Phys Of Neurons & Synapses

Question 1

Resting membrane potential of neurons is established by:

A. Ion pumps
B. Unequal conc of charged ions
C. Membrane channels selectively permeable to certain ions
D. A and C
E. A and B
F. all of the above

Answer 1

F. All of the above

Question 2

Patient presents with defective neuronal transmission. You suspect an inability to maintain a hyperpolarized resting membrane potential. Which of the following is likely defective?

A. ATP production
B. Down regulation of Ach gated Na+ channels
C. Closed K+ channels at rest
D. Ca2+ channels at pre-synaptic membrane
E. B and D
F. A and C
G. All of the above

Answer 2

G. A and C.

ATP necessary to fuel Na+/K+ pumps —> responsible for 3 Na+ out/2 K+ in (hyperpolarized membrane)

Leaky K+ channels —> allows ion flow in response to electrical or concentration gradients to maintain her polarization)

Both are vital in maintaining hyperpolarized resting membrane potential

Question 3

For each phase of AP give:
A. Depolarization and/or hyperpolarization
B. Which channel(s) are responsible

1. Rising phase
2. Overshoot
3. Falling phase
4. Undershoot

Answer 3

1. Depolarization, opening of voltage-gated Na+ channels due to reaching threshold potential
2. Depolarization past 0mV, slow closing of voltage-gated Na+ channels
3. Rapid hyperpolarization, rapid K+ outflow
4. Hyperpolarization under resting potential, slow close of K+ channels

Question 4

1. Most K+ channels @ _________

2. Most Na+ channels @ _________

Answer 4

1. Axons

2. Node of Ranvier

Question 5

Neurotoxins typically target and block:

A. Ligand gated ion channels
B. Vesicle fusion and exocytosis
C. Ion channels
D. Neurotransmitter reputable by pre-synaptic neuron

Answer 5

C. Ion channels

Question 6

A physician administers Lidocaine locally as an anesthetic. Lidocaine will block synaptic transmission so that the patient does not feel excruciating pain. Which of the following does Lidocaine inhibit?

A. Voltage gated Na+ channel
B. Voltage gated K+ channel
C. Voltage gated Ca+ channel
D. Ach binding to ligand gated Na+ channel

Answer 6

A. Na+ channel

Question 7

Patient presents with muscle weakness. Upon further testing you determine that the patient has an inability to generate an AP at post synaptic neurons. How would you treat this condition?

A. A drug that increases GABA release into synaptic cleft to hyperpolarize postsynaptic neuron
B. A drug that increases GABA synthesis to help increase depolarization of postsynaptic neuron to threshold potential
C. A drug that increases Glutamate reputable by pre synaptic neuron to hyperpolarize postsynaptic neuron
D. A drug that increases Glutamate release into synaptic cleft to help increase depolarization of postsynaptic neuron to threshold potential

Answer 7

D. A drug that increases Glutamate release into synaptic cleft to help increase depolarization of postsynaptic neuron to threshold potential

Glutamate binds to post synaptic ionotropic receptors that have Na+ pores. Glutamate binding to receptors opens ligand gated Na+ pores and causes an Na+ influx. Na+ influx depolarizes membrane to threshold potential. Threshold potential causes opening of voltage gated Na+ channels at axon hillock causes AP down axon of post synaptic neuron.

Question 8

Patient presents with muscle tetany or overstimulation of muscles characterized by many low magnitude nerve impulses causing muscle twitching. Upon further testing you determine that the patient has abnormally depolarized rVm of post-synaptic neurons. How would you treat this condition?

A. A drug that increases opening of voltage gated Ca2+ channels causing increased release of GABA that causes influx of Cl- and hyperpolarizes postsynaptic neuron making it harder to fire
B. A drug that increases GABA synthesis to help increase depolarization of postsynaptic neuron to threshold potential by Cl- influx
C. A drug that increases Glutamate synthesis to hyperpolarize postsynaptic neuron making it harder to fire
D. A drug that increases Glutamate synthesis to help increase depolarization of postsynaptic neuron to threshold potential
E. A drug that increases GABA synthesis to hyperpolarize postsynaptic neuron by GABA-gated Na+ influx making it easier to fire

Answer 8

A. A. A drug that increases opening of voltage gated Ca2+ channels causing increased release of GABA that hyperpolarizes postsynaptic neuron making it harder to fire

GABA binds to post synaptic ionotropic GABA-gated Cl- channels. Causes influx of Cl- which hyperpolarizes the membrane making it more difficult to reach threshold potential necessary to elicit an AP.

Question 9

During a patients yearly physical you observe a diminished patellar tendon reflex. What is the most likely reason for this?

A. Defective voltage-gated Na+ channels that cause AP on afferent neurons innervating muscle spindle that synapse with motor neurons and release Glutamate to activate motor neuron ligand-gated Na+ channels
B. Defective stretch-sensitive channels that cause AP on afferent neurons innervating muscle spindle that synapse with motor neurons and release Glutamate to activate motor neuron ligand-gated Na+ channels
C. Defective stretch-sensitive channels on efferent motor neurons innervating muscle
D. Defective stretch-sensitive channels that cause AP on afferent neurons innervating muscle spindle that synapse with motor neurons and release GABA to activate motor neuron ligand-gated Na+ channels

Answer 9

B. Defective stretch-sensitive channels that cause AP on afferent neurons innervating muscle spindle that synapse with motor neurons and release Glutamate to activate motor neuron ligand-gated Na+ channels

1. Stretch-receptors cause AP on 1a afferent axons
2. 1a afferent axons synapse with motor efferent neurons
3. 1a axons release Glutamate
4. Glutamate binds to and opens Na+ channels on motor neuron
5. Na+ influx causes threshold potential in motor neuron
6. Opening of voltage gated ion channels in motor neuron
7. AP elicited
8. Ach released at quad muscle causing patellar tendon reflex

Question 10

Patient presents with Myasthenia gravis characterized by muscle weakness throughout body and patient has inability to smile properly affecting her overall lifestyle as her family thinks she is always angry with them. Which of the following is likely causing this issue?

A. Increase in Glutamate release
B. Abs against GABA receptors
C. Abs against Ach nicotinic receptors
D. Increased Ach binding to nicotine content receptors

Answer 10

C.

In MG, Abs decrease/block binding to Ach nicotinic receptors. This causes an inability to open Na+ channels that caused threshold potential and thus cause inability to elicit AP

Question 11

Patient presents with Lambert-Eaton syndrome causing muscle weakness to limbs and face. What is most likely cause?

A. Abs against voltage-gated Ca2+ channels at pre-synaptic neurons
B. Abs against voltage-gated Ca2+ channels at post-synaptic neurons
C. Abs against voltage-gated Na+ channels at pre-synaptic neurons
D. Abs against ligand-gated Na+ channels at post-synaptic neurons

Answer 11

A.

L-E is caused by autoimmune abs against voltage-gated Ca2+ channels at pre-synaptic neuron. These channels cause Ca2+ influx that initiates nt exocytosis. Nt exocytosis is responsible for threshold potential that elicits AP.