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Phys Lect 10
Question | Answer |
---|---|
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). |