Action Potential Propagation, Synaptic Transmission, Neuromuscular Junctions Flashcards
Lectures 5/6
How do action potentials spread down the axon?
Wave-like motion as neighboring molecules diffuse (causing action potentials)
Fun fact on invertebrates
very few of their axons are myelinated
Why don’t action potentials travel in both directions?
On the “back side” of an action potential the sodium channels are INACTIVE
Why do we notice a decrease in voltage at neighboring axon locations?
Charges diffuse passively along axon (looses “umph” as it goes)
Which is faster passive diffusion or active current flow?
Passive diffusion!
Axon length constant
lambda- (about 1-2mm) is how far down the axon it takes for the voltage to decay to 37% of its original amplitude
Is passive diffusion sufficient for the action potential to travel fully down the axon?
No! It wouldn’t make it to the end for most
Describe the Nodes of Ranvier
-voltage gated Na+ and K+ channels
-no myelin here
-action potential regenerated here
Where does the diffusion of action potentials occur?
In myelinated areas
Def: saltatory conduction
-fast/slow/fast/slow
-action potential “jumps” down axon from one Node of Ranvier to the next
Do the action potentials move quicker at the Nodes of Ranvier or through the myelin?
Through the myelin, by diffusion
Which neurons conduct faster- myelinated or unmyelinated?
Myelinated, b/c regenerated at each node
Where are neurotransmitters stored?
In vesicles in the axon
What happens when an action potential invades the presynaptic terminal and causes depolarization?
Voltage-gated Ca2+ channels open
What does Ca2+ do in synaptic transmission?
-causes vesicles (containing neurotransmitters) to fuse with membrane
-leading to exocytosis (burst out)
Following exocytosis what happens to the released neurotransmitter?
It diffuses across the synaptic cleft and binds to receptor molecules on the post-synaptic membrane
For case purposes: lets say the release of the neurotransmitter (glutamate) into the synaptic cleft binds to receptor molecules… does that mean glutamate will be the molecule entering the post-synaptic cell?
Not necessarily, may open sodium gates
Do neurotransmitters only open postsynaptic channels?
No, they can close channels as well
How does the postsynaptic current (influx of ions into cell) change the excitability of the cell?
The ions cause excitatory or inhibitory potential
What happens to any neurotransmitters left in the synaptic cleft?
Removed by glial cells (support neurons) or degraded by enzymes
Synaptic cleft
-small space bwtn presynaptic (axon) and postsynaptic (dendrite)
Def: dendritic spines
-contact points on the postsynaptic neuron
-small projections of cell membrane
When do omega formations occur?
-when Ca2+ enters and synaptic vesicles fuse to membrane (to release contents)
What is a quanta?
-unit of measurement
-meant to describe the amount of NT in one vesicle
What is the purpose of having various proteins?
-complex structure/function
-create, load, and release synaptic vesicles
What is the budding process?
-recycling of synaptic vesicles
Once Ca2+ causes exocytosis what happens to the presynaptic vesicles?
-fuse with membrane
-pull in HRP from outside cell (endocytosis)
-axon notices
-this temporary vesicle joins up with endosome
What is the endosome?
-Large vesicle made up of vesicle membrane
-collects/reforms vesicles
Why are tracer molecules like (HRP) necessary for budding?
-recognizable by endosome
How are SNARE complexes activated?
entry of Ca2+ into the presynaptic terminal
What is the purpose of SNARE proteins?
-aid in the release of neurotransmitters
-help bind to membrane (“dock”), then tear vesicle
Name the four most common local anesthetics
Procaine, lidocaine, novocaine, cocaine
What are local anesthetics used for?
-used to block action potentials from being sent to CNS (NO PAIN!!)
How do local anesthetics (procaine, lidocaine, novocaine, cocaine) work?
bind with and block Na+ channels (no depolarization)
describe how reversible antagonists work
they eventually unbind (from Na+ channels) and the anesthetic wears off… like at dentist
Tetrodotoxin (TTX)
-blocks Na+ channels IRREVERSIBLY
-puffer fish and some other poisonous creatures synthesize TTX as a protective mechanism
What is TTX and what would happen if too many channels are blocked?
Tetrodotoxin- won’t unbind for Na+, so if too many blocked (OVERDOSE! and death from asphyxiation)
Fugu
-puffer fish prepared by highly certified Japanese chefs (tightly regulated)
glutamatergic synapse
-most common excitatory synapse in nervous system
-glutamate released from presynaptic membrane
-open channels that allow Na+ to flow into postsynaptic membrane (make neuron more positive)
Neurons store _______ of neurotransmitter(s)
one type
Neurons receive _______ of neurotransmitter(s)
various kinds
GABAergic synapse
-most common inhibitory synapse
-GABA released
-open Cl- channels (make neuron more negative)
EPSP
-excitatory postsynaptic potential
-make more positive
IPSP
-inhibitory postsynaptic potential
-make more negative
How are action potentials initiated in the postsynaptic neuron?
The postsynaptic currents sum together, if threshold is reached - BAM! - action potential
Which cells receive the most action potential inputs?
Purkinje cells (cerebellum)… hundreds of thousands
Which cells receive a lot of action potentials?
Pyramidal cells (cerebral cortex)… tens of thousands
Where are alpha motor neurons located?
ventral horn of spinal cord
What do alpha motor neurons connect to?
-their axons connect to a group of muscle fibres
How do Acetylcholine (ACh) receptors work?
-both K+ and Na+ can flow through, but more Na+ enters than K+ leaves
-NET: depolarization (more positive)
