Neurons and Synapses: Topic 6.5

Question 1

Draw and label a motor neuron (and know the function of each structure).

Answer 1

LOOK AT NOTES - BE ABLE TO DIAGRAM AND LABEL!

Dendrites receive chemical signals from sensory receptors or other neurons and transform them into electrical signals which are sent to the cell body
The cell body (soma) contains the nucleus, cytoplasm, and organelles and is key for metabolism and summation of input signals
Axons carry signals away from the cell body to the end of the axon/axon terminal/synaptic terminal buttons (where neurotransmitters are released for communication with other neurons or effectors)
The myelin sheath is made up of Schwann cells and forms an insulating layer on the axon that increases the speed of the signal along axon through saltatory conduction
The Nodes of Ranvier are spaces in between the Schwann cells that contain membrane proteins - Na+/ K+ channels and pumps

Question 2

Describe the role of the sodium-potassium pump in maintaining the resting potential.

Answer 2

Sodium-potassium pumps in the membrane of the axon maintain the resting potential
Using ACTIVE transport (ATP), sodium-potassium pumps pump 3 Na+ ions OUT of the axon while pumping 2 K+ ions INTO the axon
Result: OUTSIDE of neuron is more positive compared to inside of neuron (outside of axon and inside of neuron are POLARIZED)
Creates a negative resting membrane potential of -70mV
Resting potential is the difference in electrical charge across the plasma membrane when a neuron is AT REST (when it is NOT sending an impulse)

Question 3

Explain how an impulse (action potential) is propagated down the length of a neuron (including the role of myelin).

Answer 3

From the Notes:
1. Depolarization: Voltage-gated Na+ channels open (when threshold potential of -55mV is reached) and Na+ rushes INTO axon (more Na+ outside of cell), causing more Na+ channels to open – domino effect (propagation) down the axon – membrane potential becomes more POSITIVE
2. Repolarization: K+ channels open (and Na+ channels close) and K+ rushes OUT of axon – domino effect down the axon – membrane potential becomes more NEGATIVE - becomes hyperpolarized)
3. Resting potential restored (by sodium-potassium pumps: 3 Na+ OUT for every 2 K+ IN): This period called refractory period (another action potential CANNOT be fired until this period is complete - until the resting potential AND Na+/ K+ ion concentration gradients are restored)
NOTE: In myelinated neurons, action potentials travel FASTER down the axon because ion channels are ONLY positioned BETWEEN myelinated portions (at the Nodes of Ranvier) - called SALTATORY CONDUCTION (also require LESS ATP to return to resting potential)

• Understand that a nerve impulse is only initiated if the threshold potential is reached
• Understand that an action potential consists of depolarization and repolarization of the neuron
• Understand that propagation of nerve impulses is the result of local currents that cause each successive part of the axon to reach the threshold potential
• Understand that myelination of nerve fibers allows for saltatory conduction

From a Worksheet Markscheme:
a. nerve impulses are action potentials propagated along axons of neurons
b. resting potential is -70 mV
OR
relatively negative inside in comparison to the outside
c. Na/K pumps maintain/re-establish «the resting potential»
d. more sodium ions outside than inside «when at the resting potential»
OR
more potassium ions inside than outside «when at the resting potential»
e. action potential stimulates «wave of» depolarization along the membrane/axon
f. «when neuron is stimulated» if threshold potential is reached Na* channels open
g. sodium ions diffuse/move in
h. «Na* move in» causing depolarization / inside of the neuron becomes more positively charged than the outside of the neuron
i. potassium ion channels open
OR
potassium ions diffuse/move out
j. «K* move out» causing repolarization
k. local currents
OR
description of Na* ion diffusion between depolarized region and next region of axon to depolarize
I. myelination increases propagation speed/allows saltatory conduction
Accept any of the points clearly explained in an annotated diagram.

Question 4

Analyze an oscilloscope trace showing changes in membrane potential during and after an action potential.

Answer 4

LOOK AT NOTES - Neurons and Synapses slide 9: https://docs.google.com/presentation/d/1_bIioMJbcD-tG_0Jhk4KTCNhslaYdGuyCdzCcOL8s10/edit#slide=id.p10
AND WORKSHEETS

Resting potential, threshold potential, action potential (depolarization, repolarization), refractory period (hyperpolarization, resting potential)

Question 5

Explain the process of synaptic transmission at the neuromuscular junction (including the role of acetylcholinesterase)

Answer 5

• Acetylcholine (Ach) is a neurotransmitter (made by combining choline and an acetyl group)
• Ach is usually released by presynaptic neurons at neuromuscular junctions in order to trigger muscle contractions by binding to receptors (cholinergic/ nicotinic) in the membrane of postsynaptic muscle fibers (the motor end plate) to allow Na+ ions to diffuse into post-synaptic muscle fiber cells.
• Acetylcholinesterase/ Cholinesterase (AchE) - released by presynaptic cell or found in membrane of postsynaptic cell - continually breaks Ach down (back into choline and an acetyl group), as overstimulation of muscle fibers by Ach can lead to fatal convulsions and paralysis!
• Choline is taken back into the presynaptic cell (reuptake/ reabsorption) to be used to make Ach again

__________________
In General

1. An action potential arrives at 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/ neurons and effectors) and diffuses across the synaptic cleft
5. Neurotransmitters bind to receptor proteins (ion channels) on the post-synaptic membrane (dendrites, etc. )
6. Binding of neurotransmitter causes ion channels to open (changes their 3° structure) and:
   * Na+ ions rush in the post-synaptic cell (causing depolarization: excitatory) OR
   * Cl-ions rush into 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 presynaptic neuron (reuptake) to be assembled in vesicles again
   Note: Neurotransmitters NEVER enter a postsynaptic cell

Question 6

Discuss the use of neonicotinoid pesticides (pros and cons) and describe how they affect synaptic transmission in insects.

Answer 6

From the Notes:
Application: Blocking of synaptic transmission at cholinergic synapses in insects by binding of neonicotinoid pesticides to acetylcholine receptors

• Neonicotinoid pesticides bind IRREVERSIBLY to Ach receptors (in postsynaptic muscle fiber cell membranes) in insects
• Note: composition of Ach receptors in insects is DIFFERENT than in mammals, so neonicotinoids bind to them much more readily/ strongly than ours (effective pesticide)
• Block normal Ach binding (block/ prevent synaptic transmission)
• AchE is NOT able to break down neonicotinoids, so the effect is PERMANENT (paralysis/ no muscle contraction/ death)

Concerns include:
* Neonicotinoid use linked to reduced honeybee and bird populations
* Certain countries restricting use

From a Worksheet Markscheme:
a. neonicotinoids bind to the (acetylcholine) receptor (in insects)
b. (binding happens) in (cholinergic) synapses/at motor end plate/between motor neuron and muscles
c. neonicotinoids bind irreversibly (to receptors)
OR
(receptors are blocked so) acetylcholine is unable to bind
d. acetylcholinesterase/enzymes cannot break down neonicotinoids
e. (synaptic) transmission prevented
f. (causing) insect paralysis/death