Flashcards in Holmes 3 Deck (14):
After the peak of depolarization, the Nav channel are INACTIVATED (use of the 'stopper' instead of 'closed' gate). What does this mean?
-Stops Na flow but unlike 'closed' state, the 'inactive state is not competent to open in response to depolarization
-the 'ball' is released from the Nav channels following hyperpolarization and the membrane returns to resting potential
What is the purpose of the inactive Nav state?
Allows for direction propagation of action potentials down the axon to the axon terminals (called refractory period)
How much sodium enters the cell during an AP?
Can we fire an AP during absolute refractory? relative refractory? (after depolarization)
Yes for relative refractory if there is a more negative Vm requiring stronger depolarization current
What is saltatory conduction? Orthodromic propagation? Antidromic propagation?
Saltatory conduction: the leaping of AP in myelinated nerves between nodes of Ranvier
Orthodromic propagation: AP propagation from soma to presynaptic terminal
Antidromic propagation: Propagation in opposite direction
What is accomodation?
Increase in threshold for firing AP that occurs during prolonged depolarization
-result of Nav inactivation
-results in fewer AP generated during prolonged depolarization
T/F, APs fired from diff cells can be very diff in size, shape, and duration.
What is neuromodulation?
Molecular/ionic basis of sculpting diff patterns in action potentials
What are some toxins/medications associated with ion channels? Nav blockers? Nav inhibitors? Kv blockers?
block Nav: local anesthetics (lidocaine)
inhibit Nav: antiepileptic/anticonvulsant (phenytoin and carbamazepine)
block delayed Kv channels: antiarrhythmic drugs (dofetilide)
Tetrodotoxin (TTX) from fugu and saxitoxin (STX) from red tide are paralytic toxins that block Nav
What is propofol (diprivan)?
general anesthesia: blocks Nav channels, KILLED THE KING OF POP MJ
How can we treat severe opioid-resistant pain?
Cone snail poison
What are channelopathies? Examples?
Diseases that alter function of ion channels. Genetic or acquired
ex. arrhythmia Long QT syndrome, CYSTIC FIBROSIS, hypertension, timothy syndrome (affects voltage gated Ca channel)
What is characteristic of periodic paralysis?
One moment of enhanced excitability followed by inexcitability and weakness a few minutes later