Synaptic Transmission Flashcards
What is the neuromuscular junction
The synapse between nerve and a skeletal muscle fibre
What ion channels are in the nerve terminal end at the synapse?
All voltage gated Na+,K+,Ca2+
What is the difference in terms of gating between Na+ and Ca2+ channels ?
Na+ open first as they require lower depolarisation they will also inactive faster than Ca2+
Give an outline of what happens at a nerve terminal .
Action potential. Voltage gated Ca2+ channels open Ca2+ enters Increased calcium conc inside Causes release of neurotransmitters through exocytosis
More action potentials releases more transmitter.
True or false
True
What happens to acetylcholine ones uts been released and bound ?
Acetylcholine esterase breaks down Ach to stop continuous contraction.
What makes myeline sheath
Schwann cells
What describe the neurotransmitter receptors
They are nicotinic acetylcholine receptors. They are ligand gated ion channels that are selective to cations.
What is the effect of Na+/K+ channels opening to membrane potential?
As membrane stars much closer to Ek than to Ena there is a large driving force for Na+ entry making the membrane potential much less negative which depolarises the membrane
Calcium is unimportant in releasing receptors.
True or false
False- as calcium con is decreased so is end plate potential
How does an end plate potential initiate a muscle contraction ?
When Ach binds to receptor the influx of Na+ causes a local depolarisation this spreads to adjacent Na+ channels and Long the muscle fibres causing a contraction.
Give 2 ways that nicotinic ACh receptors can be blocked.
Competitive blocking
Depolarising blocker
Describe how competitive blocking works.
A form of competitive inhibition. When an alternate molecule binds to acetylcholine receptors but does not cause the conformational changes so the receptor doesn’t allow Na+ in and no potential is created.
Can competitive blockers be overcome?
Yes through increasing the concentration of ACh so the probability of a ACh is more likely than another molecule
Describe Mayasthenis gravis
An autoimmune disease targeting nACh receptors.
Weakness caused by decreased end plate potentials that fail to meet threshold
What is the difference between the 2 ACh receptors?
nAChR produces fast depolarisation because ligand gated ion channels
mAChR produces slow depolarisation because coupled to a G-protein which trigger cascade.
Give a summary of transmission at the neuromuscular junction.
Summary of transmission at the neuromuscular junction:
• Action potential arrives at the motoneurone terminal where it opens voltage-
gated Ca2+ channels.
• Ca2+ entry initiates exocytosis of vesicles containing ACh.
• ACh binds to nicotinic ACh receptors on the muscle end-plate, causes them
to open and the flow of cations causes a depolarization called the end-plate
potential.
• The end-plate potential depolarizes the adjacent muscle membrane and
activates voltage-gated Na+ channels, thereby initiating an action potential in
the muscle fibre which then contracts due to excitation-contraction coupling.
• nACh receptors can be blocked competitively by d-tubocurarine – this causes
paralysis.
• Drugs such as succinylcholine are known as depolarizing blockers and work
by causing inactivation of the Na+ channels adjacent to the neuromuscular
junction.
