what is anhedia
loss of ability to feel pleasure for no apparent reason
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what is affective disorder
means its caused by mood/emotion.
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what times of reactive and endogenous depression
reactive is after a bad situation and endogenous is for no reason
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what is the genetic concordance for depression
mz- 60% dz- 15%. suggests genetics, concordance for bipolar is higher
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does stress and trauma increase suseptibility
no but it does increase the chance of atatck if they've had it already
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what is SAD
less sunlight or lack of light therapy
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another form of time induced depression
postpartum- lasts up to 3 months. has to be a least a month to be diagnosed. 10% of mums
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what are the 4 classes of drugs for depression
monoamine oxidase inhibitors, tricyclic antidepressants, selective monamine-reuptake inhibitors, mood stabalizers
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what does MAO oxidise do in the body.
it breaks down noradrenaline and adrenaline in the body
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what are monamines
they are neurotransmitters like noradrenaline, dopamine and serotonion
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how were monoamine oxidise inhibitors discovered
originally made for tuberculosis but found it left them less concerned about their disorder.
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how does it work
it inhibits MAO oxidise. its an enxyme which is responsible for breaking down the monoamine neurotransmitters
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what is a side effects of it
the cheese effect- makes cheese, wine and pickles harmful to blood pressure. because, MAO oxidise normally metabolises tyramine which is bad for bp but its being inhibited
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how do tricyclic antidepresents work
they have chemical structures with 3 rings of atoms. first used as an anti-schizo drug. they block the reuptake of serotonin and noradrenaline.
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what are selective monoamine reuptake inhibitors
they serotonin agonsists (agonists make receptors work, antagonists bind and stop them), they stop the reuptake of just serotonin. leaves more in the synapses
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what did the discovery lead to
the making of selective noradrenaline-reuptake inhibitors
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how do mood stabilizers work
anti-depressants usually cause mania, lithium is used to interfere with the second message system in neursons. only really helps severe
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what are the 3 structures that appear abnormal in a depressed persons brain
amygdala, hippocampus, medial prefrontal cortex- even the connections between
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what is the monamine theory of depression
based on the fact that the 3 sucessful drugs are agonists of the monoamines and they work
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what do autopsys show which support that, what is up-regulation
more noradrenaline and serotonin receptors, this is 'up-regulation' meaning that when theres not enough of a neurotransmitter in a body, it makes compensatory receptors.
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what is neuroplasticity theory
antidepressents increase transmission of monoamines but results dont start for weeks. therefore it cant be the synapse it must be to do with further down. so is it a change in neuroplasticity
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what changes in neuroplasticity
a decrease in amygdala, prefontal and hippocampus.
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MEMORY 1- who was hm
epileptic man who had the medial temporal lobes removed and therefore couldnt make longterm memories. he couldnt remember new adress or people he's met.
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what type of amnesia did he have
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what was his digit span and what is the average
after 25 trials most people can do 15 but he could only do 6
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what is block tapping memory span task and what does it test
repeating pattern of taps, shows that the amnesia is in all sensory modalities. shows global amnesia
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what was hm's
normal of 5 bt he couldnt do 6 even if repeated 12 times
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how did he perform in the mirror drawing task and what did it show in hm
indicated it wasnt all long term tasks because he got better at tracing the star even though he has no recollection of doing the task before. indicates retention
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what is the incomplete picture task and what did it show in hm
5 sets of fragmented drawing, have to say what it is and if you dont get it they add more lines. he got better at doing it and but couldnt remember
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what did hm show in classical conditioning
retained the eye puff 2 years on
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what is emplicit memory
semantic and episodic, conscious.
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what were hm episodic memory problems
with consolidation, moving stuff from lt to st.
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what type of memory does medai lobe amnesia mostly effect
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what is implicit memory
procedural, priming, unconscious
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what were the 3 major contributions of hm
1) medial temporal lobes are important for memory. 2) his surgery got rid of lt and not st, there are different models for storage. 3) the fact he got better without knowing it shows he had implicit and explicit memory
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how do amnesic patients perform in a reptition memory test (what is one)
its when you give a word with spaces like _e_l_o. amnesic patients perform just as well which shows they are just as intelligent. shows they have the 2 stores
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who was KC
motorbike accident, medial temporal lobes. he had good semantic memory (facts about his life) but poor episodic. understood everything fine but just couldnt recall an event. could even remember the score you'd told him earlier but not when you'd told
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what is global cerebral ischemia
blood supply to the brain is lost and effects medial temporal lobes
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who was RB
man who has surgery go wrong and got really bad ischemia. his pyramidal cell layer was damaged which is in the CA1 subfield of the hippocampus
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what did this suggest
that hippocampal damage is what causes temporal lobe amnesia
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what is korsakoff syndrome caused by. what parts does it damage
a lack of thiamine. neocortex, hippocampus, cerebellum and causes antero and then retrograde amnesia at the end
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why is it hard to know which part causes the amneisa
because the damage is very diffuse. could be damage to the mamillary bodies in hippocampus
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MEMORY 2- ANIMAL MODELS. what did the non-matching to sample task do and find in monkeys
removed medial temporal lobes and got them to look under object for food and see if they went for same object. removed, went from 90% sucess to chance levels.
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what happened when they lesioned just the hippo and then the whole medial temporal. what did this show
whole medial temporal lobes similar results to when they JUST lesioned the hippocampus. which shows that its to do with this. BUT its hard not to remove rhinal cortex too so is it that
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what happened when you did it to rats
because you can seperate and do JUST the hippo, they found that they performed well when hippo removed but when rhinal cortex, amygdala and hippocampus- big effects
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what research showed that rhinal cortex drive memory loss
bilateral medial temporal cortex- always severe effects. bilateral hippocampus removal- moderate deficit. amygdala removal- no effect
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what question does this cause
if the hippocampus isnt that crucial, why when rb damaged a really small bit of hippocampus (CA1 subfield) did he have such bad problems
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what did they discover about the hippocampus that might explain this
because all the research was to do with object recognition, maybe this shows that the hippocampus is to do with specific memory of object recognition.
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what could explain the fact that rb damages were so bad
ichemia. damages and disrupts other brain regions. it over excited the CA1 region and kills connected brain parts
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how does ischemia work
too much glutamate is released when loss of oxygen and glucose happens, the hippocampus has lots of glutamate so is susceptible
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how did pinel test that the hippocampus is what makes the ischemia worse rather than does the damage
didnt remove hippo, gave ischemia- memory impaired. remove hippo, give ischemia- not impressed hippocampus- memory isnt impaired
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what does it show that if you take the hippocampus out first there are no memory problems
ischemia causes the hippocampus to damage the rhinal cortex. no hippo, rhinal cortex cant be damaged.
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ischemia kills body parts
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evidence that the hippocampus is for spatial memory
taxi drivers have massive hippocampus's
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what do bilateral hippocampus lesions do
they dont effect memory tasks but they do effect spatial memory
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what happens during morris maze if you remove hippo
cant remember where the platform is
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what happens during the radical arm test, what is it
8 arms and some are baited with food, intact rats will start only going to the baited arms after a while. this shows reference memory. if you dont visit the same arm twice this shows working memory. rats reduced in both
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what are place cells
cells that only fire when youre in a specific place. dont have them when you first enter an environment. indicate where they think they are
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how do hippocampal place cells obtain spatial info?
grid cells
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what are grid cells
etorhinal neurons with loads of place cells on that look like graph paper, to map stuff out
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what to etorhinal grid cells respond to and how
respond reflexively to location
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what do hippocampal cells respond to
place and other features of environment
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do humans and monkeys have place cells
no, but this could be because all the tests are done on them when they're stationary, wheras rats and mice and birds are actually navigating environments
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what is the cognitive map theory of hippocampal functions
different systems specialise in memory for different information. hippocampus is for spatial
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why is the hippocampus so useful for episodic memory according to the cognitive map theory
because you need spatial information/context to recall sequences of events.
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what is a fact that challenges this regarding place cells
they fire due to more than location, also depend on recent/pending behaviour
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what have studies shown to challenge this
that hippocampal damage affects tasks with no spatial evidence
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MEMORY 3- what is hebbs learning rule
learning happens in the synapse and long-lasting changes in efficiency are made by synaptic transmission
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in terms of classic conditioning how can this be seen
for it to happen, learning clearly needs to take place in the neuron. so you have a neuron for bell and a neuron for salivation and the neuron for salviation begins to fire without the bell- learning has happened
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describe neurotransmission
electricl neurotransmission travels from cell body to axon, at the synapse it becomes chemical transmission, when the neurotransmitter is released. it then crosses the synapse and binds to cleft, illicits response.
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what happens when the response has started
the neurotransmitter binds to the receptor (usually an ion channel) and it opens, reaches post synaptic membrane potential. reaches certain threshold and post synaptic neuron fires!
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explain synaptic transmission
neurotransmitter in vesicles excited by action potentioal, fuses to synaps and releases whatever inside into cleft. the receptor and neurotransmitter intereact and action occurs.
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how are they cleared from the cleft
either through difussion or re-uptake by transporters
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how does hebb think memories are stored in neurons
an axon on cell a excited cell b over and over and over, growtn/metabolises to change both the cells so that a becomes more efficient at firing at b
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what does this mean
the chemical part of neurotransmission gets better and faster, the pre-synaptic neuron gets better at firing at the post-synaptic neuron
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what is this process called when in the brain
long-term potentiation
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bliss and lomo experiment into rat hippocampus
used inventro (bits of brain on glass) to stimulate hippo with single electrode
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whats it called when you go into the hippocampus
the perforant path
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what are the first cells you get to in the hippocampus and then the next things you reach
the dendrite gyrus, then CA3 and CA1 subfields
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how do they test ltp
they put electric stimulation into the presynaptic neuron which causes synaptic transmission, give a massive amount of stimulation loads, soon when you give 1 pulse gives the same response as loads
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how long does this work
week. sometimes months
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what is absoltely necessary for long term potentiation to occur
co-occurence, needs to be firing as the pre-synaptic and the post-synaptic
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what does this have to do with memory
ltp effects are seen in most brain parts to do with learning and memory
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what have other experiments found
that smaller electricity has same effect
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what happens if you stimulate ltp in a rats hippocampus until saturation
they cant do the morris maze
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what does knock out mice say about ltp
when you take it out, they cant do spatial learning
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what are the criticims of the ltp experiments
would it happen irl not with massive stimulation
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how can we see evidence of it in behavioural conditioning
behavioural conditioning produces the same changes as ltp in the hippocampus
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how can we see evidence of it in drugs
drugs that influence learning effect ltp positiviely
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what neurotransmitter is responsible for ltp
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what is glutamate
main excitatory neurotransmitter, 80% of synapses are glutamatergic
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what are the receptiors for ltp
ionotrophic receptors, ion channels. glutamate binds to them and the receptors and the channel opens to let them in or out
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what is the most common type of ionotrophic receptor
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what is another ionotrophic receptor for glutamate
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what is it permable to
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why is NMDA usually blocked
because a molecule of magnesium which is positively charged blocks it (because its negatively charged)
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how does it become open
when the cell is depolarised and gluatamate binds to
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why does the magnesium float away and allow calcium in
because the inside of the cell becomes depolarised meaning it becomes positively charged and magnesium is positively charges so its repelld
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what does this result in
memory formation !!!!!!!!!!!!
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so how does the pulse in ltp do this
the blast of electricity to perforant path results in depolarising neuron, magnesiam flies off, NDMA receptor activated- glutamate released- memory formed
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so what actually is it that causes the long term changes
the influx of calcium
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how does calcium do this
by activating protein kinases in the neuronal cyto-plasm. calcium changes the protein synthesis that changes the cell
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recap: what does a cell HAVE to be to produce ltp
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what did this lead to the discovery of
there must be something that signals the cell what the pre-synaptic is doing
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what did this mean
we knew that activity in the neuron makes actual changes to the structure.
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what does the fact ltp occurs in the postsynaptic neuron indicate
that a signal is going back from post synaptic to the pre synaptic
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what is it that takes this signal in the NMDA receptors
nitrous oxide
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when and where is it made
when calcium influx happens, its made in the post-synaptic and diffuses back into the pre-stynaptic, strengthens it
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ALZHEIMERS- what age do you get it, how common in over 65's and over 85's
young as 40, 10% over 65 and 35% over 85
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what happens in the early stages?
decline in attention and memory
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what are the intermediate stages
confusion, irritability, anxiety
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last stages
loss of bladder, basic functions, swallowing= terminal
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what do you need for definite diagnosis
autopsy, no known cause
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what is the assessment for it, stages of diagnosis
mmse, simple calculations, recall objects, simple drawing tasks etc. score= diagnosed with cognitive impairment, leads to alzheimers diagnosis
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what are the big neurological changes that occur
ventricles (fluid filled spaces) get bigger, hippo and rhinal cortex shrink, frontal brain stars delaying over time. neurons die
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what are amyloid plagues
aggregate lumps of protein. clumps of scare tissue.
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what are they made from
the protein amyloid which is present in normal brains but in small amounts. so we dont know why its toxic
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what is the gene that makes the amyloid precurser gene
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where is the amyloid plaque pre-cursor gene located, who does this affect and how
on the 21st chromosom and downsyndrome ppl have an extra one so their chances of having alzheimers are 150% more than us, by around 40
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where is amyloid usually in the brain
hippocampus, amygdala- medial temporal lobe- memory. also in inferior cortex- posterior pareital and prefrontal cortex, involved in cognitive functions
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is alzehimers genetic
50% higher chance of getting it if someone related to you has it
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how many gene mutations are associated with it
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what did a study using transgenic mice show
made a mouse with loads of APP, so loads of plaques, their brains looked like a human with alzheimers does.
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where were most of the plaques
like humans, in medial temporal lobes (hippo, amygdala, entohinal cortex)
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what did they not show
they didnt have neurofibrially tangles which is werid
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so what did they do after that
inserted them with 3 alzheimers genes and they then got amyloid plaques and neurofibrially tangles
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what is the alzheimers risk factor gener
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where are neurofibrillary tangles
inside the cell
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how do they affect the neurons
basically, neurons have sticks on them called microtubules which hold their shape. tau (which is a protein associated with microtubules) gets in a muddle and loses its shape, so it falls off the microtubule and gets tangles on the floor
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why is this toxic
because microtubules need tau to stop them degenerating
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what are the main drugs for treatment
cholinesterase inhibitors,
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3 types of these
donepezilhydrochoride, triastigmine and galantamine
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what doe cholinesterase ihibitors do
they basically block the reuptake of acetychloine
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what is acetycholine
its a major neurotransmitter (which is in the PPT and nucleus basia) it projects all over the cortex and is very important for cognitive functions
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so why would it make sense that these help alzheimers symptoms
alcetylcholine is broken down by cholinesterase, if you block that from doing that you boost functions!
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what are NMDA receptors antagonists
another drug used, stops glutamate overexcitment which we know from ischemia causes damage! too much kills cells
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what does an NMDA receptor do when its overexcited
lets in too much calcium and kills cells. so blocking the NMDA receptors stops this
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what has stem cell treatment shown
injecting foetal cells into transgenic mice can grow brain cells- improved object recognition in mice
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GENETICS 1- what are dichotomous traits
when it has to be one thing and not a combination (eye colour etc)
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what is a true breeding line
when interbred species all same trait (pea plants all white seeds)
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what did mendalin discover
noticed that if you bred brown and white plants, you got all brown seeds. then if you bred those offspring, you get 3/4 brown and 1/4 white
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what did he label this
dominent and recessive genes.
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what would hapen if you had two dominants, two recessives and 1 of each
2 doms, youd have that trait, 2 rec, youd have that and one of each, you'd have a 3/4 chance of dominent and 1/4 recessive
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who is more likely to have a trait like colour blind
because a man has an x and a y so if they get a recessive gene they are much more likely to get the trait, even if they only have one, as the y chromosome is recessive so wont cancel out
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whats a phenotype
the actual observable trait
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whats a genotype
the genetic material that makes the trait (GG/Gy/gg)
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what is an allele
two genes that control the same gene, so the dad genes have an allele and the mum does (categories like eye colour, depression etc) and the alleles come together to give offspring the gene
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what does homozygous mean
two of the same gene is the reason you got the train (GG,yy)
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what is heterozygous
two different genes for a trai (Gy)
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what did mendalin also think about genetics
that you inherit 2 random factors from mother and father
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how would you work out inheritance
punit square
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“A” is a dominant gene for the ability to *whatever* and “a” is a recessive gene for inability to *whatever*. Which of the following couples could possibly have both a child who does and doesnt
answer would be both couples would have to have Aa and Aa
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where do genes live
on chromosomes which are thread like structures in nucleus of cell. they come in matched pairs, one gene (allele is on each of the pair)
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what us an autosomal gene
not a sex gene, equal in male and female
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who would be more likely to have a recessive gene is on an x chromosome who will be more common to get it
males because less chance of y chromosome counteracting because its so small
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what are chromosomes made from
DNA, live in nuclei of cell
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what is meiosis
cell division that produces gametes
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what are gametes
male or femlale cells (egg or sperm). have half the normal numbers of chromosomes, so when the sperm and the egg combine you get a zygote
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what is the process
there is one allele on each chromosome of a pair, meiosis produces gametes, the mum and dads chromosomes divide and one from each pair goes to each gamete so that it has a full set of chromosomes and becomes a zygote
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what creates genetic diversity
random divison in meoisos
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how else is it ensured
chromosomes are lined up in their pairs and randomly switch over and cross to produces genetic recombination
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what are the 4 sequences of nucleotide bases attached to on a strand of DNA
phosphate and deoxymise
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what are the 4 nucleotide bases
adenine, thymine, guanine and cytosine
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which ones always pair up
adenine and thymine and guanine and cytosine
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what does the sequence of these bases determine
your genetic code
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what does the structure of DNA allow for
replication because they are the exact same and one strand will unwind and replicate
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what is the exception to the rule that chromosomes are matched pairs
sex chromosomes
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what are traits that influence genes of sex chromosomes called
sex-linked traits
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which genes control all sex linked traits
genes on the x chromo bc the y is too small bc men r trash !
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what two things does DNA do when it unwinds
makes babies or makes prot
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what protein does it usually make
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what is the process of protein syntheisis
DNA unravels and makes RNA from the exposed genes, becomes mRNA which attaches to the ribosome. tRNA brings amino acids to the mRNA and they mix and become proteins (enzymes, monamines etc)
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what is the process of making mRNA acc called
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what is the process of turning it into protein called
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what is a gene mutation
when 1 base gets swapped for another
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example of gene mutation- phenylketonuria.
causes you to not be able to translate or transcribe, therefore metabolise, phenylketonuria so you get too much accumlating (no enzymes to break it down) and therefore have brain damage
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what is ontogeny and phylogeny
life time, evolutionarily
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define heritability
an estimate of variance in a characteristic within a population that is due to diferences in heritibility
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what can heritiablity go up to
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how do you study heritability
looking at twins, comparing coefficiants in mz and dz twins for traits
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why is it specific to population
because its also heavily effected by environment. if the soil is good, both plans will thrive, if its bad, only the tall ones will thrive. if its in the same environment you can judge the actual heritability
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why does heritability increase over time
because genetic tendencies make us choose similar environments and that shapes us to become more and more similar
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how does this happen from a baby
early/prenatal small chances increase with environment and amplify effects
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what is the condordance of twins in depression
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what is the risk gene for depression
tryptophan hydroxylase
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what is the amino acid which is used to synthesise serotonin
tryptohan (get it from diet)
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so what happens if you have the tryptohan hydroxlyase gene
you make 80% less serotonin
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what study showed this
87 depressed patients and 219 control patients, 9 depressed had the mutation and 3 normal had mutation
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what was further found about the 3
family history of mental health problems
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what is example 2 of gene mutation, serotonin transporter
there are long and short forms, if you have the short form, more risk. the amygdala responds much more to fear than normal people
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what was caspi's study into this
5 year diaries for stressful event, measured depressed symptoms in those with the long and short form
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what did he find
no diff in stressful events, no diff in depression BUT if you had both the enviromental (lots of events) and the gene you are more likely to be depressed
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what is this evidence for
stress diathesis model
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what was tyrons experiment into rats
bred rats to be maze-dull or maze-bright. stayed bright/dull for 21 generations. used fostering technique to ensure it wasnt just being taught that did it
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what did this show
you can breed any observable trait. selective breeding for 1 trait causes many other traits to emerge alongside it. shows that genes act as CRITERION for other genes
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what showed this
maze bright better at learning and had less fear but werent any more intelligent, less fear isnt natural
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how did environmental impact get shown
study showed that this only happened in an impoverished environment
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what does the bird song stuff mirror
humans learning language
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phase 1 of bird song
sensory stage- first few days, hear adults and genes make them only acquire songs of same specieis
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phase 2
sensorimotor, because to subsong, refine to resemble adult song, adults sing their songs back to them or they wont develop
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phase 3
rentention, some species are age limted learners and some are open-ended.
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what are the two neural circuits that control birdsong
comes from the high vocal centre of the syrinx (voice box) desending motor pathway and learning is mediated by anterior forebrain pathways
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what are the 3 cool things about a canary learning
left descending motor pway plays bigger role, like human lang with left hemisphere. 2) vocal centre 4x bigger in males. 3) doubles in summer due to more light- more testosterone and shrinks again in fall. 4) new neurons grow as a result (neurogenisis
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NEUROANATOMY- what is the cna
brain and spinal cord
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what is the pns
somatic and autonomic nervous system, everything else
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what is the somatic nervous system
interacts with external environment, has afferernt and efferent nerves.
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what are afferent nerves
carries stuff from the sensory (muscles) to the CNS (brain etc)
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what are efferent nerves
carries stuff from the CNS to the muscles
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what are the the two types of of efferent nerve
sympathetic- stimulate and organise energy resources and parasympathic- conserves energy
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what is the automic nervous system
internal environment, links between sensation and action
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what is the blood-brain barrier
special structure of cerebral blood vessles which stops toxic molecues getting to brain
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what are the 3 types of neuron
multi, bi and unipolar
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what are clusters of cells and bundles of axons called in the CNS
nuclei, tracts
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what are clusters of cells and bundles of axons called in the PNS
ganglia, nerves
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what are glial cells
increase speed and efficiency of axons in cns
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what are schwann cells
guide axonal and neruonal regeneration
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what are golgi stains
used to see overall shape of neuron
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missl stains
only binds to cell bodies so we can tell how many are in a neuron
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what is the dorsal, anterior, posterior and ventral parts of brain
top, front, back and bottom
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what is a coronal cut, saggital and horizontal
down from side view, down from front view and across from side view
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what are the 4 major regions of the spinal cord
cervical, head/neck/hands/arms. thoracic- chest/breath/abs. lumar- legs/feel. scaral- bowel/bladder/sexual funcs
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what is the dorsal and ventral root of the spins
dorsal is at the back and is AFFECTIVE- affected by world. ventral is at the front and EFFECTIVE- effects the world
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what is in the forebrain
telencephalon and diencephlaon
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what is in the midbrain
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what is in the hindbrain
metencephalon, melencephalon
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what is the myelencephalon
medulla- sits in posterior of brain, base of spinal cord. carries signals between rest of brain and the body
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pons + cerebellum
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what is the pons
latin for bridge, relay structure between cortex
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what is affective disorder


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what times of reactive and endogenous depression


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what is the genetic concordance for depression


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does stress and trauma increase suseptibility


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