What is the direct result of the arrival of an action potential at the telodendria?
Opening of voltage gated calcium channels.
Describe the importance of voltage-gated calcium channels in the pre-synaptic neuron.
These voltage gated Ca2+ channels allow the influx of Ca2+ into the neuron. When this occurs, synaptic vesicles fuse with the P.M., and release NT into the synaptic cleft.
What is found in abundance in the telodendria?
Mitochondria (used to generate ATP for Na/K pump activity)
Describe (overall) how action potentials are transmitted between cells.
The action potential is transmitted from neuron to muscle via the neuromuscular junction.
Reset the membrane potential for the propagation of the next action potential.
Binds the NT vesicle to the dense bar prior to NT release; "tether"
Unkown function; thought to help "anchor" the NT vesicle prior to NT release
Acts to increase the surface area for neuron/end plate/receptor interaction.
Degrades ACh in the neural cleft; prevents tetany
Receives NT to produce depolarization of end plate
Acetylcholine receptors have __ alpha subunits, and require binding of two ACh molecules to open.
Responsible for production of the local potential on the motor end plate.
2 ACh molecules binding to the ACh-R; produces an opening to the lingand-gated ACh-R; this opens the channels and allows Na+ to enter the muscle at the sarcolemma
Ways by which ACh is removed from the synaptic cleft
Re-uptake (using ATP driven pumps)
Diffusion (random and slow)
Destruction by acetylcholinesterase
ACh is produced in the _____.
How does ACh binding cause transmission of the action potential?
1) Two ACh molecules bind to the ACh-R
2) Binding causes the opening of sodium channels, which causes a LOCAL potential
3) If the local potential is large enough, voltage-gated Na+ channels are opened, and THESE produce the "end plate potential" that moves down the sarcolemma
What is the voltage of the "end plate potential"?
These are formed at the plasma membrane to form new vesicles for ACh received from the liver.
Clathrin coated pits (become vesicles)
Methacholine binds to ACh-R and acts to ____.
produce depolarization of the motor-end plate
Carbachol acts to ____ and produce depolarization of the motor-end plate
bind to ACh-R
Nicotine binds to ACh-R and produces _____
end plate depolarization
How do methacholine, carbachol, and nicotine continue to bind to ACh-R and produce potentials?
By being non-susceptible to breakdown by ACh-Esterase
What drug inhibit AP transmission?
Competitievly binds to ACh-R, preventing depolarization through ACh binding
What drugs prevent functioning of acetylcholinesterase?
Neostygmine, physostygmine, diisopropyl flurophosphates
Explain the pathophysiology of myasthenia gravis.
Auto-aby are formed against ACh-R; as a result, there is muscle weakness due to destruction of -R and no action potentials.
Explain the treatment of myasthenia gravis
Because of auto-aby mediated destruction of ACh-R, neostigmine is used to inhibit acetylcholinesterase. This ACh-E inhibition allows enough free ACh to remain in the synaptic cleft to (hopefully) bind to any free ACh-R and trigger an action potential.