Neurons, Synapses, Muscles, and Movement Quiz Flashcards
Diagram and label the structures of a motor neuron.
Be able to describe the function of each structure in a motor neuron.
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
Define membrane potential
The membrane potential is the difference in electrical charge across the plasma membrane
Neurons have a difference in charge across their membranes due to the distribution of positively-charged ions (Na+ / K+)
Electrical signals are created by changing membrane polarity
* Polarity of a neuron at rest is the resting potential (-70mV)
* Polarity of a firing neuron is the action potential (+30mV)
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)
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)
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”
The inside of the cell is negative with respect to the outside (internal and external environment are POLARIZED).
Inside the cell (at rest = more negative):
Cations: LOTS of Potassium (K+) and few sodium (Na+)
Anions: proteins, sulfate, phosphate (collectively A-) and few chloride (Cl-)
Outside the cell (at rest = more positive):
Cations: LOTS of Sodium (Na+) and few potassium (K+)
Anions: chloride (Cl-)
Know what an action potential is (and that it is an all or nothing event) and which direction it travels through a neuron.
Once the threshold voltage of -55mV is reached, an ACTION POTENTIAL (nerve impulse) is generated and propagated (sent) down the axon
(An action potential is an ALL-or-nothing event!)
Explain how an impulse is generated in a neuron and propagated down the axon (events of an action potential) - Know this one in A LOT OF DETAIL!!!
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.
Be able to analyze/ interpret information in oscilloscope traces (graphs) showing membrane potential changes over time during an action potential and when a neuron is at rest.
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)
Explain the role of the myelin sheath in saltatory conduction.
In myelinated neurons, action potentials travel FASTER down the axon because ion channels are ONLY positioned BETWEEN myelinated portions (at the Nodes of Ranvier). This is called SALTATORY CONDUCTION (also requires LESS ATP to return to resting potential)
Identify the structures involved in synaptic transmission in diagrams.
LOOK AT NOTES (Axon, synaptic vesicles, synapse, neurotransmitter, receptor, dendrites)
LOOK AT WORKSHEET (#6a from the Neurons and Synapses worksheet)
Explain the steps of synaptic transmission (in general).
- An action potential arrives at END of the axon (the axon terminal/ synaptic knob)
- Calcium channels open and calcium ions rush INTO the axon terminal/synaptic knob
- 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
- Neurotransmitter is released (by exocytosis) into the synaptic cleft (space between neurons/ neurons and effectors) and diffuses across the synaptic cleft
- Neurotransmitters bind to receptor proteins (ion channels) on the post-synaptic membrane (dendrites, etc. )
- 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) - 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
Explain the steps involved in synaptic transmission (at the neuromuscular junction) when ACh (acetylcholine) is the neurotransmitter.
- 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
Explain how neonicotinoid pesticides work, why they are effective (and not harmful to humans), and what concerns there are with their use.
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
Draw and label all of the parts of a sarcomere (and be able to identify all of these parts in electron micrographs too). Parts to label/ identify: sarcomere, Z line, A band, I band, H band, actin (thin filaments), myosin (thick filaments)
LOOK AT NOTES - Muscles and Movement slide 12 and 13: https://docs.google.com/presentation/d/1zSmgUCOdpqvUUWLLZMuVysbrHRaw2usPf0H6gPR9FOs/edit#slide=id.p16
LOOK AT WORKSHEET - #15 from the Muscles and Movement worksheet
Be able to identify a relaxed versus contracted muscle by looking at the above structures in an electron micrograph of a sarcomere (so you should know what happens to each structure in the sarcomere as a muscle contracts)
LOOK AT NOTES - Muscles and Movement slide 18 AND 19: https://docs.google.com/presentation/d/1zSmgUCOdpqvUUWLLZMuVysbrHRaw2usPf0H6gPR9FOs/edit#slide=id.p21
- The length of the sarcomere shortens during muscle contraction. (Z lines get closer together)
- The length of the actin and myosin filaments does not change during muscle contraction (they simply slide past each other).
Explain, IN DETAIL, the steps of muscle contraction.
From the Notes:
1. Nerve impulse/ action potential arrives at the neuromuscular junction (between a motor neuron and a muscle cell) and acetylcholine (Ach) is released into the synaptic cleft
2. Ach binds to protein receptors on the sarcolemma (muscle fibre cell membrane)
3. Sodium channels open (on sarcolemma and in t-tubules) and sodium ions rush into the muscle cell, causing calcium channels (on sarcoplasmic reticulum) to open and release calcium ions
4. Calcium ions bind to troponin (on actin filaments), causing troponin to change shape, moving tropomyosin and exposing the myosin-binding sites on the actin filaments
5. ATP is hydrolyzed to ADP + Pi, providing energy for the myosin heads to bind to (form “cross bridges” with) the actin filaments
6. Myosin heads move/ change shape/ bend, which pulls the actin filaments toward the center of the sarcomere (myosin filaments and actin filaments slide past each other) - this is called the “power stroke” - and the muscle contracts (shortens the sarcomere)
7. ATP binds to myosin, releasing it from actin/ breaking “cross bridges”
Note: myosin can then hydrolyze ATP and bind to the next myosin binding site on actin to pull it in even farther in/ shorten the sarcomere even more
Note: actin and myosin fibers do NOT change their length during muscle contraction – they merely slide past each other to bring the Z lines of the sarcomere closer together.
- This cycle (myosin heads attaching to actin, power stroke, and detachment) continues as long as ATP and calcium levels remain high in the sarcoplasm.
Note: each “cycle” shortens the sarcomere 1%, and hundreds of these cycles occur each second during muscle contraction!
From a Worksheet Markscheme:
a. myofibrils «in muscle fibers/cells»
b. sarcomeres «are the repeating units in muscle/myofibrils»
c. sarcomeres arranged end to end / sarcomeres shorten during muscle contraction
d. actin and myosin/overlapping protein filaments/ diagram to show sarcomere with actin and myosin overlapping
e. dark and light bands in sarcomeres»/ diagram to show this/light bands narrower when muscle is contracted
f. thick filament is myosin and thin filament is actin/diagram to show this
g. nerve impulses stimulate contraction/cause depolarization of sarcolemma/T-tubules/trigger release of calcium from sarcoplasmic reticulum
h. calcium ions released from sarcoplasmic reticulum
i. calcium ions bind to troponin
j. troponin causes tropomyosin to move/exposes binding sites on actin
k. ATP hydrolyzed to ADP/ used to provide energy for myosin «heads» to form cross-bridges with/bind to actin
l. myosin heads move/change shape/swivel/cock / myosin heads cause the power stroke
m. myosin filaments pull actin towards center of sarcomere/more overlap between actin and myosin/Z-lines move closer
n. ATP is used «to provide energy»/cause cross-bridges to break
o. intercostal/abdominal/diaphragm muscles contract «to cough»
Marks can be awarded for any point made clearly on an annotated diagram.
