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Phys Lect 10

QuestionAnswer
How can nueromuscular transmissions be modified within the axon/terminal bouton? Affecting the process of synaptic vesicle release at the neuromuscular junciton
What happens to the EPP at the nueromuscular junction when: the presynaptic Na+ channels are blocked? Diminished or non-existant. The Na+ influx is needed to activate voltage gaited Ca+ channels which in turn cause the release of neurotransmitter into the synaptic cleft.
What happens to the EPP at the nueromuscular junction when: the presynaptic Ca2+ channels are blocked? Dimished or non-existant. the Ca2+ influx causes the release of the neurotransmitter into the synaptic cleft.
What happens to the EPP at the nueromuscular junction when: AChE is inhibited? The EPP becomes larger as more ACh lingers in the synaptic cleft and continues to bind to ACh receptors. **Normally AChE will breakdown ACh and allow its re-uptake into the pre-synaptic neuron.
What happens to the EPP at the nueromuscular junction when: the ACh receptors are blocked? deminished or non-existant. If not all of them are blocked then the EPP can still be generated, however not as fast so patient will present with muscle weakness
Where are V-snares and what are the two main types? They are proteins on the vesicles within the axon terminal. 1.Synaptotagmin. 2.Synaptobrevin.
Where are T-snares and what are the two main types? They are proteins on the axon terminal membrane. 1.SNAP-25. 2.Syntaxin.
What causes the interaction of V and T-Snares which leads to the release of neurotransmitter Ca2+ influx causes them to interact, twist, and leads to the fusion of the veiscle to the axon terminal membrane. Releasing them via EXOcytosis.
Where does Botulinum toxin come from? Clostridium botulinum. Found in canned goods/veggies
What does Botulinum toxin do? **Prevent Neurotransmitter release.** cleaves the T & V-SNARE proteins, preventing the vesicle to be tethered to the terminal membrane which means they can not fuse and release the ACh into the neuromuscular junction. **Causes muscle weakness.
Is there just one input influencing a motor neuron? NOOO C'mon man. The neuron must integrate multiple EPSPs and IPSPs at the spinal cord level.
What are two critical regions for generating an AP in a motor neuron? 1.Axon Hillock (this is where the AP first gets generated). 2.Initial Segment.
what is an EPSP? IPSP? EPSP: Excitatory post-synaptic potential. Causes opening of Na+ channels in the axon hillock. IPSP: Inhibitory post-synaptic potential. Causes the influx of Cl- and efflux of K+ which prevents the generation of an AP by making the mem. pot. more neg.
Why doesn't an EPSP generate an AP in the dendrite? Becuase there are very few Na+ channels there, so the EPSP passively travels to the Axon Hillock where it can generate and AP. **Decreased Na+ channel density = Increased Threshold**
Spatial Summation occurs inside the neuron as EPSPs and IPSPs collide as they approach the axon hillock. They add together or cancel eachother out. **Therefore one IPSP could cancel out one EPSP.
Temporal Summation Rapid firing/ high frequency of one EPSP will summate in the dendrite and build on eachother as they travel to the axon hillock.
Difference between Spatial and Temporal Summation? Spatial: Multiple inputs. Temporal: Single input firing rapidly.
Where does tetanospasmin come from? Clostridium Tetani
How/where does tetanospasmin work? It acts only in the CNS on inhibitory interneurons. It affects V-SNARES which prevents the IPSP from being released. **This leads to unopposed EPSPs and constant muscle contraction.
What is the mechanism causing muscle spasms and contraction? Inhibition of Inhibitory Interneuron synaptic vesicle release on to an Alpha motor neuron in the spinal cord (Glycine).
Created by: WeeG