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BISC306 Lecture Notes - Lecture 6: Resting Potential, Tetraethylammonium, Tetrodotoxin

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School
University of Delaware
Department
Biological Sciences
Course
BISC306
Professor
Cain William

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Document Summary

Voltage clamping reveals nature of ion currents during ap: injected current into cell; the inward current went more negative, so positive"s must be moving into the cell. Changes in conductance of na+ and k+ during an action potential: the voltage is change in voltage during the action potential. Problem: imagine a cell 10micrometers in diameter. Assume it has an internal [k+] of 140 mm and a membrane potential of 0 mv. All else staying the same, what % of internal potassium ions would have to leave the cell to bring the membrane potential to -65 mv: surface area = 4*pi*r2, volume = 4/3 * pi * r3. Decreasing capacitance increases the speed of voltage change. Early efforts to measure the conduction velocity of nerve impulse: frog nerve-muscle preparation, in the 19th century, hermann von helmholtz measures the conduction velocity in a frog nerve. At that time many believed that the signal would be too fast to measure.

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Related Questions

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 Loewi’s 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

Santiago Ramon y Cajal’s theory of dynamic polarization refers to the:

(a)membrane potential of a neuron at rest.

(b)membrane potential of a neuron firing action potentials.

(c)opening and closing of gated channels in the membrane.

(d)one way flow of information in neurons from dendrites to axon terminals.

(e)one way flow of information in neurons from axon terminals to dendrites.

Over the course of scientific history, there are many examples of scientists reaching the right conclusion for the wrong reasons. When Schwann first proposed that the nervous system was made of individual cells, he based it on observations of:

(a)synapses.

(b)dendrites

(c)axon terminals.

(d)astrocytes.

(e)Nodes of Ranvier.

The synaptic cleft was finally seen in the 1950s. What prevented scientists from seeing it earlier?

(a)The resolution of the light microscope.

(b)They were looking in the wrong place.

(c)Their tissue was not appropriately stained.

(d)Myelination of the axons.

(e)all of the above

The resting membrane potential of a neuron is approximately:

(a) +65 V

(b) +65 mV

(c) -65 V

(d) -65 mV

What is largely responsible for the resting membrane potential in a neuron?

(a)Axonal insulation by myelin

(b)Voltage-Gated Sodium Channels

(c)The Action Potential

(d)Potassium Leak Channels

Which of the following would DECREASE the propagation velocity of an action potential down an axon?

(a)Increase in axon diameter

(b)Increase myelination between nodes of Ranvier

(c)Remove myelination between nodes of Ranvier

(d)Decrease density of voltage-gated Na+ channels except at the Nodes of Ranvier

The resting membrane potential of a neuron can be estimated using the:

(a)Nernst equation

(b)Goldman equation

(c)Hodgkin and Huxley equation

(d)Ohm’s law

18. What would happen to the resting membrane potential of a neuron if you added K+ to the extracellular fluid?

(a)Resting membrane potential would increase (become more positive)

(b)Resting membrane potential would decrease (become more negative)

(c)Resting membrane potential would not change

(d)Resting membrane potential would be abolished

. Which of the following statements is FALSE for Graded Potentials

(a)Magnitude changes with magnitude of triggering stimulus

(b)Magnitude decreases with distance from initial site

(c)Cannot be summed

(d)No refractory period

In the nervous system, the strength of the stimulus is coded into:

(a)The frequency of action potentials generated

(b)The amplitude of action potentials generated

(c)Both the frequency and amplitude of action potentials generated

(d)The duration of individual action potentials generated

Ion movement during both the depolarization and repolarization phases of an action potential are the result of:

(a)active transport pumps along the neuron membrane.

(b)diffusion of ions down their electrochemical concentration gradients.

(c)negative feedback loops.

(d)All of the above

At the peak of the action potential, the membrane potential is:

(a)Exactly at the Na+ equilibrium potential

(b)Greater (more positive) than the Na+ equilibrium potential

(c)Above 0 mV but less positive than the Na+ equilibrium potential

(d)0 mV

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.