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69 Cards in this Set

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What is the most important thing to remember about the presynaptic mechanisms in chemical neurotransmission?
Calcium plays the KEY role - release of all chemical NTs is dependent on Ca uptake into the presynaptic terminal.
What causes calcium uptake by the presynaptic terminal?
Depolarization of the presynaptic terminal - which opens Calcium channels.
How does the amount of Calcium influx into the presynaptic terminal affect synaptic transmission?
Amt of Ca2+ influx -> amount of NT release -> size of postsynaptic potential.
How do we know that the opening of Ca channels at a presynaptic terminal is voltage dependent, not via Na/K channels?
Because Ca influx still happens even if channels are blocked with TTX and TEA.
Why is it thought that calcium influx is directly related to NT vesicle release?
Because in a freeze-fractured cell the calcium channels are in rows parallel with synaptic vesicles.
What is the ACTIVE ZONE?
The region of the presynaptic terminal membrane where there are rows of adjacent NT vesicles
Where are the ACh receptors found at in a synapse?
On skeletal muscle postsynaptic membranes at the tops of junctional folds.
3 Functions of Vltg-gated Ca2+ Influx at Presynaptic terminals:
1. Increased formation of CDPK
2. Mediates Vesicular fusion w/ Plasma Membrane
3. Increases diameter of the fusion pore complex allowing exocytosis to occur
In what 2 states are synaptic vesicles stored?
1. Attached to the cytoskeleton
2. Docked to the PM
What happens when calcium influxes into the presynaptic nerve terminal?
It complexes with Calmodulin to activate Ca/Calmodulin-dependent protein kinase.
What does Ca/Calmodulin-depend. protein kinase do?
Phosphorylates Synapsin
What is Synapsin?
A protein that anchors synaptic vesicles to the cytoskeleton - when phosphorylated, they're freed
What happens to vesicles when freed from Synapsin?
Rab3A targets them to the membrane active site for docking.
What is Rab3A a member of?
The Ras proto-oncogene family
When is Rab3A activity on/off?
Rab3A-GTP guides vesicles to the release site; then hydrolysis to GDP results in Rab3A-GDP which is inactive.
What prevents vesicles from leaving the active site once they're docked?
Rab3A-GDP - it is incapable of guiding vesicles anywhere.
How does Ca increase exocytosis of NT?
1. Mediates fusion of the protein that's the vesicle portion of the pore complex to the terminal membrane
2. Increases the diameter of the fusion pore complex.
What is Post-Tetanic Potentiation?
The result of intense activity (AP freq) at a presynaptic nerve with the result of increasing the EFFECTIVENESS of the synapse.
What allows for the amplitude of postsyn potentials to remain elevated in PSP?
Elementary form of memory - Ca saturates its buffer system in the presynaptic terminal longer and results in RESIDUAL conc.
What changes in potential occur during post-tetanic potentiation?
-Presynaptic AP magnitude is UNCHANGED (b/c all or nothing!)
-Postsynaptic Em is INCREASED in ppn to the increased freq of presynaptic APs
Why is PTP called a form of 'cellular memory'?
Because it's electrical activity being stored as biochemical information ([Ca]i)
What is the most common function of Axo-axonic synapses?
Presynaptic inhibition
How is Presynaptic inhibition achieved?
By regulating the amount of calcium influx at voltage-gated channels.
Where is the site of synapse between an axo-axonic synapse?
Inhibitory axon contacts at the presynaptic axon terminal.
What is the action of the inhibitory neuron in presynaptic inhibition?
Depressed Ca current into the presynaptic terminal, to decrease the amplitude of the postsynaptic potential.
List 3 possible mechanisms for how Presynaptic inhibition works:
1. Selectively open K+ channels to hyperpolarize Em and shut Ca channels
2. Activate ionotropic GABA-gated Cl- channels to decrease presynaptic axon AP amplitude and prevent voltage-gated Ca channels from even opening
3. Activate metabotropic receptors that inhibit NT release by other mechanisms than Ca influx
What is the effect of activating ionotropic Gaba-gated Cl- channels?
Cl- influx short-circuits the axonal AP and decreases its amplitude.
What is a non-Ca-dependent mechanism of presynaptic inhibition?
Activation of metabotropic receptors that can directly inhibit 1/more steps in the NT release process.
At what site in the mammalian CNS does presynaptic inhibition occur?
At the first synapse of mechanoreceptors in the CNS.
Where are the cell bodies for mechanoreceptors?
In the dorsal root ganglion.
What is a Nicotinic receptor?
An ionotropic receptor activated by ACh.
What is the definition of an Ionotropic receptor??
A channel in which the RECEPTOR FUNCTION and EFFECTOR GATING FUNCTION are carried out by the same macromolecule (but in different domains).
What is the definition of a metabotropic receptor?
A channel in which the RECEPTOR FUNCTION and EFFECTOR GATING FUNCTION are carried out by 2 separate molecules (2nd msgr).
What are the constituent subunits of the AcH receptor?
2 Alpha
1 Beta, yamma, and delta.
What activates the AcH receptor?
Binding of 2 ACh's to the alpha subunits - changes the ion channel conformation.
What happens when the ACh-gated channel is opened?
Na and K flow down their electrochemical gradients (in opposite directions).
What makes up each subunit of the ACh receptor?
4 membrane-spanning sequences that are hydrophobic, a-helices (20 aa each).
How do the 5 subunits come together to make the pore of the AcH receptor?
They orient themselves so the M2 chains together make the pore walls.
What determines the opening/closing of the AcH receptor channel pore?
Movement of 5 amino acids - one per each of the 5 subunits.
When an Ach receptor is activated, what ion will flux more, Na or K? Why?
Na - because the net electrochemical force is much greater for it.
What does the depolarizing current caused by Na influx at ACh receptor channels generate?
An endplate potential - typically up to about -20 mV
What are the features of an EPP?
What is Curare?
A drug that competes with AcH for ACh receptor sites - prevents the EPP from reaching threshold.
Under normal physiological conditions what is always the result of an EPP?
Action potential is always generated.
When is an AP NOT generated by an EPP?
In the presence of Curare
How is an EPP different from an AP?
EPP = local, nonpropagated, caused by opening nonspecific ion channels via AcH binding.
AP = transient, propagated, caused by voltage opening specific ion channels for Na/K
How is an EPP different from an EPSP or IPSP?
EPSP/IPSPs are neuro-neuronal synapses, EPP is neuromuscular.
EPSP/ISPSs do not always result in an AP; can be SUMMATED spatially/temporally.
For Na/K, which net electrochem gradient is higher at:
-Resting Em (-90 mV)
-0 mV
Resting Em: Na gradient is higher so it will influx
0 mV: K gradient is higher so it will outflux
What is the mechanism of an IPSP?
An IPSP will summate with an EPSP to result in the EPSP being below threshold and no significant depolarization.
What type of potential is an IPSP?
What CAUSES IPSPs in the CNS?
Glycine - an inhibitory transmitter that hyperpolarizes the postsynaptic membrane by opening Cl- channels in it.
What is the Ecl for mammalian motor neurons?
MORE NEGATIVE than the resting Em - so opening Cl channels will HYPERPOLARIZE the membrane.
What neurotransmitter in the CNS causes EPSPs?
How exactly does Glutamate act?
Similarly to ACh by opening nonspecific Na/K ion channels, which then opens voltage gated channels.
What would happen to EPSPs generated at denrites on neurons if there were no axon hillock?
They would just decay and die.
What happens to EPSPs generated on dendrides as they travel along a neuron?
They decay exponentially
Why does an EPSP decay?
Because it has a finite LENGTH CONSTANT and TIME CONSTANT.
How can an AP be generated at an axon hillock if an EPSP has decayed so much by the time it gets there?
The axon hillock has a threshold Em very close to resting Em because it has a high density of v-gated Na channels.
What is the Eth at the axon hillock?
-55 mV - only 10 mV higher than resting Em
What is the Axon Hillock termed?
Site of Integration
Why is the Axon Hillock the Site of Integration?
Because that's where all the EPSPs and IPSPs will summate and determines whether an AP will be generated or not.
What is the net ionic current for a membrane potential of 0mV?
NET Current = 0 because the inward sodium current is equal to the outward potassium current.
What is the membrane potential generally achieved by EPSPs in the CNS?
0 mV
What can you deduce from the fact that EPSPs produce a membrane potential of 0?
The channel opened by Glutamate allows permeability of both Sodium and K
What would result if you gave a neuron an EPSP and clamped its membrane at +60?
Potassium would flow out alot more than sodium because the cell wants to become less positive.
What happens for the normal resting membrane at Em = -60 when you give it an EPSP?
Sodium flows in because that is much stronger of a gradient pulling on it.
Membrane threshold in normal cell is what:
-35 mV
Membrane threshold at Axon Hillock is what:
-55 mv
So what is the Axon Hillock?
The site of integration - if an EPSP or IPSP impinges here, it will determine the type of effect.