Lecture 3 - Lucas

Question 1

2 types of synapes

Answer 1

electrical and chemical

Question 2

how do electrical synpases make contact

Answer 2

make direct contact between excitable cells via connexons (protein channels)

Question 3

4 features of elctrical synapses

Answer 3

fast and synchronous signal transmission.
Non-selective ion movement.
Always transmits signals (no fine-tuning or modulation).
Bidirectional.

Question 4

how do chemical synapses make contact

Answer 4

Utilize neurotransmitters to bridge a synaptic cleft.

Question 5

features of chemical synapse

Answer 5

Slower but more versatile.
Can modulate signal strength and response (e.g., excitatory vs. inhibitory).
More prone to disruption (things going wrong)
Unidirectional.

Question 6

3 key parts of neuromuscular junction

Answer 6

Presynaptic terminal (vesicles of acetylcholine, ACh).
Synaptic cleft.
Postsynaptic membrane with ACh receptors (ligand-gated Na⁺ channels).

Question 7

5 steps of signal transmission

Answer 7

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

Question 8

SNARES reside on 2 places

Answer 8

on vesicle
on presynaptic membrane in active zone to facilitate fusion of ach vesicles into the presynapse

Question 9

Explain Excitation-Contraction Coupling (ECC)

what do t tubules do

Answer 9

T-tubules propagate the action potential deep into the muscle fiber.

Question 10

Explain Excitation-Contraction Coupling (ECC)

what happens in this step

Answer 10

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.

Question 11

What Happens During Repeated Stimulation with sustained levels of calcium
Sustained Ca²⁺ Levels:

Answer 11

Prolongs contraction, but can lead to fatigue without ATP replenishment.

Question 12

Ending Contraction

What happens at the point of the ending contraction

Answer 12

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

Question 13

Latency

Definition:
Phases:

Answer 13

Delay between excitation and contraction.

Excitation → Ca²⁺ release → Force generation → Muscle shortening.

Question 14

is the nmj a slow or fast chemical synapse

Answer 14

a fast chemical synapse due to ligant gated channels, but still inherently slower than electrical synapses

Question 15

which type of chemical synapse is slow

Answer 15

G protein coupled receptors

Question 16

is nmj strong or weak, fast or slow, epsp or ipsp

Answer 16

strong, fast, epsp

Question 17

What happens in Myasthenia Gravis?

Answer 17

Antibodies block or destroy ACh receptors, reducing muscle responsiveness and causing weakness.

Question 18

Why does the NMJ release excess ACh vesicles?

Answer 18

Ensures signal transmission reliability even under suboptimal conditions.

Question 19

Explain how parvalbumin allows for superfast muscle contraction

Answer 19

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.

Question 20

asides for ligand (ach) gated ion (na) channels on the post membrane, what else is there

Answer 20

voltage na channels

Question 21

why are g protein coupled receptors slow

Answer 21

uses secondary messengers

Question 22

why is the nmj fast

Answer 22

direct ion channel activation through ligand gated ion channels, rapid depolarization, immediate Na influx

Question 23

which neurotransmitters are ipsp

Answer 23

glycine or gaba

Question 24

where do ipsp happen

Answer 24

in neurons within CNS where inhibitory signals modulate neuronal firing and prevent excessive excitation.

Question 25

How Could Signal Transmission Be Disrupted on the Presynaptic Side of the NMJ?

Answer 25

• calcium doesnt go in to release ach vesicles into synapse
  -ca doesnt allow ach to fuse with pre membrane into synapse

Question 26

Why Is the Release of ~125 Vesicles (When Only ~15 Are Sufficient) Useful?

Answer 26

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