Exam 1 Flashcards
describe the resting membrane potential (using K)
so… the RMP is determined when there is an electrical and a chemical gradient. The membrane has channels in it that allow K to leave the cell. However, the K in the cell is accompanied by a negative anion. So when the K leaves, its negative counterpart cannot leave (The K only leaves because there is wayyy more K inside the cell then outside, so it goes down its concentration gradient). So now the K is gone, but the inside becomes more negative, which will attract the K to come back into the cell. This is the electrical gradient pulling it back in. This then leads to the RMP of K to be -94mV
what is the RMP of K
-94mV
RMP of Na and a how it works
So, the Na has a much higher concentration outside the cell then inside. The Na will enter the cell, causing a more (-) environment outside of the cell, and more (+) inside the cell. The (+) inside of the cell repels further Na from entering, which leaves the RMP of Na to be +61mV.
What has a very large impact on the resting membrane potential?
passive diffusion (channels about 90%) and only about 10% from the Na/K ATPase pump.
which ion is the membrane more permeable to (K or Na)
K+
Describe the active transport of both K and Na
There is much more K inside the cell then outside. The Na is higher on the outside then the inside. So, the pump will send 3Na out of the cell, and bring 2 K into the cell. This uses ATP. The break down of ATP will cause a conformational change that brings the Na out and the K inside.
Where is there more K
inside the cell
where is there more Na
outside of the cell
where does the K get pumped
from out to in (against its concentration gradient)
Where does the Na get pumped
from inside to outside
ratio of K in to Na out
every 3Na out there is 2 K pumped in
why is the Vm closer to that of K then Na
the membrane is far more permeable to K then it is to Na, therefore the the RMP is closer to the -94mV (-70 to -90mV)
the resting membrane potential will be closest to the ion with the ____ permeability
greatest
How does the Dr. Death thing work
Dr. Death administered KCl to patients who wanted to die. This increased the K concentration outside of the cell. Since there is more K inside the cell then out, it usually wants to leave the cell. However, when K is higher on the outside, there is less of a drive for K to leave. If K does not want to leave, no RMP. No RMP means that there is no excitability for cells, can’t breath or heart stops and that is death.
What are the 5 ion channels at the cleft
- Voltage gated Ca channels, which cause Ca to rush into the axon, and release the NT ACh.
- ACh goes across synaptic cleft, and then binds to nicotinic receptors (causes a conformational change and Na influx)
- Then the local depolarization causes voltage gated Na channels to open for more depolarization and AP
- At the T-tubule, the DHPR opens and Ca is released.
- The Ryanodine receptors (RyR) open on the SR and Ca is released into the cytoplasm.
Botulinum toxin
Blocks the ACh release from the nerve terminal. Doesn’t go across and open the Na channels which will open the Na voltage gated channels and cause the AP to release the Ca. NO CONTRACTION
Curare
Competes with the ACh (pushes ACh away and prevents binding)
Tetrodotoxin
puffer fish, inhibits Ca
Neostigmine
AChEsterase inhibitor. ACh has more time in the cleft to be picked up by nicotinic receptors. For a contraction
what does neostigmine help treat
myasthenia gravis (this is when your body makes antibodies against ACh receptors, so there aren’t as many receipts to bind the ACh to. there is a normal amount of ACh but not enough receptors. So the neostigmine helps to keep the ACh in the cleft so more can be picked up by the remaining receptors
Hemicholinium
blocks the choline re-uptake (need choline to make ACh, so when this is blocked, don’t make as much ACh, which depletes stores, which will mean not enough for sufficient contractions, and therefore tired fatigue much MUCH quicker.
how can you increase the conduction velocity of a nerve firing
by increasing the fiber size (increase diameter to decrease resistance)
also by myelinating.