Neurons and Synapses Quiz

Question 1

Be able to define membrane potential.

Answer 1

The difference in electrical charge across the plasma membrane.

Question 2

Be able to explain the role of the sodium potassium pump in maintaining the resting potential of a neuron (and be able to define resting potential and know that it is negative for neurons)

Answer 2

Resting potential - the difference in electrical charge across the plasma membrane when a neuron is AT REST (when it is NOT sending an impulse). It is negative (-70mV) for neurons.

Using active transport (ATP), sodium-potassium pumps in the axon membrane pump 3 Na+ ions out of the axon while pumping 2 K+ INTO the axon. This causes the OUTSIDE of the neuron to be more positive to the inside of the neuron (outside of the axon and inside of the neuron are POLARIZED). This creates a negative resting membrane potential of -70mV.

Question 3

Know the relative (where there is more versus where there is less) concentrations of sodium and potassium inside and outside of a neuron when it is “at rest”

Answer 3

Inside the cell (at rest = more negative)
- Cations: LOTS of potassium (K+) and few sodium (Na+)

Outside the cell (at rest = more positive)
- Cations: LOTS of sodium (Na+) and few potassium (K+)

Question 4

Know what an action potential is (and that it is an all or nothing event) and which direction it travels through a neuron.

Answer 4

An action potential is a nerve impulse that is generated and propagated DOWN THE AXON after a stimulus causes a voltage-gated ion (Na+) channel to open in the axon membrane and reaches a threshold voltage.

Question 5

Be able to explain the role of the myelin sheath in saltatory conduction.

Answer 5

The myelin sheath is an insulating layer on the axon. It is made up of Schwann cells and it helps increase the speed of the signal along the axon because ion channels are ONLY positioned BETWEEN myelinated portions. This is known as saltatory conduction. Saltatory conduction requires less ATP to return to resting potential.

Question 6

Be able to explain the steps of synaptic transmission.

Answer 6

1. An action potential arrives at the END of the axon (the axon terminal/synaptic knob).
2. Calcium channels open and calcium ions rush INTO the axon terminal/synaptic knob.
3. Calcium ions interact with vesicles (containing neurotransmitter) stored in the axon terminal, causing them to migrate to and fuse with the membrane of the axon terminal/synaptic knob.
4. Neurotransmitter is released (by exocytosis) into the synaptic cleft (space between neurons and effectors) and DIFFUSES across the synaptic cleft.
5. Neurotransmitters bind to receptor proteins on the post-synaptic membrane (dendrites, etc.)
6. Binding of neurotransmitter causes ion channels to open (changes their 3 degree structure) and:
   - Na+ ions rush into the post-synaptic cell (causing depolarization: excitatory) OR
   - Cl- ions rush in the post-synaptic cell (causing hyperpolarization: inhibitory)
7. Enzymes break down neurotransmitters into two or more fragments (ion channels close on postsynaptic membrane) and their pieces diffuse back into the presynaptic neuron (reuptake) to be reassembled into vesicles again.

Question 7

Be able to explain the steps involved in synaptic transmission (at the neuromuscular junction) when ACh (acetylcholine) is the neurotransmitter.

Answer 7

When acetylcholine (ACh) (made by combining choline and an acetyl group) is the neurotransmitter, it is often released by presynaptic neurons at neuromuscular junctions by in order to trigger muscle contractions. It does so by binding to receptors (cholinergic/nicotinic) in the membrane of postsynaptic muscle fibers to allow Na+ ions to diffuse into post-synaptic muscle fiber cells.

Question 8

What is the role of acetylcholinesterase?

Answer 8

Acetylcholinesterase (AChE) is released by the presynaptic cell or found in the membrane of the postsynaptic cell. It continually breaks ACh back down into choline and an acetyl group to prevent overstimulation of muscle fibers by ACh, as that can lead to fatal convulsions and paralysis. Choline is taken back into the presynaptic cell (reuptake/reabsorption) so it can be used to make ACh again when needed.

Question 9

Be able to explain how neonicotinoid pesticides work, why they are effective (and not harmful to humans), and what concerns there are with their use.

Answer 9

In insects, when neonicotinoid pesticides bind IRREVERSIBLY to acetylcholine receptors at cholinergic synapses, this leads to the blocking of synaptic transmission, as normal ACH binding is blocked. AChE is not able to break down neonicotinoids, so the effect is permanent.

However, neonicotinoid pestacides don’t permanently bind to ACh receptors in mammals (humans). This is because the composition of the ACh binders in insects is DIFFERENT than those of mammals. Hence, neonicotinoids bind to insect’s ACh receptors more strongly than ours.

However, there are some environmental concerns, as use of neonicotinoid pesticides have correlated with decreasing honeybee and bird populations. Some countries even banned the use of the neonicotinoid pestacides.