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Rogers and Kesner (2003)
aim: to determine the role of acetylcholine in the formation of spatial memory
procedure:
30 rats
put in maze and familiarise themselves with it
randomly allocated two conditions
con 1- injected with scopolamine
con 2- saline solution
ten minutes before maze
injections directly into hippocampus
encoding memory asses- average no. of errors made on day one for first 5 trials and last 5 on day one.
put food in one of the corners for them to find.
findings:
scopolamine group too longer and more mistakes
did not affect retrieval of memories that were already created
acetylcholine plays important role in spatial memories.
Rosenzweig et al (1972)
aim: investigate whether environmental factors such as a rich or impoverished environment would affect the development of neurons in the cerebral cortex.
procedure:
three male rats
randomly allocated three enviornments
control- three rats in cage
impoverished- each rat in individual cages without toys and maze
enriched- 10-12 rats in cage with stimulus objects and toys
all groups had water and food
30-60 days in environment
killed to study brain anatomy
findings:
anatomy different in EC and IC
increased thickness and weight of cortex in EC
EC greater activity in neurone in cerebral cortex associated with the transmission of acetylcholine- important in learning and memory
follow up- 30 mins a day in enriched environment= same changes in brain as original study
Meaney et al (1988)
aim: determine the effect of glucorticoids (stress hormones) on memory.
procedure:
independent samples design
randomly allocated 2 conditions
treatment group- newborn rats for three weeks from birth to weaning. Taken from mothers of 15 minutes in plastic container with paper towel. Brushed for 15 mins to simulate grooming of mother rat.
control group- taken from mother and did nothing
put into pool of milky water.
tracked the rats route they sought to get to the platform in the pool
findings:
high levels of glucocorticoids in early life effects rats in old age
increased exposure to adrenal glucocorticoids accelerated hippocampus neuron loss and cognitive impairments in aging.
rats taken from mothers at young age has a messier route not as direct.
neglected rats- hippocampal cell loss and spatial memory deficits
stroking rat= activation of genes responsible for stress response- epigenetics
when rat is stressed it releases cortisol that goes to hippocampus binding to glucocorticoid receptor sites, which shuts down fight or flight.
over stimulation = hippocampal cell death.
Newcomer et al (1999)
aim: investigate if high levels of stress hormone - cortisol- interfere with verbal declarative memory
procedure:
had clynical interview with physician before to check if they were fit for the experiment
double-blind
condition 1- high level cortisol- tablet of 160mg cortisol on each day. Blood levels similar to major stressful events
condition 2- low level of cortisol- tablet of 40mg cortisol each day. Blood levels of minor surgical procedure.
condition 3- placebo- control group
asked to listen and recall paragraph everyday
did the paragraph before without the dosage and there was no difference
findings:
high cortisol- impaired memory and worst verbal memory
no difference between low cortisol and placebo
con 2 and 3 got better overtime because of practice
Friedman et al (1994)
aim: support the lipostatic theory and investigate what is the feedback mechanism.
procedure:
OB mouse- genetic mutation leading to hyperplasia- lack of control over eating
surgically attached OB mouse with a lean mouse so they shared blood supply.
hypothesis- if hormone that controls wait it should be transferred to OB mouse
if harmon in OB leading to overeating- lean mouse gain weight
findings:
OB mouse lost weight
discovered leptin- hormone that tells us we are done eating- we feel full.
Caspi et al (2003)
aim: examine the role of the 5htt gene in depression
procedure:
gene is two short= depressions cut of stressful life event
newzealand 26 year olds
group 1- short
group 2- one short one long
group 3- long
mutation- short
stressful life event survey- financial, employment, health, relationships
assessed for depression
findings:
one or more short- symptoms of MDD and intrusive thoughts
strongest with 3 or more events
inheriting the short gene is not enough but the interaction between short gene and no. of stressful events = depression
Cases et al (1995)
aim: investigate correlation between low levels of MAOA and aggressions
procedure:
genetically modified male mouse- gene that regulates production of monoamine oxidase A (enzyme that breaks down serotonin and norepinephrine, was knocked out.
days 11 and 16- signs of low MAOA like frantic running, violent shaking during sleep and biting
adult males- signs of aggression
resident-intruder test- mouse put in a cage of another mouse
findings:
control- sniff other mouse
transgenic mice- threatening hunched position with both female and male intruder mouse
autopsies- increase of serotonin, dopamine and norepinephrine
serotonin 6-9 times higher than control
MAOA-deficient mice- aggressive behaviour
aggressive behaviour is due to interaction with MAOA deficiency and social and enviornmental factors.