Lecture 3 - Lucas Flashcards
2 types of synapes
electrical and chemical
how do electrical synpases make contact
make direct contact between excitable cells via connexons (protein channels)
4 features of elctrical synapses
fast and synchronous signal transmission.
Non-selective ion movement.
Always transmits signals (no fine-tuning or modulation).
Bidirectional.
how do chemical synapses make contact
Utilize neurotransmitters to bridge a synaptic cleft.
features of chemical synapse
Slower but more versatile.
Can modulate signal strength and response (e.g., excitatory vs. inhibitory).
More prone to disruption (things going wrong)
Unidirectional.
3 key parts of neuromuscular junction
Presynaptic terminal (vesicles of acetylcholine, ACh).
Synaptic cleft.
Postsynaptic membrane with ACh receptors (ligand-gated Na⁺ channels).
5 steps of signal transmission
Action Potential: Opens voltage-gated Ca²⁺ channels in the neuron.
SNARE Proteins: Facilitate ACh vesicle fusion with the presynaptic membrane.
Exocytosis: ACh is released into the synaptic cleft.
ACh Binding: Binds to ACh receptors, allowing Na⁺ influx into the muscle fiber.
Excitatory Postsynaptic Potential (EPSP): Depolarization triggers voltage-gated Na⁺ channels, propagating the action potential
SNARES reside on 2 places
on vesicle
on presynaptic membrane in active zone to facilitate fusion of ach vesicles into the presynapse
Explain Excitation-Contraction Coupling (ECC)
what do t tubules do
T-tubules propagate the action potential deep into the muscle fiber.
Explain Excitation-Contraction Coupling (ECC)
what happens in this step
T-tubules propagate the action potential deep into the muscle fiber.
Voltage-gated sensors on T-tubules trigger Ca²⁺ release from the SR.
Activates voltage DHPR receptor which activates RyR (calcium sensitive) on the SR to release Ca²⁺ into the cytosol.
Ca²⁺ binds to troponin, shifting tropomyosin to expose actin binding sites (TN-I, TN-C, TN- T, TM)
Enables the cross-bridge cycle to proceed.
What Happens During Repeated Stimulation with sustained levels of calcium
Sustained Ca²⁺ Levels:
Prolongs contraction, but can lead to fatigue without ATP replenishment.
Ending Contraction
What happens at the point of the ending contraction
ACh enzymes breaks down ACh in the synaptic cleft and diffuses it away.
ATP-dependent pumps return Ca²⁺ from cytoplasm to the SR, stopping the cross-bridge cycle (contraction)
Tropomyosin re-covers actin binding sites
Latency
Definition:
Phases:
Delay between excitation and contraction.
Excitation → Ca²⁺ release → Force generation → Muscle shortening.
is the nmj a slow or fast chemical synapse
a fast chemical synapse due to ligant gated channels, but still inherently slower than electrical synapses
which type of chemical synapse is slow
G protein coupled receptors
is nmj strong or weak, fast or slow, epsp or ipsp
strong, fast, epsp
What happens in Myasthenia Gravis?
Antibodies block or destroy ACh receptors, reducing muscle responsiveness and causing weakness.
Why does the NMJ release excess ACh vesicles?
Ensures signal transmission reliability even under suboptimal conditions.
Explain how parvalbumin allows for superfast muscle contraction
A calcium-binding protein that rapidly sequesters Ca²⁺ in the cytoplasm.
Speeds up Ca²⁺ removal from troponin, enabling faster muscle relaxation and readiness for the next contraction.
asides for ligand (ach) gated ion (na) channels on the post membrane, what else is there
voltage na channels
why are g protein coupled receptors slow
uses secondary messengers
why is the nmj fast
direct ion channel activation through ligand gated ion channels, rapid depolarization, immediate Na influx
which neurotransmitters are ipsp
glycine or gaba
where do ipsp happen
in neurons within CNS where inhibitory signals modulate neuronal firing and prevent excessive excitation.
How Could Signal Transmission Be Disrupted on the Presynaptic Side of the NMJ?
- calcium doesnt go in to release ach vesicles into synapse
-ca doesnt allow ach to fuse with pre membrane into synapse
Why Is the Release of ~125 Vesicles (When Only ~15 Are Sufficient) Useful?
excess vesicles creates a large safety margin for confirmed depolarization even if ach receptors are blocked or something or if there is disease like Myasthenia Gravis that lower receptor functionality.
- quick depolarization
