What gated channels are involved?
What ions are involved?
These questions prompt me to pull out my notes from anatomy and physiology, and review nerve function. It's awful how much I forget, but because the subject matter of my studies keeps circling around the the same topics, I get lots of review and retain a little more each time. So here I go, rewriting the questions and overstudying.....because I want to understand.
How is an action potential (nerve impulse) propagated down the axon of a neuron?
An impulse begins when the initial stimulus causes the trigger zone in the nerve to reach a threshhold. A nerve can take some stimulation before it fires. The trigger zone of a nerve is where the cell body becomes the axon, or the "neck" of the nerve. Nerves can be triggered in the middle, too, causing phantom pain or referred pain.
A nerve impulse is an all or nothing event; there are no bigger or smaller impulses. Once the threshhold is reached, it begins. The impulse doesn't travel, but rather the membrane potential change in one location influences the next location to change. When triggered, Na+ ions rush into the cell (action potential), which triggers K+ ions to flow out (returning the membrane to the resting potential).
The resting membrane potential of a nerve cell is -70 millivolts. It is not zero because the cell regulates the in/outflow of ions (selective permeability), and maintains an electric charge gradient across the membrane--more negative on the inside. When the nerve is stimulated, the Na+ channels open and Na+ comes in, changing the charge ot +50 millivolts: an action potential. This is the threshold that must be reached. The last stage at that location is that the voltage sensitive K+ channels open and K+ goes out, restoring the -70mV resting potential. Meanwhile the impulse is working its way down the axon.
Impulse propagation is slow when the nerve is nonmyelinated, and called continuous conduction. The impulse moves about 1-4 miles per hour. Some pain, touch and pressure sensors esp in the viscera have this lag. Also the short axons in the CNS are nonmyelinated.
When the nerve is myelinated the propagation of the nerve impulse is by saltatory conduction. Myelin is mostly sphingomyelin, a lipid insulator, so the current skips across from node to node, speeding up propagation to 250-300 mph. Myelin also helps keep the resting membrane potential by confining the ions near the cell surface to a very small area. When the myelin sheath leaks you get dystrophies.
What gated channels are involved?
Na+, K+
What ions are involved?
Na+, K+
What about Ca+? Where does it come from? It is involved in activating the SNARE complexes to release vesicles into the synaptic cleft, but not in nerve impulse propagation...?