excitable cells
cells that produce electrical signals when stimulated
like nerves or muscles
when a membrane is excited, what are the stages it does thru and what defines this change?
there is a charging time, maximum voltage time and then a decay.
Length constant defines how fast the signal decays over a certain length of a neuron- the larger the length constant the slower it decays
active conduction
- what is used to spread electric signal across a large distance like down the leg
- there is no decay over the distance
what is the structure of a voltage gated Na channel and how many states go along with it?
- the voltage gated Na channel has two gates-an inactivation and activation gate.
- There are three states: during the CLOSED state the inactivation gate is open and the activation gate is closed
- in the OPEN state, both gates are open allowing Na thru
- in the INACTIVATED state, the inactivation gate is closed and the activation gate is open
- In order to let Na thru again, you must go thru the closed state and start over
Voltage Gated K channels- how many states and how many gates?
-has one gate and two states- closed and open
How are action potentials generated?
- the membrane starts at a resting state with Na and K voltage gated ion channels being closed.
- then, depolarization (make membrane less neg) opens the membrane up to A Na channel
- the rising phase of the actin potential causes further depolarization and more Na voltage gated channels to open
- falling phase- closes sodium influx and opens voltage gate K channels letting K out. (membrane repolarizes)
- undershoot- K volt. gated channels remain open and then close causing all to go back to resting phase
when the membrane potential goes up (gets less negative) what happens to Na and K channels?
-Na channels open, reach a max voltage and then close allowing K channels to open
Local anesthetic
-Na channel blocker that blocks action potential and decreases pain sensation by binding on outside of Na channel, inside and in the bilayer
what does tetrodotoxin do? where is it from? symptoms?
from a puffer fish, it’s a Na voltage gated channel blocker
causes weakness, dypnea, and oral paresthesias caused by a lack of being able to generate an action potential
If ouabain is used, what occurs?
- Ouabain is a Na/K ATPase pump inhibitor (poison)
- it makes it stop pumping Na and K but the chemical concentration gradients take time to degrade and a large axon can fire thousands of action potentials via Na and K voltage gated channels before the Na and K concentrations are depleated
AP threshold
- action potential threshold
- the lowest amount of depolarization or lowest voltage that allows Na channels to go into fast, positive feedback loop
- once threshold is reached, action potential generation Is no longer dependent on stimulation
what influences AP threshold?
k channels
na channels
ca2+ concentration
how does Ca2+ influence AP threshold?
- when calcium is low, it makes the AP threshold go to almost resting state
- smaller amount of depolarization needed to reach threshold
symptoms of low ca2+
neuropsych probs
neuromuscular irritability- chvostek’s sign, Trousseau sign
cardiovascular probs
autonomic probs
Chvostek’s sign
- tapping near ear where facial nerve is causeing contraction of eye, mouth or nose
- sign of hypocalcemia 2/3 of pt but 10% of normal people have it
Trousseau’s sign
- MORE specific for hypocalcemia than chvostek’s sign
- in 94% of hypocalcemic pt
- if put a B.P cuff on pt and increase above systolic pressure, it triggers muscle spasm in hands
Hypercalcemia
- action potential threshold is increased and moves further away from resting membrane potential as external Ca++ conc increases
- larger amount of depolarization needed to reach threshold
how is the calcium concentration related to sodium channels and action potential?
- as calcium concentration increases the threshold for action potential gets higher
- the more the calcium, the less likely the Na channels are open for depolarization of the membrane
Relative refractory period?
- a second response (second action potential) from the membrane can be elicited but at a greater “cost” (ie strength or duration of stimulus is higher)
- represented by the hyperpolarized state with the K channels open
Absolute refractory period
- a second membrane response impossible regardless of strength or duration of stimulus
- represented by Na channel activation and inactivation
how does action potential propagation work?
-via a sequential propagation down the neuron that extends to either side of the stimulus
what prevents bidirectional flow of an action potential across neurons and prevents weirdo firing in our systems?
- axons have an axon hillock
- the hillock has the lowest membrane AP threshold so they generate the first AP
- the structure of the hillock allows only unidirectional flow down the axon
- the AP travels down the axon via propagation
how is the axon width related to the velocity of the action potential across the axon
the bidder the diameter the faster the axon conducts action potentials
what purpose does myelin serve and what is it made out of? Overall affect of myelination?
- electrical insulation
- proteins, lipids, cholesterol
- it decreases axon membrane capacitance and increases membrane resistance to give insulation
what cells do myelin cover in the peripheral nervous system? central?
- peripheral = schwann
- central = oligodendrocytes
node of ranvier
- breaks in myelin sheath where current is propagated -straight down the node rather than in the internodal space.
- since the current can only go thru via the nodes of ranvier, the rest of the current bounces off the membrane and forms a loop along the axon
why is conduction so fast in myelinated axons?
-because the axon doesn’t waste time forming a AP on the myelin covered portion and because myelin causes capacitance to be lower
multiple sclerosis
- demyelination via autoimmune disease of the CNS
- demyelination of oligodendrocytes responsible for not only myelination of CNS but nutritional (trophic) support to axons
guillain barr syndrome
- causes demyelination of PNS (schann cells)
- cause muscle weakness and paralysis
- usually follows infections like stomach bugs or respiratory infection
- can recover because unlike CNS, PNS can remyelinate =IMPORTANT