Biological Paper 1 Flashcards

1
Q

research methods & MRI

A

Maguire 2000s

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2
Q

localisation

A

Maguire 2000s

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3
Q

neuroplasticity (neural pruning & neural network)

A

Maguire 2000s

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3
Q

neurotransmitters

A

Rogers & Kesner 2000s

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4
Q

hormones

A

Meaney 80s

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5
Q

evolutionary explanations for behaviour

A

Wedekind 90s

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5
Q

pheromones

A

Wedekind 90s

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6
Q

genes / genetics

A

Gottesman & Shields 90s

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7
Q

genetic similarity

A

Gottesman & Shields 90s

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7
Q

the brain & behaviour ERQ

A
  • Meaney 80s localisation
  • Rogers & Kesner 2000s neurotransmitters
  • Cases 90s neurotransmitters
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8
Q

the hormones & behaviour ERQ

A
  • Meaney 80s hormones
  • Weaver 2000s hormones
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9
Q

the genetics & behaviour ERQ

A

Cases 90s genes

Weaver 2000s genes

Van Oortmerssen & Bakker 80s genes

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10
Q

Cases 90s Study

A

AIM (genes & brain)
- to investigation the correlation between low levels of MAOA, enzyme which breaks down serotonin, and impulsive aggression

PARTICIPANTS/IV
- transgenic mice (experimental group) genetically modified to produce less MAOA
- control mice (unedited genes)

METHOD
- Transgenic mice—were genetically modified to remove a gene that produces MAOA enzyme which is a protein which degrades neurotransmitters such as serotonin, norepinephrine, & dopamine to see how excess levels of these neurotransmitters would impact aggression

  • After the rats reached maturity a test simulating an intruder entering the cage was conducted—where another mouse entered the cage of the mouse.

RESULTS
- Transgenic mice were quicker to attack the intruder (impulsive) & adopted a threatening position
- more offensive aggressive behaviour e.g. biting the experimenter
- control mice would sniff the intruder mouse
- Autopsies of the mice brains’ showed an elevated serotonin levels

IMPLICATIONS
- MAOA-deficient mice exhibited more aggressive, and impulsive behaviour possibly due to increased serotonin levels as a result of less MAOA
- The MAOA deficiency causes a predisposition towards impulsively aggressive behaviour
- MAOA, enzyemes, and neurotransmitters are determined by genes which influence behaviour

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11
Q

Maguire 2000s Study

A

AIM (MRI, neuroplasticity, localisation)
- study the ability for the brain to undergo plastic changes in response to increased navigational requirements

  • determine the role of hippocampus in spatial memory

STUDY
- Correlational Study
- Quasi-experiment

PARTICIPANTS/IV
- 16 taxi drivers from London
- 50 control
- all right handed

METHOD
- MRI (magnetic resonance imaging) scan of participants brains

  • analysed with pixel counting for size of hippocampus
  • & VBM (voxel-based morphometry) for density/volume of hippocampus

RESULTS
- post-interior hippocampus significantly larger
(Pixel counting)

  • volume of post-interior hippocampus correlated with amount of time spent as taxi driver
    (VBM)

IMPLICATIONS
- environmental pressures to learn navigation of London made the brain plastic to increase volume & size of post-interior hippocampus

  • post-interior hippocampus stores spatial information
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12
Q

Rogers & Kesner 2000s Study

A

AIM (neurotransmitters)
- to determine the role of acetylcholine in the formation and retrieval of spatial memory

PARTICIPANTS/IV
- 30 rats

METHOD
- All rats acclimated to a maze and its objective to find food in the opposing corner of the maze, but before the maze was able to be transferred to long-term memory
Then rats were randomly allocated into 3 groups:
- 1) injected with scopolamine—a drug which blocks the reception of acetylcholine by post-synaptic neurons, and thus preventing acetylcholine, a neurotransmitter expected to help form memories, from functioning, as acetylcholine cannot travel from one neuron to another. As there is a significant number of acetylcholine receptors in the hippocampus which is known for memory storage.
- 2) inject drug physostigmine which blocks an enzyme: cholinesterase which naturally breaks down acetylcholine from receptor proteins on the post-synaptic neurons to return the neurons to their resting potential when no nerve impulse is being sent, thus more acetylcholine than typical.
- 3) injection with a placebo saline solution. These injections were made into the hippocampus.
- After being injected the rats were measured to see how long it would take them to find food they had previously located over 2 days.
formation of spatial memory was assessed by averaging the number of errors the rats made on the 1st 5 trials of the maze on day 1 compared to the last 5 trials of day 1
the retrieval of spatial memory was assessed by comparing the average number of errors made on the last 5 trials of day 1 to the 1st 5 trials of day 2

RESULTS
- The scopolamine group took longer to learn the maze, and made more errors—higher average number of mistakes on the last 5 trials on day 1 thus deficit in memory formation
- The scopolamine did not appear to affect the retrieval of memories that had already been created
- The increased acetylcholine group had increased spatial memory formation with less errors compared to made in the last 5 trials on the 1st day compared to the 1st 5 trials on the 1st day
- However, the increased acetylcholine group showed a deficit in memory retrieval on the 5 trials of the 2nd day compared to the 1st 5 trials of the 1st day

IMPLICATIONS
- This suggests acetylcholine plays an important role in the formation of spatial memories, as the low acetylcholine rats were confused and lost although they were had learned the maze previously.
- However, excess acetylcholine, as demonstrated by the high acetylcholine group, may hinder spatial memory retrieval

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13
Q

Meaney et al (1988): aim, study, participants, method, results, implications

A

AIM (hormones, brain
- to determine the effect of glucocorticoids (stress hormones) on memory

STUDY
- true experiment

PARTICIPANTS
- Condition 1 rats: experimental group, not handled normally, neglected, removed from mother
- Condition 2 rats: control group, handled normally, staying in care of mother

METHOD
- After the rats reached maturation, they were individually placed in a container with milky water and had to escape by finding a platform
- This experiment was repeated multiple times to see whether the rats would use their memory to reach the platform more effectively
The route the rats took across trials was tracked

RESULTS
- The neglected rats secreted more glucocorticoids in response to the stressful maze than the control rats
The neglected rats also took more ineffective routes to the platform at old age
- At later ages the neglected rats had elevated basic glucocorticoid levels at rest than normal rats, since the neglected rats were exposed to a long period of stress which caused the cortisol or glucocorticoid levels had to increase to remain high, which then became the neglected rats’ baseline
- Accelerated hippocampal neuron loss and thus spatial memory deficits in the neglected rats due to the higher glucocorticoid whereas, this effect was almost absent in the control rats

IMPLICATIONS
- The higher level glucocorticoids from prolonged stress leads to hippocampal neuron loss which causes reduced spatial memory abilities

14
Q

Wedekind (1995): aim, study, participants, method, results, implications

A

AIM
- to determine whether female attraction of males body odour are dependant on MHC genes which can be expressed through scent

STUDY
- laboratory experiment

PARTICIPANTS
- 49 females & 44 males (uni students)

METHOD
- all participants had MHC genes identified

  • male participants were asked to wear a shirt for 2 days straight
  • on day 3 females smelt the shirt and ranked the odour from 1-10

RESULTS
- females consistently preferred smell of men with dissimilar MHC genes to their own

IMPLICATIONS
- pheromones released in our scent plays a role in initial attraction

  • pheromones are determined by our genes, so our genes may dictate our initial attraction
  • we are attracted to differing genes because that will create genetically diverse offspring
14
Q

Van Oortmerssen and Bakker (1981): aim, study, participants, method, results, implications

A

AIM
- to investigate genetic influence on aggressive behaviour by determining whether aggression can be selectively bred

STUDY
- true experiment

PARTICIPANTS
- Wild mice found in a barn that underwent selective breeding
- Control group of mice that were not selectively bred

METHOD
- The mice underwent a ‘resident-intruder’ test—the same as Cases—and the mice with the shortest latency attack (most aggressive) were selectively bred to produce a strain of aggressive mice
- Latency scores were studied over 11 generations of mice

RESULTS
- The latency scores gradually shortened with each generation, and the selectively bred aggressive mice were quicker to respond with aggression towards intruder
- The aggressively bred mice attacked within 5 minutes whereas, 22% of the control mice attacked within 5 minutes

IMPLICATIONS
- Genetic basis for aggression, as aggression can be bred and inherited

14
Q

Gottesman & Shields (1991): aim, study, participants, method, results, implications

A

AIM
- examine the relationship between genes and developing schizophrenia

STUDY
- Field survey

PARTICIPANTS
- 57 pairs of twins
- 24 monozygotic (MZ) (100% shared genes)
- 33 dizygotic (DZ) (50% shared genes)

METHOD
- 1 of the twins from each pair already had SZ which they had found from hospital records

  • then researchers interviewed other twin W/O SZ from the pair and obtained their hospital records to find their likelihood of also having SZ

RESULTS
- MZ twins have 48% chance of developing SZ if other twin has SZ
- DZ twins have 17% chance

IMPLICATIONS
- concluded that genetic inheritance plays a role in developing SZ and related psychiatric disorders

//some info is missing check SAQ from prelims last year//

15
Q

Weaver et al (2004): aim, study, participants, method, results, implications

A

AIM
- to investigate the impact maternal nurturing or neglect on epigenetic changes to the way the brain responds to stress in rat maturation

STUDY
- quasi-experiment

PARTICIPANTS
- Rats biologically from high-affection mothers fostered by low-affection mothers
- Rats biologically from low-affection mothers fostered by high-affection mothers

METHOD
- The matured rats were then placed into stressful situations such as physical restrainment for 20 minutes to examine the two rat groups’ response to stress with blood samples before and after stressful situation
- Additionally, genetic mapping technology was used to determine patterns of methylation of the gene sequence from when the rats were new borns and also at maturation

RESULTS
- The rats raised by low-affection mothers irregardless of biological relation had methylation of glucocorticoid receptor (GR) promoter gene, which means less glucocorticoid receptors in the hippocampus for cortisol, thus had higher levels of cortisol and stress hormones and were more stressed
- Conversely, rats raised by high-affection mothers rarely had methylated GR promoter genes which means more receptors in the hippocampus for cortisol, with lower levels of corticosterone
- These differences occurred although the gene sequence did not differ, ultimately due to the epigenetic changes from nurturing or neglect.

IMPLICATIONS
- The environment impacts the gene expression which affects behaviour
- Vulnerability to stress may be result of methylation of a gene responsible for the production of stress hormone receptors (GR Promoter gene) which would reduce stress

16
Q

conceptual understanding / explanation for neural network/pruning

Linking Maguire to neural pruning

A
16
Q

conceptual understanding of MRI
Linking Maguire to technique

A
17
Q

conceptual understanding of synapse (inhibitory vs. excitatory)

A
17
Q

conceptual understanding of neurotransmitter

A
18
Q

conceptual understand of pheramones

A
19
Q

conceptual understand of hormones

A
20
Q

conceptual understanding of agonist vs antagonist

A
21
Q

definitions of genes

linking genes to study

A
22
Q

linking genetic similarity to study

A
23
Q

linking evolutionary explanations for behaviour to study

A
24
Q

Rogers & Kesner (2003) ethics & TRREVG eval

A
25
Q

Cases et al (1995) ethics & TRREVG eval

A
26
Q

Meaney et al (2000) ethics & TRREVG eval

A
27
Q

Van Oortmerssen and Bakker (1981) ethics & TRREVG eval

A
28
Q

Weaver et al (2004) ethics & TRREVG eval

A