Questions and Answers
What role does soluble α-SNAP play in synaptic transmission?
How does botulinum toxin affect synaptic transmission?
What happens to the intracellular calcium concentration [$Ca^{2+}$]i after fusion completion?
Which protein is responsible for the recycling endocytosis of synaptobrevin?
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In the context of Lambert-Eaton myasthenic syndrome, what does a positive antibody study for voltage-gated calcium channels indicate?
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What is the main function of the N-ethylmaleimide–sensitive factor (NSF) in the SNARE complex?
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Which of the following statements best describes the process of synaptic transmission?
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What initiates the process of vesicle fusion at the presynaptic terminal?
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Which component of the SNARE complex is located in the presynaptic membrane?
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Study Notes
SNARE Protein Functionality
- Composed of v-SNAREs (from vesicle membranes) and t-SNAREs (from target membranes).
- Key v-SNARE includes Synaptobrevin.
- Key t-SNAREs include Syntaxin-1 and SNAP-25.
Synaptotagmin
- Functions as a calcium sensor during exocytosis.
- Binds Ca2+, promoting neurotransmitter release.
Docking and Priming Stages
- After docking near the presynaptic membrane, Sec-1/Munc18, Munc13, and RIM facilitate SNARE complex assembly.
- Priming stage 1 involves coiling of SNARE helices, forming a stable trans-SNARE complex.
- Priming stage 2 sees complexin insertion into the trans-SNARE complex, preventing premature fusion.
Calcium Influx and Fusion
- Voltage-gated Ca2+ channels allow calcium influx aligning with presynaptic active zones.
- Ca2+-bound synaptotagmin binds acidic phospholipids, displacing complexin and initiating fusion-pore opening.
Synaptic Transmission Sequence
- Membrane fusion occurs when the fusion pore opens, leading to neurotransmitter release.
- Following fusion completion, intracellular calcium levels decline rapidly through PMCA and mitochondrial uptake.
SNARE Protein Recycling
- Soluble α-SNAP binds to the SNARE complex and recruits NSF ATPase, leading to protein recycling.
- Synaptobrevin undergoes recycling endocytosis, while syntaxin and SNAP-25 remain for subsequent vesicle fusion.
Botulinum Toxin Effects
- Botulinum toxin prevents vesicle exocytosis by occupying binding sites on SNARE proteins, inhibiting neurotransmitter release.
- True statements regarding its mechanism do not include preventing action potentials or calcium channel opening.
Gap Junctions in Electrical Synapses
- Comprised of two connexons, permitting communication between adjoining neurons.
Key Neurotransmitter in Neuromuscular Junctions
- Acetylcholine is the primary neurotransmitter involved.
Saxitoxin Poisoning Case
- Symptoms include vomiting, diarrhea, and facial numbness after consuming potentially contaminated mussels, indicating possible saxitoxin exposure.
Lambert-Eaton Myasthenic Syndrome (LEMS)
- Positive antibody studies for voltage-gated calcium channels suggest LEMS in a patient with small cell carcinoma and muscle weakness.
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Description
Explore the intricate process of neurotransmitter release involving SNARE proteins and calcium signaling. This quiz covers key components like v-SNAREs, t-SNAREs, and the role of synaptotagmin in exocytosis. Test your knowledge on the sequence of events leading to synaptic transmission.