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30 Cards in this Set
- Front
- Back
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what kind of transmission do ligand-gated ion channels conduct? |
fast transmission - dependent on selectivity of channel or driving force or ion concentration |
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What kind of transmission do metabotropic/GPCR channels conduct? |
slow transmission - amplifies things: signal = many molecules of diffusible messengers produced; space = amplified greater space away from receptor site; time = long-lasting signals |
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what type of receptors does glutamate bind to? |
on postsynaptic cell: - AMPA - NMDA - KAR - all are cation channels and ionotropic receptors - all are selectively permeable to K and Na |
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NMDAR components |
- has Mg+ blocks - depolarization is required to remove Mg+ block - requires Glu and glycine binding to remove Mg+ block - coincidence receptor b/c of this |
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What is GABA synthesized from? |
glutamate |
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What is the GABA transporter? |
GAT |
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What is GABAa selective for and what kind of receptor is it? |
- GABAa is selective for chloride - when GABAa receptors are active, Cl- enters the cell - ionatropic receptor |
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what type of current is followed in voltage clamp experiments? |
- positively charged ionic current is followed (Na, K) |
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what does outward current show in a voltage clamp experiment? is it depolarization or hyperpolarization? |
- it shows either negative ions are going in and/or positive ions are going out of the cell - it is hyperpolarization (a mountain) |
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what does current clamp measure and which direction is depolarization? |
- measures voltage - peak shows depolarization (opposite of voltage clamp) |
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what is measured in extracellular recordings and what does it show? |
- mV is measured - downward mV = net negative ions in the extracellular space |
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what does whole cell voltage clamp measure? |
- current is measured - currents can be action potential dependent or independent |
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what are miniature IPSCs/EPSCs and how can they be measured? |
- measure by using TTX to block sodium channels - spikes are spontaneous fusing of vesicles and release of neurotransmitters presynaptically |
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Reversal Potential for Glu and GABA |
- glutamatergic reversal potential = 0 (almost always) - hold at Glu's reversal potential IOT measure GABA IPSCs (b/c Glu current = 0 at rev pot b/c of driving force) - current measured at GABA rev pot = Glu EPSP |
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Cumulative probability (stair steps) |
- shifts in cumulative probability plot = changes in spontaneous and mini events |
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Can you interpret spontaneous post synaptic currents based on frequency or amplitude? Why/why not? |
No, because spontaneous PSCs are action potential dependent; APs contaminate the data, so nothing can be interpreted based on freq or amplitude |
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What do miniature post synaptic currents indicate with changes in frequency? |
changes in frequency = presynaptic changes in the # and probability of release (note: silent synapses are the exception here) |
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What do miniature post synaptic currents indicate with changes in amplitude? |
changes in amplitude = postsynaptic changes in receptor numbers, properties, etc. - currents shown are a summation of the single channel openings (greater amplitude = more channels open) |
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What does simple integration do when measuring action potentials? |
- simple integration = additive = spatial or temporal summation - integrates IPSPs and EPSPs in post-synaptic cell to determine if an AP will fire |
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Which is fast and which is slow? AMPA, NMDA receptors |
- AMPAR = fast - NMDAR = slow |
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what are silent synapses? |
- mini-EPSCs with NMDARs - baseline: block NMDARs with Mg+ - add AMARs, which will allow Glu to bind and depolarize membrane enough to remove Mg block, thus allowing Glu to bind to NMDAR - a Mg+ - free solution gives the same result (Glu can bind to NMDARs) - silent = NMDAR is there, but can't be used b/c of Mg block |
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What is special about ionotropic glutamate receptors? and what are ionotropic glu receptors? |
- subunit composition can change, which changes the reaction of the receptor - ionotropic glu receptors synaptic = AMPAR, NMDAR perisynaptic = KAR, mGluR |
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what are the various NMDAR types? |
- synaptic - perisynaptic (from spillover of neurotransmitter) - extrasynaptic (modulating glial cells) - presynaptic (on terminal, axon) |
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What are the various mGluR receptors? |
- all are slow GPCRs - Type I = increase IP3 via PLC - Type II = decrease cAMP via adenylyl cyclase - receptors use signal, space, time amplification - can alter presynaptic release probability and postsynaptic responses |
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what does GABAb do? |
GPCR that modulates K+ |
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what does GABAa do? |
GPCR; targets different subtypes for a specific therapeutic response |
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what does extrasynaptic GABAa do? |
- causes shunting (a leaking membrane) - increase in noise and increase in resting potential - shunting occurs b/c ions leak out of open channels |
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what does excitatory GABA do and when does it occur? |
- occurs in development and in a disease state - can occur with prolonged GABAa receptor activation (initially hyperpolarized with Cl into the cell, but Cl buildup eventually leads to HCO3 leaving, resulting in depolarization) |
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What can cause degradation of an EPSP? |
- distance - how tight the membrane is (membrane resistance) - how much amplification there is (based on nearby channels) - intrinsic properties of the AP (degrading, fast, etc) |
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non-linear summation of EPSPs - how can this happen? |
- the composite EPSP's amplitude does not equal the sum of the EPSPs contributing - when synapse 1 (further from soma) is activated first, EPSP=smaller b/c driving force is smaller when synapse 2 is activated due to partial depolarization - high freq stimulation/depolarization at the same site=smaller driving force=smaller EPSPs |
