Neuron Action Potential And Synapsis

Question 1

What happens to Voltage-Gated Fast Na+ Channels with chronic hyperkalemia?

Answer 1

They remain in “inactivated state”

Question 2

What happens to membrane excitability with chronic hyperkalemia?

Answer 2

Reduced membrane excitability

Question 3

These channels are crucial for repolarization in cells/neurons?

Answer 3

Voltage-Gated K+ Channels!!

Question 4

These channels are crucial for cell/neuron depolarization ?

Answer 4

Voltage-Gated Fast Na+ Channels

Question 5

What common substances block Voltage-Gated fast sodium Channels?

Answer 5

1. “Caine” local anesthetics
2. Tetrodotoxine TTX (pufferfish)
3. Saxitoxine STX (shellfish)

Question 6

What common substances block inactivation for Fast Na+ Channels ?

Answer 6

1. Batrachotoxine BTX (frog).

2. Ciguatoxine CTX (fish).

Question 7

Presynaptic membrane Channels necessary for the release of Ach in the NMJ?

Answer 7

Voltage-gated Ca++ Channels .

Question 8

Receptors for Excitatory Postsynaptic Potential (EPSP)?

Answer 8

1. Nicotinic receptors.
2. NMDA receptors.
3. Non-NMDA receptors.

Question 9

Receptors for Inhibitory Postsynaptic Potential (IPSP)?

Answer 9

1. GABA receptors

2. Glycine receptors.

Question 10

Nicotinic vs muscarinic receptor?

Answer 10

1. Nicotinic = ganglionar and ion channel

2. Muscarinic = target organ and G- protein coupled channel

Question 11

Name ion disturbances that cause decreased neuronal excitability/conduction?

Answer 11

1. Hypokalemia
2. Hypercalcemia
3. Chronic Hyperkalemia

Question 12

Name neurological conditions with demyelinization or loss of neurons which cause decreased neuronal excitability:

Answer 12

1. Gullian Barrè Syndrome (GBS).
2. ALS.
3. Old Age.

Question 13

What toxins/drugs can cause decreased neural excitability?

Answer 13

1. Local anesthetics (“Caine” drugs).
2. TTX.
3. STX.

Question 14

What NMJ conditions cause decreased neural excitability?

Answer 14

1. Myasthenia Gravis.
2. Lambert Eaton Syndrome.
3. Botulinum.
4. Depolarizing and Non-Depolarizing NM Blockers.

Question 15

Name ion disturbances that cause increased neuronal excitability/conduction?

Answer 15

1. Acute Hyperkalemia

2. Hypocalcemia.

Question 16

Name neurological conditions with demyelinization or loss of neurons which cause increased neuronal excitability:

Answer 16

1. MS.

Question 17

What toxins/drugs can cause increased neural excitability?

Answer 17

1. Batrachotoxine (BTX)

2. Ciguatoxine (CTX)

Question 18

What NMJ conditions cause increased neural excitability?

Answer 18

1. AchE inhibitors

2. Latrotoxin (LTX).

Question 19

Pathologic alteration in Miasthenia Gravis?

Answer 19

Antibodies vs postsynaptic Ach receptors (Nicotinic)

Question 20

Pathologic alteration in Lambert Eaton Syndrome?

Answer 20

Antibodies vs Presynaptic Ca++ Channels

Question 21

Latrotoxin (black widow) pathologic alteration in the NMJ?

Answer 21

Opens presynaptic Ca++ Channels –> ⬆️Ach release

Question 22

Botulinum toxin action mechanism for flaccid paralysis?

Answer 22

Destroys proteins necessary for Ach vesicle release in presynaptic membrane. —> (⬇️) Ach is released.

Question 23

Succinylcholine binds to this receptor to cause depolarizing neuromuscular block?

Answer 23

Nicotinic Ach receptor in postsynaptic membrane

Question 24

Succinylcholine is what type of neuromuscular blocker?

Answer 24

Depolarizing NB.