Neuroscience- whole course

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what does schizoprenia mean
the breakdown of interaction between motion, thought and action
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how much of the population get it
1%
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what is echolia
vocalised repetition of whats been said
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what are positive symptoms
the excess of normal function
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what are negative symptoms
the loss or lack of normal function
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name 5 positive symptoms
1) delusions (of grandeur or control. 2) hallucinations. 3) inappropriate affect (no approp emotion to pos/neg events. 4) incoherent thought (illogical thinking) 5) odd behaviour (hygiene, talk in rhymes)
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name 5 negative symptoms
1) affective thinking (no emotional expression. 2) Alogia (absence of speech. 3) Avolition (absence of speech). 4) Anhedonia (can't experience pleasure. 5) Catatonia (motionless or awkward positions)
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over what period shouls symptoms reoccur for diagnosis?
over 1 month
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what is the chances of getting if if relative has it?
10%
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what is the concordance rate in mz and dz twins
mz- 45% dz- 10%
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what do adoption studies tell us about it
you were more likely to have it if your biological parent had it not your adoptive, shows you inherit the potentional and experience effects if you get it or not.
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how do they know this?
children of twins where one has it and one doesn't, incidences of getting it are just as high in the children of the twins who doesn't have it
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what other factors have been suspected to be involved
infections, autoimmune reactions, toxins, traumatic injury, stress, birth complications.
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what was the first drug that was discovered to treat it and how was it discovered
chlorpromazine, was used as an antihistamine but found to calm the patients. In schizophrenics, it seemes to activate those who are blunted and calm those who were agitated.
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what is reserpine and how was it discovered
was used in indian folk medicine, taken from snakeroot plant. It reduced symptoms but is not used anymore bc of dangerous decline in blood pressure.
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what are the two similarites between reserpine and chlorpromazine
1) they take 2-3 weeks to work. 2) they both produced parkinson's like symptoms.
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what do these symptoms tell us
suggest that both the drugs were acting on the same mechanim, which was related to parkinsons. Now we know that parkinsons is due to a lack of dopamine in the nigro-striatal pathway, does it suggest schizo is due to too much?
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how was the dopamine theory born
1) reserpine and chlorpromazine were known to break down the synapse vesicles for dopamine and other monamines. 2) cocaine and ampethamines were known to increase chances of schizophrenia and also known to increase dopamine and monamins in the brain.
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how does reserpine do this?
it depletes the vesicles so the amount of DA released is reduced. The DA just goes back into the cell- it pops vesicles!
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how does chlorapromazine do this
its an antagonist, it binds to the DA receptors and stops them working. Feedback signal increases dopamine, broken down in synapse, results in less dopamine metabolites
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what is an agonist
makes a receptor work- illicits response!
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what is an antagonist
binds to receptor and stops it working.
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how do reserpine and chlorapromazine differ in the way they stop dopamine
they both antagonise transmission of dopamine. Reserpine depletes dopamine and chlorpromazine binds to its receptors
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what happens to dpamine levels when the drug is taken? what does this mean?
extracellular levels stay the same, carson and lindquist said that the blocking of receptors sends a signal to the presynaptic neuron to tell it to release more dopamine and then MORE is broken down in the synapse. results in more metabolites
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what does this mean
its not more dopamine that causes schizophrenia, its more activity in the receptors!
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what are the conclusions of DA theory (related to drugs)
basically, drugs that reduce dopamine neurotransmission (chlora,reserp) reduce psychotic symptoms. Drugs that increase it (coke,ampeth) increase them.
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how do we know the efficacy of a drug?
the better they are at binding to dopamine receptors
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how do we test drug efficacy?
add radioactive dopamine to monkey striatums with a lot of receptors in, rinse it off anf see how many dopamine molecules are left. less molecules left- better at working!
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what does high affinity mean
more effective, high affinity of dopamine receptors
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what is the exception to this rule?
haloperidol. It was very potent but it left a lot of dopamine receptor sights. so had low affinity
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what is the explanation for this
there are 5 subtypes of dopamine receptors. chlorpromazine binds to D1 and D2 and haloperidol just binds to D2
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what does this suggest
that schizophrenia is caused by hyperactivity of specifically D2 receptors. if a drug is better at binding to D2- its better at reducing symptoms.
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what are dopamine receptors
when they bind to a reception, changes the G protein that makes chances in the cell. it is either positively or negatively couples with adenlyate cyclase.
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what is adenlytle cyclase
an enzyme that sens messages in the cell
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which receptors are positiviely or negativley coupled with adenlyate cyclase?
D1- positively. INCREASES DOPAMINE. D2- negatively. DECREASES DOPAMINE
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what has now been found about d1 and d2 receptors
there are subtypes. D1- D1 + D5. D2- D2 + D3 + D4
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therefore what receptors do drugs target to treat schizophrenia?
D2.
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what is a limitation of DA theory?
receptors other than DA receptors are involved, such as glutamate and serotonin.
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DRUG ADDICTION Q'S. Describe oral injestion
dissolves in fluids in stomach, goes into bloodstream. Unpredictable because absorbing through digestive tract is heavily influences by amount/type of food in there
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describe oral injestion
strong, predictable, bypasses digestive tract.
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how can you inject, 3 ways
1.) subcutaneously- just under skin (fatty tissue). 2) intramuscularly- into large muscles. 3) intravenously- directly into veins. delivers directly into brain.
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risks of injecting
you can't intervene well if you've overdosed or allergic reaction. can result in scar tissue, collapsed veins.
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describe inhalation
through capillary network in lungs. difficult to regulate intake.
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desribe administration through mucus membranes (nose, mouth, rectum)
drugs go straight towards central nervous system. stopped by the 'blood-brain barrier' which stops dangerous chemicals from going into neurons in the cns
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what is metabolism
the action of drugs is decided by the enzymes in the liver, they turn active drugs into nonactive forms. means it can't go through the blood-brain barrier anymore
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what does administration affect and how
makes it more addictive if its quicker
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what is tolerance
a shift in the dose-response curve. dose of drug and size of effects that gives
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what can tolerance be
same dose having less effect or more drug gives same dose
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what is cross tolerance
drug produces tolerance to other drugs that use the same mechanism
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does tolerance have to be for all effects of a drug
no, you can be tolerant to some effects and not others. you can actually have 'drug sensitisation' to some effects.
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last feature of tolerance
not unitary- no single mechanism, many adaptive changes have to happen in the nervous system to reduce it
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what are the 2 types of change that happen during tolerance
metabolic tolerance and functional tolerance
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what does metabolic tolerance do
it reduces the amount of drugs getting to sites of action, means more enzymes to break it down are made by the body
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what does functional tolerance do
it reduces amount of activity of the sites of action- you can get conditioned drug tolerance. environment its taken, addicts die if don't take it in usual setting
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what is withdrawal
when the opposite of the drug affects happens.
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what does this suggest
suggests it uses the same neural mechanisms as tolerance
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how does this work
exposure to drug causes compensatory changes in nervous system to produce tolerance.
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what is the difference between contingent and conditioned toleratance
tested the anti-convulsant effects of alcohol by injecting them with alcohol either before or after stimulating them with electicity to cause a seizure. rats who recieved the alcohol before didnt become tolerant to its anticonvulsant effects
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what happened to the rats who has alcohol injected after the seizures and what does this show
they did become tolerant to the effects of it, shows you can become tolerant to some effects
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what is conditioned tolerance
you are maximally tolerant in envirornment you took it
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how did they test this
injected rats with heroin in novel or distinct environment, overdose more likely in new enironment.
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explain conditioned tolerance
conditioned stimulas gives bigger and bigger conditioned response when its in the same environment ro compensate, counteracts effects of drug
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what is enteroceptive stimuli
external stimuli like environment
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what are interoceptive stimulu
internal such as thought and feelings which can also reduce the full effect of the drug
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how is drug sensitivity tested
rats became more sensitive to the motor effects of meth if dont in the same enviroment
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how does tobacco work,what is the withdrawal. how likely to get addicted and what percentage quit
it acts on nicotinic cholinergic receptors in brain. withdrawal makes you anxty and irritable. if you experiment, 70% become addicted. 20% of quitting attempts are sucessful
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is there a genetic componenet to tobacco
yes, 56% concurance in mz twins.
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how does alcohol work, genetic? risks? depressent or stimulant
particles are soluble in fat and water so its absorbed by all parts of the body. depressent, high dose dampen neural firing, low dose- stimulant. 50% genetic, its a diuretic and increases blood in kidneys
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how do you become tolerant and what are the 3 stages to proper withdrawal
liver becomes better at metabolising it more quickly. 1) 5-6 hours after, tremors headaches etc. 2) 15-30 hours convulsing. 3) day after- lasts a day or 2, deliruium, hallucintions, hypothermia, tacycardia
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what can high consumption of alcohol produce
korsakoffs syndrome. memory loss etc, causes scarring of liver
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what does repeared cocaine result in
become sensitised to motor and convulsive effects
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what does ampthetime have in common
both block dopamine transporters which normally remove dopamine
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how do opiates work
bind to endorphines and enkephalines. can get through blood-brain barrier.
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why do addicts keep going back when they are detoxified
positive incentive theories, not just dependance, they want the good effects
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what is intracranial self stimularion
test that shows that humans and rats will give themselves small bursts of electrical stimulation, because it goes to pleasure centers in brain
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what does this suggest
that the brain parts used in this are the same bits activated when taking drugs
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what is the mesotelencephalic dopamine pathway
a system of dopaminergic neurons that project from the mesencephalon (midbrain) into different parts of the telencephalon
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what is it composed of
the substantia nigra and the ventral tegmental
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what happened to his memory
he couldnt form long term memories anymore. had anterograde amnesia
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EMOTION AND THE AMYGDALA. what is the common sense theory
stimulus, feeling, physicological response
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what is james lange's theory
stimulus recieved and interpreted by cortex, triggers changes in autonomic and somatic nervous system. then that triggers conscious feeling
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cannon bard theory
stimulus and the autonomic and somatic feeling at same time as conscious feeling.
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what did james lange think was the role of somatic and autonomic arousal
emotional experience depends completely on it
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what did cannon bard think
that they are completely seperate, no causal relationship
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what does modern biopsychology think
that the three factors of emotin (autonomic, somatic and conscious feeling) can all effect each other
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what is sham rage
you remove the cortex in cats and they become completely reactive to any form of stimulus
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what was concluded in the experiments on sham rage
if you removed the cortex up to the hypothalams but if you lesioned that it didnt. shows the hypothalamus is heavily involved in aggresion and the cortex is involved in inhibiting it
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what did papez say about the limbic system
emotion is controlled by it, its interconntected nuclei and tracts that ring the thalamus
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what parts of the limbic system are important to emotion
hypothalamus and hippocamput, and amygdala and prefrontal cortex
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whats the experiment for the facial feedback hypothesis
if you watch videos of angry people you feel more angry and same with happy and sad
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what gives us evidence of emotion in the limbic system
voluntary and involuntary smiles, limbic system is connected to facial muscles and pyramidal motor tracts, they end up on different muscles on the face/mouth. shows limbic is involved in genuine emotion. voluntary ones use the pyramidial system
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what is kluver bucy syndrome
anterior temporal lobes in monkeys removed and they became highly sexual, towards objects and anything, had no fear. resulted from damage to the amygdala
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what are the neual mechanisms behind fear conditioning
painful and auditory stimulu gets paired in the amygdala. long term potentiation means fear is conditioned in the hippo and amygdala. auditory thalamus projects to the auditory cortex, projects to lateral nucleus in amygdala and so does the hippocamp
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what else also projects to amygdala and what happens when it reaches it
prefrontal cortex also projects, when it reaches the response stars (freezing, hormons, blood pressure)
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what can ptsd patients tells us about the amygdala and what happens when you lesion it
once learnt in amyg, you cant unlearn from there. if you lesion it, cant be fear conditioned. ptsd patients get alzheimers and it comes back because they lose prefrontal cortex
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what does the amygdala damage in humans do
if you have a stroke and its damaged, you cant recognise fear. draw fearful faces.
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when is your amygdala less activated
when youre rating someone as trustworthy
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what kind of people have smaller amygdalas
psychopaths, autistic people and solo climber (not activation when thinking of it
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what role does the autonomic nervous system play in emotion according to james
different patterns in ANS activity produce different emotional expereinces
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cannon bard
all emotional stimuli produce the same ANS pattern
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what does evidence suggest
that its between total specificity and total generality, not enough evidence that they all produce a different pattern but evidence that they dont all produce the same
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STRESS N THE IMMUNE RESPONSE. describe model 1
anterior-pituitary adrenal-cortex model. stressors make adrenocorticotrophic hormone ACTH, comes from anterior-pituitary. causes release of glutocorcoids like cortisol
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describe model 2
sympathetic nervous system adrenal medulla- stressors activate SNS and that releases noradrenaline and adrenaline from the adrenal medulla
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in 1990's what was discovered about stress
that it causes inflammatory responses, increases cytokines in the blood which is now considered a major stress hormone
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what prompted research into stress
the idea that physicological disorders have a psychological element
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what condition started this
gastric ulcers, people who had them had heli-bactor pliori but so do 75% of people who dont have them
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what makes up the immune system
the innate and the adaptive immune system
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describe the innate immune system
quick and first to respond.
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what are pathogens
disease causing cells
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what are phagocytes and whats the most famous
cells that eat pathogens, macrophage
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what ate cytokines
small cell-signalling proteins like lymphokines that are producted in immune cells
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describe process of innate
pathogens have antigens on them (sticky things). phagocytpes have toll-like receptors on which bind to surface on pathogen when injured cells send signals. releases cytokines and triggers other cells like the adaptive immune system
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4 differences of the adaptive immune system
slower to respond, has a memory, reacts against specific antigens, slower evolved
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what are the main cells in the adaptive
lymphocyres which are white blood cells. produced in bone marrow and thymus gland. stored in lymphatic system until needed
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what are the two main types of lymphocytes
t cells and b cells
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what is t-cell mediated immunity
a macrophage (famous phagocyte) starts to eat pathogen. t-cells attracted, two kinds of receptor. one attaches to phagocytes and one to specific foreign antigens. one binds to macroghage and kills all cells infected and the macrophage
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how do vaccines work
give small amount of like pathogen so body immune system defeats it and remembers this
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explain antibody (b-cell mediated) immunity
b cells bind to foreign antibodies and multiply to develop antibodies that go and kill pathogens. memory cells are produced in process, gives vaccines their prophylactic effect
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what about this means it makes sense that stress weakens immune system
t cells and b cells have receptors on them for glutocorticoids (stress hormones like cortisol). also, lympacytes have receptiors for adrenaline and noradrenaline
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what does acute stress do to the immune response
short term effects of cytokines are good for body. happens so quickly as its done in the innate which can be helpful to the body. EURESS
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what does chronic stress do to the immune resposnse
after a while the tcells and bcells become too busy receiving all the glutocoid and words less
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why does stress change your chances of getting an infection in the first place
1) the immune system has redundant areas, effecting 1 has little effect, 2) stress produes short lived changes, there is compensation in other ares for the decline in other
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what was cohen's study into stress and health
gave 394 healthy students nose drops, measured their stress before. the highly stressed ones got colds
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how does stress effect the hippocampus
cortisol is in the blood and goes to brain. the hippocampus has a lot of glutocorcoids in it. reduction in dendritic branching, less neurogenesis. get worse at hippo dependent tasks like spacial and episodic memory
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what was found in rat babies with stressed mums
produced less glutocorcoids when had a relaxed mum
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VISION. what is vision doing
converting radiation (light) into neural impulses. neural models created to guide eye movements
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what regulates the amount of light that goes into the eye
the iris, a donut shaped band. enters the retina through the pupil (which is a hole in the iris)
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what is pupil adjustment about, what happens in light and dark
compromise between sensitivity and acuity. light- constrict. dark- dilate
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what is happening during pupil dilation
more light is allowed in to the eye, projects onto a large surface area- overlap=more blurry
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what is happening during pupil constriction?
less light allowed in- projects to smaller area- less blurry
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what does the lens do
directs however much light has been allowed in towards the retina.
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what are cilliary muscles
they hold the lens in place. allows for constriction and dilation.
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what is the cornea
helps lens to focus, contributes 75% focusing power
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what is pupil accomodation
the process of the lens changing shape to focus on different distance
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what are zonules
a supportive ligament that holds lens in place
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what are the 3 steps for accommodation for close stuff
the cilliary muscles contract, cilliary body with extra zonules moves closer to lens. tension reduced, lens rounds up- reduces focal distance and creates sharp image
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what are the 3 steps for accomodation for far away stuff
the cillirary muscles relax, cillirary body with extra zonues moves further from lens, tension increase and lens flattens, increases focal distance
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what are the photoreceptors
rods and cones
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what do we have most of
mostly rods but in the fovea we have loads of cones, focus of our gaze
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what is the fovea and where is it
the fovea is located in the mancula. centre of the retina
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what is a bipolar cell.
they get input from the photoreceptors and output to the ganglian cells. includes horizontal and amacrine cells
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what do bipolar cells allow
low level processing in the retina
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what happens when the light hits the photoreceptors
it interacts with photo pigment which starts a chain of events for visual signals
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what happens when the signal reaches the ganglian cells
they leave in a big cluster through the optic disc and become the optic nerve. this is your brain's blind spot because its where the signals go
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why dont we see our blind spots
we dont notice our blind spots because 3 eye movements- tremours, saccades and drifts. keep image moving on retina so it doesnt disappear
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why do we have a blind spot
we have a blind spot because all our vision cant be foveated so we are constantly scanning 3 times a second so that visual information fills in the gaps. integrates all info together
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what is cone-mediated vision called
photopic vision.
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what is rod-mediated vision called
scotopic vision
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what does photopic vision do
each cone connects to one biopolar- good acuity and bad sensitivity
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what does scotopic vision do
hundreds of rods connect to a single bipolar call- poor acuity but good sensitivity
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how do we see colour
if we had a single receptor it would be greyscale, two or more= see in colour. can differentiate wavelength from intensity (actual colour from brightness) colour is seen by 2 or more photoreceptors being activated
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how many people are colour blind
8% of men and 0.5% of women
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what is colour blindess. whats the most common
its a lack of or sensitivity of a cone. most common one- deuterachomoly. cones shift towards red, hard to differentiate
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what is the sclera
the white of the eye, tough layer of connective tissue
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what is the choroid
tissue layer between retina + sclera, has many blood vessels. provides oxygen and glucose to the eye
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what is red eye
light flashes and reflects off blood in choroid
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why do animals have reflective layer on their eye
called the tapetum lucidum
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VISION 2- what is the function of photoreceptors
converting light into neuro signals
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who was HM
epileptic man who has his temporal lobes removed to stop his seizures
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what is visual transduction
moving light into neuro signals
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what is rhodopsin
red pigment that absorbs light
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what is lateral inhibiton
that bands get light towards the edges in a visual illusion
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how was it first identified
ommatidia in horseshoe crab
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what are mach bands
non existent stripes of brightness and darkness running adjacent to edges.
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how does later inhibiton work
basically the stronger a light, the more intensly it fires and this means it inhibits the cells next to it and makes them appear darker. they send sideways projections to neighbours
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what are on centre/off surround retinal fields
light going on to central region causes inhibiton of other cells. amplifies the centre-surround difference
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what happens if there is loads of light on the centre and the surround
cant reall see much because lateral inhibiton cancels it out
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what happens if light is just on the centre
the eye really likes it, very focused vision
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what are humans ommatidia called
horizontal cells
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what is the most common visual pathway
retina-geniculate- striate
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what happens in it
signals go from retina to visual cortex via the geniculae nuclei. axons of retinal ganglian cells do down to the retinal-geniculate-pathway
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what does ipsilaterally and contralaterally mean
contralaterally- crosses over. ipsilaterally- same side
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what are p layers
input from cones. small cell bodies that are responsive to colour. fine detail, slow moving objects, object identification, scene analysis
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what are m layers
large cell bodies, lumincance change, on/off movement, rods produce input.
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PARKINSONS. how many people get it.
1-2% elderly population.
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what is bradykinesia, akensia
bradykinsiea- very slow movement. akinsia- no movement
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what type of disorder is it
idiotpathic, not single cause
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what is it a deficiency of
its deneration of the substantia nigra which is part of the midbrain and part of the basal ganglia. the substantia nigra projects to the striatum.
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what makes up the striatum
the putamen and the caudate
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what is the basal ganglia
the basal ganglia is key to movement.
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what is parkinsons a deficiency in
a lack of dopamine in the nigrostriatal pathway
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what does autopsy of people with parkinsons show
lewy bodies which are clumps of proteins in the dopamine filled neurons of the substantia nigra
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in a normal person, what role does the striatum play
the striatum is at rest and the globus pallidua is constantly active which dampens down the motor cortex (laterl inhibiton). if you 'transiently excite' the striatum, it switches off inhibition of the globus pallidus and you start movement.
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what is it in the striatum that causes this?
its dopaminergic input that transiently excited the striaum and therefore movement. without dopamine, you cant inhibit the motor cortex, the globus pallidius gets stuck on!
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what is the surgical idea
to lesgion the globus palidius and cortex. works in animals but too risky in humans.
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what is the drug treatment idea
you inject l'dopa that goes into the brain and makes dopamine.
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does it work
works for a short period of time, about 3 years, and then it stops working
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describe deep brain stimulation
you have an electrode inserted into the brain that overexcites the basal ganglia so that it stops working. globius pallidius is temporalily switched off to inhibit cortex
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what does neurotransplantation
repairing damaged to cells by putting embryonic cells near by that mature and replace the damaged cells. donor tissue intergrates with host
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how did they do it in monkey
bilateral transplantation of foetal cells in substantia nigra- treated the MPTP (what the frozen addicts had) in monkeys. the cells survived and started releasing dopamine
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what about in humans?
promising results but then after a year patients began writhing and ****
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what is adrenal medulla neurotransplantation
putting patients own adrenal medulla cells which release dopamine in d'orta- he died
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what is non neural neurotransplantation
planting non neural cells to stop neural degeneration and guide neural regeneration.
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how did they test this in rats
limited the blood flow in brains which damaged hippocampus and stopped them at morris maze. then they treated them with virus's that were genetically modified to release AIP, reduced the symptoms!
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what resulted in the MPTP model of parkinsons
the frozen addicts who gave themselves parkinsons by injecting MPTP which turned into the toxic MPP+ in the brain
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sum up what parkinsons is
ITS A LACK OF DOPAMINE IN THE NIGROSTRIATAL DOPAMINE PATHWAY WHICH IS IN THE BASAL GANGLIA. THE DOPAMINE NEURONS STUFF INTO IT AND THOSE CELLS DIE
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where is the nigro striatal pathway!!! drill in
THE BASAL GANGLIA
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how much of the brains dopamine is in the basal ganglia
80%
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what does the basal ganglia project down to
cortex and cortex prohects into basal ganglia.
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how much of the population get it

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1%

Card 3

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what is echolia

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what are positive symptoms

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what are negative symptoms

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