Biological Paper 1 Flashcards
research methods & MRI
Maguire 2000s
localisation
Maguire 2000s
neuroplasticity (neural pruning & neural network)
Maguire 2000s
neurotransmitters
Rogers & Kesner 2000s
hormones
Meaney 80s
evolutionary explanations for behaviour
Wedekind 90s
pheromones
Wedekind 90s
genes / genetics
Gottesman & Shields 90s
genetic similarity
Gottesman & Shields 90s
the brain & behaviour ERQ
- Meaney 80s localisation
- Rogers & Kesner 2000s neurotransmitters
- Cases 90s neurotransmitters
the hormones & behaviour ERQ
- Meaney 80s hormones
- Weaver 2000s hormones
the genetics & behaviour ERQ
Cases 90s genes
Weaver 2000s genes
Van Oortmerssen & Bakker 80s genes
Cases 90s Study
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
Maguire 2000s Study
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
Rogers & Kesner 2000s Study
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