger, Melis and Tomasello (2011)** - Chimps prefer to reach goals on their own. Only change ways if benefit from collaborating.
* Chimps can cooperate, but not with the same motivations as humans.
**_Social Learning_**
* Human culture unique because over generations changes are adopted and further ellaborated in the next.
* **Tennie, Call and Tomaslleo (2009)** - Human social learning more about process than product. We modify culture over time and cooperate as want others to learn. Social motivations for conformity.
The unique social skills and motivations of humans are a scaffold for developing human cognitive skills.
117
Is theory of mind unique to humans? Provide evidence for this
TOM is knowing what others see.
* **Hare, Call and Tomasello (2000)** - Food in middle of room. Subordinate goes for food only they can see. Know dominant cannot see it, so safer.
* **Hare, Call and Tomasello (2001)** - Both see food being hidden. Subordinate understands what others have seen.
* Also know what others intend. Chimp waits longer if clumsy.
**_False Belief Tasks_**
* **Hare, Call and Tomasello (2001)** - Don't understand that some have a false belief of world. Some sort of theory of mind, diff from humans. Understand others in terms perception, goal psycholog.
118
Explain whether or not tool use is unique to humans
**_Insight_**
* **Kohler (1925)** - Apes could demonstrate insight from suddenly grabbing food out of tube. However, could be carrying known behavs from past. Might not happen immediately.
* **Epstein et al. (1984)** - Pigeons solve banana and box prob.
Instrumental Incentive Learning
**_Imitation_**
*
