Lectures 8 & 9 Outline Flashcards

Question

What are the 5 phases of the AP?

Answer 1

1. Resting Potential 2. Threshold 3. Rising Phase 4. Falling Phase 5. Recovery Phase

Answer 2

a period of time where you can't fire an AP or it is much more difficult to fire an AP

Answer 3

is the period during which a cell can absolutely NOT fire another AP - happens when a cell starts to fire an AP in the rising phase. why? b/c during the rising phase all the Na+ channels are already opening as fast as they can

Answer 4

some of the Na+ channels are still inactivated but NOT ENOUGH of them to be able to fire an AP easily - IOW, enough have recovered to be able to fire an AP, but the cell has to be stimulated more strongly than it did a the beginning in order to fire that AP (b/c a significant amount of those Na+ channels are not available they are inactivated)

Answer 5

1. Na+/K+ ATPase --> only plays a role in establishing & maintaining the RMP 2. Na+ may change by 0.00017% - under normal physiological circumstances, the Na+ concentration inside the cell does not change

Answer 6

Single AP - will wait a period of time & then it will fire another AP (most similar to normal APs) Tonic AP - some neurons fire APs all by themselves - don't need any GPs to stimulate their MP to get to a threshold - the neuron is just firing spontaneous APs (one after another, after another) Bursting AP - will fire a couple of APs, then you get an afterhyerpolarization, then eventually it depolarizes enough to fire another couple APs - literally fires them in bursts

Answer 7

1. Normal conditions (RMP is @ -70mV) - small stimulus was not enough to bring it to the threshold, so it doesn't fire an AP 2. But with a stronger stimulus it brought the cell to the threshold & then it fired an AP 3. Hyperkalemia: increased extracellular K+ concentration - then you depolarize the MP - kidney failure for ex - you are bringing it closer to the threshold to fire an AP so now the small stimulus IS enough to bring it to the threshold & you get an AP * can cause increased excitability or an increased ability to fire APs 4. Hypokalemia: decreased extracellular K+ concentration - then it will hyperpolarize the MP & the large stimulus that previously went past the threshold is not long (large enough) to get to the threshold - therefore, you don't see an AP, where you might have seen one before * can lower excitability or make it harder to fire APs

Answer 8

1. Initial state: normal ion gradients, RMP ~ -70mV - very high density of Na+ channels at the Axon Hillock (trigger zone) - VG Na+ & K+ channels distributed along the axon 2. During an AP, Na+ rushes into the axon causing depolarization 3. Some Na+ is attracted to the nearby areas (local current flow) - this causes depolarization of the nearby axon to ITS threshold (the hillock is now recovered) 4. Na+ enters, causing depolarization - again local current depolarizes the adjacent segment to threshold - AP moves down the axon as a traveling wave of depolarization

Answer 9

1. Myelination - increases velocity b/c insulated areas mean less leakage of Na+ & K+ - also means less ATP used - myelination allows axons to be smaller, so you can fit more into a space 2. Increase axon diameter - increases velocity b/c as the axon radius becomes larger, internal resistance decreases (inverse square relationship) ** large diameter axons can really speed up axonal conduction of AP, but myelination allows even faster conduction in less space

Answer 10

PNS: Schwann cells - each Schwann cell wraps around a length of the axon sort of like a cinnamon roll (just curls around & around & around making an insulating layer) - think cinnamon roll CNS: Oligodendrocytes - can form a myelin sheath on a # of different axons - think octopus

Answer 11

- myelin is formed from concentric layers of glial cell membrane (in development) - layers of membrane are excellent insulators (prevent the conduction of ions out of the axon - prevent the leakage of ions) - very few ion channels myelin sheaths, or in the axonal membrane beneath (few leak or VG) - myelination increases electrical efficiency of the axons (more faster & more robust - less chance an AP will fail) - up to 200 layers!

Answer 12

lower high

Answer 13

myelin sheath form insulating segments along axon - formed by concentric layers of glial cell membranes compacted together separated by nodes of ranvier Na+ channels found at very high density at nodes of Ranvier, K+ channels found nearby instead of traveling as a wave, the action JUMPS from node to node: Saltatory Conduction - b/c of this they travel much faster

Answer 14

conduction slows when current leaks out of the previously insulated region b/t the nodes - a depolarization that comes down the axon will stimulate an AP there, but then when that depolarization tries to travel in this newly unmyelinated area, it causes a leakage of ions out through the membrane & the AP WILL FAIL (NEUROlogical consequences from this: loss of info from where that info is supposed to travel) - no longer have layer of insulation in this region of axon & so end up with more leakage of the ions after you lose that myelin sheath - won't be effectively conducted b/c very few VG Na+ channels (not enough to actively propagate an AP)

Answer 15

NEUROlogical consequences from this: loss of info from where that info is supposed to travel)

Answer 16

- autoimmune disease - unknown cause: environment, virus, genetics, cerebral blood flow - demyelination of CNS axons - multiple patterns of progression: relapsing-remitting & several progressive phases - symptoms include loss of balance, loss of speech, loss of vision, abnormal pupil reflexes, numbness, pain (SYMPTOMS ARE HIGHLY VARIABLE) - treatments include immunosuppressants, other drugs as indicated by symptoms

Answer 17

- autoimmune, days after a seemingly minor GI or lung infection - may be also associated with chronic illness such as lupus, HIV - 1976 flu vaccine (1 additional case per 100 000) - demylination of sensory, motor, & autonomic axons (PNS) - slowing &/loss of AP conduction - initial symptoms include tingling, weakness, pain in hands/feet - symptoms may rapidly progress to inability to speak, paralysis, respiratory distress - treatment may include plasmapheresis (to remove antibodies from blood) & immunoglobulin G (IGG) to inactivate circulating antibodies - most people survive, recovery may take months to years

Answer 18

all things being equal, a LARGER axon will conduct APs faster than a smaller diamater axon & all things being equal, a MYELINATED axon would conduct APs faster than a similarly sized nonmyelinated axon

Answer 19

(kills 30-100 people per year worldwide) comes from pufferfish & several other species of animals fugu is a very specific antagonist of VG Na+ channels - high affinity, high specificity - high efficacy, high potency prevents entry of Na+ into cells prevents APs in neurons & muscle lidocaine, benzocaine & other local anesthetics also block VG Na+ channels

Lectures 8 & 9 Outline Flashcards

(43 cards)