BIPN 102 Lecture Notes - Lecture 7: Axon Terminal, Reversal Potential, Membrane Potential

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silvercod749

3 Jun 2017

School

UCSD

Department

Biology/Animal Physiol & Neurosc

Course

BIPN 102

Professor

James Cooke

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Document Summary

The density of channels effects the shape and threshold of an ap. When there more voltage gated channels na+ you lower the threshold to firing an ap. This is b/c when we have a single na+ channel and a large amount of na+ channels we can reach a greater amount of. Na channels that can be opened up by the single initial na+ channel. Electromotive force is the answer to this questions. The reversal potential for na is very high and the reversal potential for. So when at rest you"re very close to the reversal potential for k+ and very far away from na+. So the electromotive force for na+ is much larger and there is a higher drive for na to enter the cell. So when at rest if you increase the permeability to na and k equally you should see depolarization b/c the electromotive force for na+ is larger than that of k+.

Related Questions

1a. all of the following are true about nerons except... (A. they produce ATP by cellular respiration, B. they are found in the central and peripheral nervous system, C. they have Na+/K+ pumps in their membranes, D. they can rapidly depolarize, E. they don't contain nucleir or mitochondria

1b. a reesting potential of -70mV ...(A. is possible because of voltage-gated sodium channels, B. is possible because of ligand-gated sodium, C. means that the outside of the neuron is more negative than the inside, D. is an IPSP that leads to threshold potential)

1c. after an action potential is triggered, the rapid increase in membrane potential to +50mV can be attributed to (A. opening of voltage-gated sodium channels, B. reversal of the direction of the sodium/potassium pump, C. opening of voltage-gated potassium, D. closing of ligand-gated potassium channels)

How does spacing apart sodium and potassium channels allow theaction potential to travel faster down the axon? This is the reasonalways cited for saltatory conduction and myelination, but mymental model of conduction tells me that the density of ion gatesalong the axon should not affect the speed of the AP.

To illustrate, consider a myelinated axon. A wave of Na+ fromaction potential site 1, a node of Ranvier, rushes into and quicklydiffuses down the axon. (It travels in both directions, butbackwards is still in the refractory period.) It diffuses throughthe myelinated region, its concentration always diminishing. Beforeit attenuates too much, however, it happens upon node of Ranvier 2,where it triggers another action potential. A new wave of Na+rushes in and the cycle repeats. This should be plain so far.

Now imagine that there is actually a node of Ranvier halfwaybetween node 1 and 2, called node 1.5. The wave of Na+, on its wayto node 2, happens to trigger an action potential at node 1.5, fromwhich a wave of Na+ pours in and either boosts the original wave orreplaces it by taking its momentum. Now the reinforced waveproceeds to node 2 and triggers it just as soon as, perhaps evensooner than, if node 1.5 had not existed. Repeatedly insert nodesat higher densities until the situation is simply lack ofmyelination, and we conclude that unmyelinated axons can transmitan action-potential-triggering wave of Na+ as fast as or fasterthan a myelinated one.

In short, my point of confusion is this: I cannot seehow a higher density of gated channels can possibly slow down thewavefront of Na+ that triggers action potentials. Ifanything, the additional influxes of Na+ should speed up theall-important wavefront, assuming that new waves really "eitherboost the original wave or replace it by taking its momentum", andalso assuming that the wavefront of Na+ is really all-important forsignal transmission, and also assuming that the mere presence of(voltage?) gated ion channels in the membrane does notsignificantly retard the wavefront.

But the usual explanation for why saltatory conduction is fasterthan continuous conduction (a fact I hope is empirically andunambiguously established) relies on the putativeslowing effect of ion channels on the signal fore. Please explainthis effect in more detail, if it is not amisconception.

Tetraethylammonium (TEA) is a drug that blocks voltage-gated potassium channels. What effect would this have on an action potential?

(a)Prevent the rising phase

(b)Prevent the cell from reaching the threshold to trigger an action potential

(c)Prevent or prolong the falling phase

(d)None of the above

The hyperpolarization phase of the action potential is due to:

(a)The opening of voltage-gated Cl- channels

(b)Prolonged opening of voltage gated K+ channels

(c)The closure of resting Na+ channels

(d)Rapid inactivation of voltage-gated K+ channels

The period when it is difficult to initiate another action potential for several milliseconds due to voltage-gated sodium channel inactivation is referred to as the:

(a)Relative refractory period

(b)Absolute refractory period

(c)Resting period

(d)Hyperpolarization period

In the human central nervous system, Gap junctions are found:

(a)Only between neurons

(b)Only between astrocytes

(c)In both neurons and astrocytes

(d)In all cells

Small molecule transmitters such as acetylcholine are synthesized in:

(a)The nerve terminal

B) The cell body and transported to the nerve terminal

C) Synaptic vesicles

D) Endoplasmic reticulum

Prior to Otto Loewiâs classical experiment, which of the following was not known:

(a)stimulation of the vagus nerve slows the heart

(b)extracts of frog heart, made following vagal nerve stimulation, slow the heart

(c)some acetylcholine effects are similar to those produced by muscarine

(d)vagal nerve stimulation releases a substance which slows the heart

Which of the following is most important in determining if neurotransmission is excitatory or inhibitory?

(a)The structure of the synapse

(b)The neurotransmitter released by the presynaptic neuron

(c)The neurotransmitter receptor

(d)The strength of the stimulus

Benzodiazepines such as Valium allosterically regulate GABA receptors by:

(a)Binding at receptor sites other than the transmitter binding site

(b)Binding at the transmitter (GABA) binding site on the receptor

(c)Blocking the action of the endogenous transmitter

(d)Mimicking the action of the endogenous transmitter

GABA-A receptors are ligand-gated Cl- channels. The equilibrium potential of Cl- is -65 mV. At the neuronal resting membrane potential of -65 mV, GABA binding to the GABA-A receptor would result in the opening the Cl- channel, resulting in:

(a)no net flow of Cl- ions

(b)Cl- inflow and hyperpolarization

(c)Cl- outflow and depolarization

(d)Cl- outflow and hyperpolarization

At the mammalian neuromuscular junction, the released neurotransmitter acts on:

(a)muscarinic receptors

(b)nicotinic receptors

(c)adrenergic receptors

(d)Beta receptors

Neurotransmitters are packaged into synaptic vesicles by:

(a)endocytosis following transmitter release

(b)presynaptic membrane transporters

(c)vesicular transporters

(d)all of the above

. Which of the following are NOT types of ion channels?

Voltage-gated

(a)Ligand-gated

(b)G protein coupled receptor (GPCR)-gated

(c)Leak channels

(d)NONE of the above

NMDA receptors are unique in that their ion channel is:

(a)Ligand-gated

(b)Voltage-gated

(c)Ligand- and voltage-gated ion channels

(d)GPCR-gated

. Which of the following is INCORRECT regarding Catecholamine neurotransmitters

(a)Includes Dopamine, Norepinerphrine, and Epinephrine

(b)Contain a Catechol Ring

(c)Synthesized from Tryptophan

(d)Are produced by neurons whose cell bodies are located in the upper brainstem

The largest and most diverse group of receptors in eukaryotes is:

(a)Ligand gated receptors

(b)Glutamate receptors

(c)G-Protein coupled receptors

(d)Allosteric receptors

The most abundant G-protein coupled receptor in the brain is:

(a)Glutamate receptors

(b)Acetylcholine receptors

(c)Cannabinoid receptors

(d)Dopamine receptors

Which of the following drugs DOES NOT block voltage-gated Na+ channels

(a)Lidocaine

(b)Riluzole

(c)Reserpine

(d)Tetrodotoxin

Sarin, a nerve gas, exerts its toxicity by:

(a)blocking nicotinic receptors

(b)inhibiting choline acetyltransferase

(c)inhibiting acetylcholinesterase

(d)inhibiting voltage-gated Na+ channels

Botulinum Toxin (BoTox) interferes with transmitter release by:

(a)cleaving protein(s) involved in transmitter release

(b)blocking voltage-gated Ca2+ channels

(c)blocking voltage-gated Na+ channels

(d)blocking voltage-gated K+ channels

Atropine is:

(a)An agonist of the acetylcholine ionotropic receptor

(b)An antagonist of the acetylcholine ionotropic receptor

(c)An agonist of the acetylcholine metabotropic receptor

(d)An antagonist of the acetylcholine metabotropic receptor

BIPN 102 Lecture Notes - Lecture 7: Axon Terminal, Reversal Potential, Membrane Potential

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