Neuromuscular Junction Flashcards
Describe the cellular characteristics of a single axon terminal
- Synaptic vesicle with acetylcholine: release neurotransmitters via exocytosis, 300,000
- Many mitochondria
- Dense bar: Anchored to the presynaptic membrane and associated with synaptic vesicles to which they are tethered by short filaments.
Describe the characteristics of a motor end pate
- Synaptic gutter (trough): groove or furrow in the surface of a sacrolemma in which the axon terminal makes contact with the sacrolemma.
- Subneural clefts are small clefts or troughs int he bottom of the synaptic trough .
- Synaptic clef: 20-30 nm wide. Very narrow but real gap between the axolemma of the axon terminal and the sacrolemma of the. Innervated muscle fiber.
Describe the structure, including subunits, of an acetylcholine-aged channel
- On sacrolemma of the skeletal muscle
- 275,000 mw
- 2 alpha proteins, 1 beta protein, 1 gamma protein, 1 delta protein
- Tublular channel remains closed until two acetylcholine molecules attach to its alpha subunits
- Acetylcholinesterase??
Where are vesicles for neurotransmitters formed in the neuron?
- 40 nm vesicles are formed in the Golgi apparatus and are carried by axonal transport in the axon terminus where they are filled with Ach.
- Ach is synthesized in the cytosol of the nerve axon terminal.
How are vesicles for neurotransmitters in the neuron transported?
- When the action potential arrives at the terminus of the axon, voltage-gated calcium channels open and calcium ions enter the axon terminus.
- Calcium ions are thought to draw synaptic vesicles closer to neurolemma next to the voltage gated calcium channels.
Compare the concentrations of calcium ion outside the axon and inside the axoplasm.
- ECF Ca2+ conc. = 1-2 mM
- Intracellular Ca2+ = <10^-6 M
How does calcium enter the axon during the transmission of an action potential?
- The action potential on the sacrolemma continues down the T tubules and activates voltage-gated dihydropyridine channels
- Dihydropyridine channels activate ryanodine receptors (ryanodine-sensitive calcium ion release channels) on the sacroplasmis reticulum membranes, allowing calcium ions to move quickly through the ryanodine receptors into the cytosol at the A-I boundaries.
- The ryanodine receptor is also activated by the calcium released into the cytosol, thus allowing more calcium ion to be released.
State the number of acetylcholine molecules that attach to each ligand-gated channel.
- 2 Ach molecules bind to each ligand-gated channel on the sacrolemma.
Define: “end-plate potential.”
- Both sodium and potassium ions pass through the channels, but sodium ions are more permeable.
- the principal effect is for large numbers of sodium ions to pass through the muscle fiber membrane (sacrolemma), creating the end-plate potential (50-70mV), which. Initiates. An action potential on the sacrolemma.
Review the steps in the skeletal muscle contraction beginning with the release of acetylcholine from the neuron.
DIAGRAM
List the mechanisms by which acetylcholine is removed from the synaptic cleft.
- Degradation into choline and acetate by acetylcholinesterase
- Reuptake of choline by axon and terminal
- Diffusion of Ach away from site
- excitation-contraction (electro-mechanical) coupling?
List examples of drugs that mimic acetylcholine but that are not broken down by acetylcholinesterase and describe their effect on muscle contraction.
Methacholine, carbachol, nicotine
- Have same effect on muscle fiber as acetylcholine
- not broken down by accetylcholinesterase
- cause spasm.
List the drugs that inactivate acetylcholinesterase and describe their effect on muscle contractions
Neostigmine, physostigmine, diisopropyl fluorophosphate
- inactivate acetylcholinesterase
- cause muscle spasms
Describe the effect of curare on skeletal muscle contraction
- prevents passage of impulses from nerve ending into muscle
Describe the underlying cause of myasthenia Travis and its effects.
- autoimmune disease
- antibodies attack acetylchoine receptors
- end plate potentials are. Too weak to initiate opening of the voltage-gated sodium channels