Week 3

Important concepts

1. Synaptic transmission

• Vesicle: Container inside cells.
• Exocytosis: Expulsion of intracellular molecules contained in a vesicle.
• Quantal: Not continuous, ice is quantal, water is not.
• Synaptic: Relating to synapses, the sites where messages are conveyed between cells.
• Junction: A place where two things meet.

2. Neurotransmitter release

• Cytosolic: Water-soluble components of cell cytoplasm
• Bouton: Neuronal component that connects to other neurons.
• Protein complex: Proteins arranged in a structure.

3. Presynaptic dynamics

• Facilitation: Amplification.
• Post-tetanic: After repetitive pulses.

4. Presynaptic modulation

• Metabotropic: Receptor that acts through a secondary messenger.
• Ionotropic: Opens or closes channels.
• Plasticity: Ability to change.

5. Electron microscopy

• Polymerize: Combine several molecules.
• Vacuum: Absence of matter.

Resources

Plain text

• 3.1.txt
• 3.2.txt
• 3.3.txt
• 3.4.txt
• 3.5.txt

PDF

• (8 MB) 3_1_SynapticTransmission.pdf
• (2 MB) 3_2_NeurotransmitterRelease.pdf
• (2 MB) 3_3_PresynapticDynamics.pdf
• (3 MB) 3_4_PresynapticModulation.pdf
• (5 MB) 3_5_EM.pdf

Videos

• 3.1
• 3.2
• 3.3
• 3.4
• 3.5

Questions

Question 3.1.1

What are the main excitatory and inhibitory neurotransmitters in the mammalian brain respectively?

• Arginine and GABAzine
• Dopamine and Glycine
• Glutamate and GABA
• Acetylcholine and Oxytocin

Question 3.1.2

What is meant by quantal release of neurotransmitter?

• All-or-none exocytosis of a synaptic vesicle
• Release based on quantum mechanics
• All-or-none action potential firing
• All-or-none activation of presynaptic ion channels

Question 3.1.3

What is the approximate diameter of a synaptic vesicle?

• 4 nm
• 40 nm
• 400 nm
• 4 um

Question 3.1.4

Neurons mainly communicate with each other at specialised junctions called synapses, with the presynaptic bouton containing many synaptic vesicles. What is the approximate length scale of a typical synapse in the central nervous system (i.e. approximate diameter of the synaptic contact area)?

• 5 um
• 500 nm
• 50 nm
• 50 um

Question 3.1.5

What is meant by volume transmission?

• Exocytosis of a large volume of synaptic vesicles
• Signals about the loudness of a sound
• Regulation of the amount of neurotransmitter release
• Exocytosis of neurotransmitter-filled vesicles into the extracellular space

Question 3.2.2

What is the dependence of neurotransmitter release upon calcium concentration?

• The release rate has a linear relationship with calcium concentration
• The release rate goes as the fourth power of the calcium concentration
• The release rates depends exponentially on calcium concentration within the physiological range
• The release rate is independent of the calcium concentration

Question 3.2.3

Which proteins form the SNARE complex?

• Synaptotagmin and voltage-gated calcium channels
• Synaptobrevin, SNAP-25 and syntaxin
• Voltage-gated sodium and potassium channels
• Rab3a, MUNC18 and synaptophysin

Question 3.2.4

How does calcium drive neurotransmitter release?

• Calcium swells up boutons and synaptic vesicles fuse with the presynaptic membrane
• Calcium interacts with charged phospholipid head-groups altering membrane properties allowing vesicle fusion
• Caclium binds to syntaxin which leads to phosphorylation of synaptotagmin causing vesicle release
• Binds to synaptotagmin, interacting with the SNARE complex, to cause vesicle fusion

Question 3.2.5

After the release of neurotransmitter, synaptic vesicles undergo what process to be able to release neurotransmitter again in the "kiss-and-run" cycle?

• Stay in the same spot and refill with neurotransmitter to be able release again
• Undergo fast active transport to the cell soma to be refilled with neurotransmitter
• Closure of the fusion pore, diffusion away from presynaptic membrane and refilling with neurotransmitter
• Undergo clathrin mediated endocytosis and fusion with golgi apparatus

Question 3.3.2

Which of the following statements about short-term synaptic plasticity is not correct:

• Short-term synaptic plasticity mechanisms predominantly occur in the presynaptic bouton
• Short-term synaptic plasticity mechanisms always increase the strength of synaptic connections
• Presynaptic efficacy depends on the recent history of synaptic activity
• Short-term synaptic plasticity typically changes the neurotransmitter release probability

Question 3.3.3

What mechanism is thought to underlie short-term syanptic facilitation?

• Facilitation results from the accumulation of Ca2+ within the presynaptic terminal
• Facilitation results from the accumulation of Ca2+ within the postsynaptic terminal
• Facilitation results from the increased efflux of Ca2+ from the presynaptic terminal
• Facilitation results from the accumulation of synaptic vesicles within the presynaptic terminal

Question 3.3.4

What mechanism contributes importantly to short-term synaptic depression?

• Broadening of the action potential waveform during repetitive firing
• Short-term depression results from the depletion of vesicles in the presynaptic terminal
• Calcium-dependent inactivation of synaptotagmin
• Short-term depression results from the depletion of Ca2+ in the presynaptic terminal

Question 3.3.5

Which of the following statements about post-tetanic potentiation is not correct:

• Post-tetanic potentiation lasts about 1 minute
• Post-tetanic potentiation can be evoked at some synapses by a 100 Hz train of action potentials
• Post-tetanic potentiation results from calcium activation of protein kinase C
• Post-tetanic potentiation depends upon correlated presynaptic and postsynaptic activity

Question 3.4.2

A metabotropic receptor typically:

• is a membrane protein with seven transmembrane regions signalling via a GTP-binding protein
• is a membrane protein with six transmembrane regions forming an ion channel pore
• is an intracellar protein signalling via kinase activity
• is a membrane protein with a single transmembrane region signalling via the extracellular matrix

Question 3.4.3

Metabotropic receptors are characterized by:

• faster activation and shorter duration of activity than ionotropic receptors
• faster activation but longer duration of activity than ionotropic receptors
• slower activation but shorter duration of activity than ionotropic receptors
• slower activation and longer duration of activity than ionotropic receptors

Question 3.4.4

Which of the following statements about presynaptic inhibition in the mammalian brain is false?

• Presynaptic inhibition can be mediated by GABA acting on metabotropic GABA receptors on the presynaptic membrane
• Presynaptic inhibition is typically mediated by inhibition of Ca2+ channels or vesicle release machinery
• Presynaptic inhibition is typically mediated by axo-axonic GABAergic synapses directly innervating axonal boutons
• Presynaptic inhibition reduces the release probability of synaptic vesicles from the presynaptic bouton

Question 3.4.5

What happens to short-term synaptic plasticity during presynaptic inhibition by a neuromodulator?

• Presynaptic inhibition typically reduces depression and thus increases facilitation
• Presynaptic inhibition typically increases depression and thus decreases facilitation
• Presynaptic inhibition converts short-term depression into long-term depression
• Presynaptic inhibition typically increases depression and thus increases facilitation

Updated on 2020-08-21.