Neurotransmitters and Chemical Synapse

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  • Created by: Sarah
  • Created on: 20-05-17 13:55
what is the criteria for transmitters? what should be NT?
present in presynaptic, released by stimulation, postsynaptic receptors, rapid removal
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what does a NT need mechanisms for?
SSRRR synthesis, stroage, release, receptors and removal
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what biogenic amines are there
catecholamines (dopamine, adrenaline and noradrenaline) and histamine + seotonin
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what neuropeptides are there?
enkephalin, substance P, B-endorphin and cholecystokinin
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features of neuropeptides?
stored in sceretory granules, only activate GPCRs, large molecules
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what are amines and amino acids stored in?
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what was dales principle
each neuron only releases one neurotransmitter
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is dales priniciple correct?
no some have neuropeptides and aa or co-factors as well
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where are no peptides synthesised? (Gly, Glu, Ach + GABA)?
synthesis localised to axon terminal by specific enzymes
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what are them non-peptides packaged into?
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what is abundant in all cells?
glutamat acid and glycine
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what is the most common excitatory NT in the CNS?
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what recpetors does glutamate bind to?
particulary AMPA, NMDA but also Kainaite receptors
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what receptor that glutamate uses is important in fast transmission?
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what happens when glutamate binds to AMPA?
receptrs triggers Na and K currents to produce an EPSP
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what often co-exists with AMPA receptors?
NMDA receptors
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what can block NMDA receptors?
coltage depend Mg2 block
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becuase of this Mg2+ voltage dependent block how does the NMDA recptors need to activated?
indirectly activated by another transmitter
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what is the major inhibitory NT in the spinal cord?
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what is the most common inhibitory transmitter in the brain?
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what do GABA-gated chloride channels do?
produce IPSPs
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why does chloride channels (gated by GABA) produce and IPSP
has a negative potential reduces influx
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where is GABA found in the brain especially?
throughout the brain especially striatum ad cortex
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too little action of GABA gives what?
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too much action of GABA gives what?
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what converts glutamate -> GABA?
glutamic acid decarboxylase
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what is presynaptic inhibiton?
one neuron supressons the action of another, doesn't have to be inhibitory transmitters can be
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what is NMDA important in?
memory and learning
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what is autoinhibition?
inhibition of inhibition gives autoinhibition or disinhibition
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what is disinhibition?
inhibiting inhibition
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what is really importnat?
inhibition- waste energy if everything was firing all the time
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what are anxiety dissolving drugs called?
anxiolytic drugs
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what do anxiolytic drugs bind to?
GABAa receptor
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what can bind to GABAa rec?
barbiturate, neurosteroids, ethanol, benzodiazepine
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what do toother chemicals that bind to GABAa do?
modulate/stimulate response to GABA, difference in intensity of binding to GABA recs, can alter rec
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what is lost in a panic A?
loss of GABAa receptors
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what system do opiates act by?
the endogenous opiate system- compounds we make bind to recs but opiates can bind to them as well
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when was opiate receptors in the brian discovered?
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what was the implication of common rec site for opiate actions?
they were endogenous so everywhere, in te 1960s discovered the opiate antagonst
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what was the opiate antagonist discovered in the 1960s?
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the discovery of opiate recs in the brain in 1973 led to the discovery of what?
several endogenous opiates (neurppetides) EED- endorphin, endorphin, enkephalin adn dynorphin
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where are peptides (including opiates) formed?
in rough ER then packaged into secretory granules
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three main ypes of opiate receptors?
kappa, sigma and mu
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what do opiates do to pain? where?
block pain signal in the spinal cord
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where regulates sensation of pain?
periaqueductal grey
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what is the amygdala important for?
regulating emotions
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whas the role of the frontal cortex to do with pain?
cognitive aspects
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what does the brain do to pain under opiate influence?
depress respiration and cough reflex (vommiting)
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opiate receptors are what kind of reeceptors?
G-protein coupled receptors
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as opiate recs are GPCRS what do they act as?
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how can opiates be used in relation to intestinl disorders?
reduces diarrhoea, decreases ddehydration
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what drug is used as a cough supressant (antitussive) that is an opiate?
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why are opiates used for analgesia?
reduces perception and emotional response to pain
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whats the problems with using opiates for therapeutic use?
analgesia is linked to dependence, tolerance and dependence dev, analgesic (Reduce pain perception) and euphoric effects linked, relieve dull visceral pain better than sharp pain
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what are the common features of diffuse modulatory systems of the brain?
core nuclei in central part of the brain (often brainstem), many neurons contact large numbers of postsynaptic neurons like a hospepipe effect
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what catecholamines are there?
dopamine, adrenaline and noradrenaline
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which transmitters are in the diffuse modulatory system?
catecholamines, serotonin and Ach
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what is serottonins chemical name (5-HT)?
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where is acetylcholine widespread?
basal forebrain, hippocampus, autonomic nerves and neuromuscular junctions
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what neurotransmitter is lost in alzeheimers?
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what is acetylcholine associated with?
sleep cycle, memory, coordination, mood and aggression
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acetylcholinesterase breaks down acetylcholine into what?
acetic acid and choline
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what enzyme makes acetylcholine? from what?
choline acetyltransferase from choline and acetyl CoA
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what does botulism do to Ach?
prevents the release
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where does acetylcholine spread out from?
potomesncephalic tegmental complex
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what can the black widow spider do to Ach?
prevents release, increases and decreases the release of Ach
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what Acetylcholinesterase inhibitors are there?
nerve gas, insecticide, alzeheimer treatments (ach lost in alzeheimers)
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what blocks the nicotinic receptors of acetylcholine?
curare, alpha-bungarotoxin
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what blocks muscarinic Ach recs?
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what is known as the pleasure centre in the dopamine system?
ventral tegmental area
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what are the catcholamne systems associated with?
movement, moot, attention, visceral function
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what converts noradrenaline to adrenaline?
phenotolaine N-methyltransferase
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what is the catchecolamine syn pathway?
tyrosine -> [tyrosine hydrozylase] -> l-dopa -> [dopa decarboxylase] -> dopamine -> [dopamine beta-hydroxylase -> noradrenaline -> [phentolamine N-methyltransferase] -> adrenaline
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symptoms of parkinsons?
tremor, rigidity, akinesia, postural changes- stoop and shuffling gait, monotonous slurred speech, no sensory loss, normal cognitive func (at start)
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what is diminshed in parkinsons?
substantia nigra
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what does the striatum inhibit?
motor function
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what is the nigrostriatal pathway?
substantia nigra sends pathways up to striatum, prkinsons deficient in parkinsons
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what does the dopamine do to the striatum normally?
dopamine from substantia nigra inhibits cells of the striatum (activates them? as striatum inhibits) by receptors, inhibiting inhibitroy cells = promote motor activity, dopamine effectively removes the inhibition of motor by striatu
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so what happens when dopamine is lost from the substantia nigra in parkinsons?
dopamine no longer inhibits the striatum from inhibiting motor activity therefore striatum is free to inhibit motor activity, increase in inhibition of motor function from the striatum
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what receptors does dopamine use o inhibit the striatum?
D2 cells
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what could be a possible treatment for parkinsons?
increase precursor L-dopa
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what is a way parkinsoism can be caused?
reserpine destroys stored of dopamine vesicles so induces parkinsonism
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what can increase he release of dopamine?
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what drug blocks reuptake of dopamine so theres increased action of it at the synapse?
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what can d2 agonists be used for?
parkinsons treatment
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d2 antaginists induce what?
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what breaks down dopamune>
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what treatment is there to inhibt MAO B therefore stop the breakdown of dopamine?
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why would you not just increase the levels of dopamine to treat parkinsons?
its cardioactive
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in L-dopa treatment what is used o stop side effects on the body?
peripheral DDC inhibitor-benserazide
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why is there problems wth L-dopa long term?
drug becomes effectively (taken orally), get dopa-induces dyskinesisa fluctatng with sudden immobility (on-off syndrome)
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where are dopamine neurons outside the substantia nigra?
cortical and the limbic system, frontal lobe, striatum, ventral tegmental area
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why is the limbic sytsem important in relation to dopamine?
emotion, memory, complex behaviours, psychosis
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where do addictive drugs target?
ventral tegmental area (pleasure centre) and nucleus accumbens
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what drugs known to go the ventral tegmental area?
heroin and nicotine
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what do antipsychotic (used to treat schizophrenia) drugs act on?
dopamine receptors
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what may antipsychotic drugs induce?
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what does dopamine do to prolactin produced by the hypothalamic-pituitary axis?
dopamine neurons inhibit prolactin secretion from the pituitary
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antagonists of dopamine on the hypothalamic-pituitary axis do what?
result in the overproduction of prolactin
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what antagonists arethese?
gynaecomastia and galactorrhoea
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what does the noradrenaline system arise from?
the locus coerueleus
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what is the noradrenaline system involved in?
multiple targets, attention, arousal, learning, memory and anxiety
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what is part of the noradrenaline system?
hyothalamus, locus coerulues, temporal lobe, sperebellum, neocortex, brainste
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how are most catecholamines got rid of?
reuptake into presynaptic terminal
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what are catecholamines metabolised by?
Catechol-O-methyltransferase (OMT) and Monoamine oxidase (MO-a)
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where is catechol-O-methyltransferase mainly
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where is monamine oxidase (MAO) mainly?
outer mitochondrial membrane
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what does MAO- A mainly break down?
noradrenaline and serotonin
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what does MAO-B breakdown?
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other than synapses (presynaptic knob) where are MAO enzymes?
in the liver and gut for detoxification
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what have MAO-inhibitors been used treat?
depression (increase serotonin+noradrenaline), parkinsons increase dopamine
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where is a key place serotonin is found?
in the raphe nuclei
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what are the major functons of serotonin (5-HT)?
mood, aggresion, circadian rhythms (Sleep), consciousness/arousal
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what do tricyclics do to treat depression?
prevent uptake of serotonin and noradrenaline
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what is a specific serotonin reuptake inhibitor used to treat depression?
fluoxetine (prozac)
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what 3 drugs used to treat depression?
tricyclis, specific serotonin reuptake inhibitors- fluoxetine (prozac) and MOA-A inhibitors
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what is the problem with MAO inhibitors?
breaks down dieterary tyramine wich is sympathomimetic and MAO-I -> hypertensive crisis
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synapses allow infomation that is what?
FESC- flexible, elaborate, subtle and complex
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how big is a normal chemical synapse?
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what kind of junction is the chemical synapse?
adhesive junction
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how do chemical synapses vary?
can shrink, grow, move, different synapses
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what do large synapses have more of?
active zones
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what is an active zone?
where NTs are released
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can synapses release transmitter from more than one active zone in a terminal?
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where are neuropeptides sythesised and then stored in?
in the soma and stored in secretory granules
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what is synthesised at the synaptic terminal?
acetylcholine, amines and amino acids
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why are some NT vesicles docked at the terminal before an action potential?
allows rapid release
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what is the outisde and inside calcium concentrations?
inside-1nM, outside 2.5nm
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what does arrival of an ap do at a chemical synapse?
opens voltage gated calcium channels which triggers vesciles to fuse and release by exocytosis
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what is quantal release?
each vesicle releases the same amount so can work out how many vesicles fused
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how much do synaptic vesciles usually contain?
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NTs once released fromt he synapse act on what 2 types of receptors?
ligand gated ionchannels (ionotropic) and G protein coupled receptors (metabotropic)
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what effect on the heart does acetylcholine binding to muscarinic receptors have?
is G protien coupled activates K channels and slows down the heart
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when Ach binds to the nicotinic receptor what does this do to skeletal muscle?
causes contraction as is ionotropic makes permeable to Na
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why does GABAa make it harder to reach threshold and produce an IPSP?
makes membrane potential more negative opens Cl channels
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ligand-gated ionchannels are what?
fast acting, open transiently in response to NT binding
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where is the acetycholine binding site in nicotinic recs?
alpha subunit
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what 3 things terminate transmission?
1) reuptake 2) breakdown 3) diffusion
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transmitter release at a fast excitatory chemical synapse geenrates what?
excitatory post synaptic potential
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merabotropic receptors features?
synaptic tranmission is slower+more complex than ligand-gated ion channels, signal amplification, multiple channels affected
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rather than directly elicit an PSP or IPSP what do GPCRs do?
act as modulators
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