L9 Neuromuscular Junction Flashcards
What is the “EPSP” called when it’s at the neuromuscular junction?
EPP- end plate potential
WHat is the name for the plasma membrane of the muscle?
Sarcolemma
What is the part of the sarcolemma that is “folded” called?
Motor end plate
What are ACh receptors called in the neuromuscular junction?
Nicotinic receptors
What are the ion channels in the motor end plate called?
Mixed-cation receptors
Because they let K+out and Na+ in
What is the motor end plate?
The PORTION of the sarcolema that is directly across from the synaptic terminal
True or False: t
he Motor End Plate is similar to the membranes of the soma and dendrites on neurons
True
True or false: The sarcolemma is electrically similar to atonal plasma membranes on neurons?
True
What are the ion channels in the sarcolemma
VOLTAGE gated Na+ and K+ channels
Wha are the ion channels in the motor end plate?
CHEMICALLY gated channels that bind acetylcholine
Is the motor end plate capable of Action potentials?
NO, it only does End Plate Potentials (EPP)
What part of the muscle propagates action potentials?
Sarcolemma
What are the two types of neuromuscular blockers that cause skeletal muscle relaxation?
Nondepolarizing blockers
Depolarizing blockers
How do Non-depolarizing blockers cause skeletal muscle relaxation?
They competitively bind to the ACh receptor (antagonists)
Ion channel does NOT open and there is no EPP
What is an example of a non depolarizing blocker that causes skeletal muscle relaxation?
Curare
How do depolarizing blockers cause skeletal muscle relaxation?
They bind to the ACh receptor (agonist) and cause depolarization (muscle contraction), but then can not be removed by AChE, and the voltage-gated Na+ channels in the sarcolemma remain inactivated for 2-3 minutes (flaccid paralysis)
What is an example of a depolarizing blocker that causes skeletal muscle relaxation?
Succinylcholine
This doesn’t actually bind to ACh receptor? It inhibits AChE?
How does botulism toxin cause muscle paralysis?
It degrades SNARE proteins and prevents the synaptic vesicles from releasing ACh into the cleft
How does black widow spider toxin cause muscle spasms and intense cramping?
It invades the lipid membranes of the presynaptic cells and induces Ca++ flow, resulting in lots of ACh to be released.
In high doses, it may cause paralysis as a result of prolonged depolarization
How does Lambert-Eaton syndrome cause muscle weakness?
It attacks the voltage gated calcium channels and prevents ACh from being released.
How could you treat Lambert Eaton Syndrome?
The autoimmune condition that attacks Calcium channels
You can give a drug that blocks the efflux of K+ from the presynaptic cell. This prolongs the period of depolarization and keeps the remaining Calcium channels open longer
What does magnesium do?
It regulates neurotransmitter release by blocking some Calcium channels (normal, healthy for a few of them to be blocked)
What does hypomagnesemia do to the neuromuscular junction?
The few calcium channels that are normally blocked by magnesium are now open, so more calcium gets in, leading to more ACh being released, causing cramps
What would hypermagensemia do to NMJ?
Block too many calcium channels, and not enough ACh gets released =muscle weakness
How do organophosphate pesticides and many nerve gases work?
They inhibit ACh Esterase and cause prolonged depolarization.
Hypercontractility followed by paralysis due to inactivation of voltage gated Na+ channels
What kind of drugs are Neostigmine and pyridostigmine?
Anticholinesterases
Inhibit acetylcholineesterase
What happens in myasthenia Gravis?
Body attacks ACh receptors causing muscle weakness
What is a drug that can help with myasthenia gravis?
Autoimmune attack on ACh receptors
Pyridostigmine- an anticholinesterase inhibitor
Allows for accumulation of ACh in cleft and makes the most of the receptors you have left
What does hemicholinium do?
Blocks reputable of choline into presynaptic terminal.
Can’t make as much ACh
