Active recall questions Flashcards
What is the mechanism by which botulinum toxin causes paralysis?
It destroys SNARE proteins required for vesicle fusion, thus blocking presynaptic vesicle release
How does myelin increase neuronal conduction velocity?
It increases membrane resistance
Which of these factors distinguishes inotropic from metabotropic receptors?
-Whether they can produce excitation
-Whether they can produce inhibition
-Whether they act via second-messenger signalling pathways
-Whether they modulate a neuron’s response to other synaptic inputs
Whether they act via second-messenger signalling pathways
Which of these factors distinguishes electrical from chemical synapses?
- Whether they allow one neuron to communicate with another
- Whether they allow signals to be inverted
- Whether they can be modified (e.g., by learning)
- Whether they allow a neuron to integrate inputs from multiple sources
Whether they allow signals to be inverted
Chemical synapses can invert signals if they are inhibitory (e.g., activity in a GABAergic neuron will usually inhibit its postsynaptic partners), whereas electrical synapses cannot invert signals
Consider a neuron where the chloride concentration is 30 mM inside and 150 mM outside. If the cell’s membrane potential is -43 mV, and the cell expresses GABA_A receptors, if you apply GABA, the cell will:
-Show no change in membrane potential (<1 mV change)
-Be hyperpolarised
-Be depolarised, but not fire an action potential
-Be depolarised, and fire an action potential
Show no change in membrane potential (<1 mV change)
The Nernst potential for chloride for this neuron is -43 mV (2.303 RT/(zF) log([Cl-]o/[Cl-]i), so opening chloride channels will cause no net movement of chloride ions, hence no change in membrane potential
Neuron A has an axon twice as wide as neuron B’s axon. If everything else is the same between the two neurons, how long is neuron A’s space constant compared to neuron B’s space constant?
A’s space constant is sqrt(2) times longer than B’s space constant
What’s wrong with this statement? “If myelin makes action potentials go faster by insulating the axon, the action potentials would go even faster if the entire axon is insulated, even the nodes of Ranvier”
Action potential can’t be regenerated without voltage-gated sodium channels at nodes of ranvier
Passive propagation of current will eventually die out even with the insulation
What would happen to neuronal conduction speed if you insert a lot of K+ leak channels into the membrane (i.e. K+ channels that are open at resting potential)?
I’d be slower
What would happen to neuronal conduction speed if you insert a lot of K+ leak channels into the membrane (I.e. K+ channels are open at resting potential)?
Decrease
(Membrane resistance goes down, shorter space constant)
Given [Ca2+]i = 0.0001 mM, [Ca2+]o = 1 mM, what is the Nernst potential of [Ca2+]?
=+123 mV
If you block vesicle endocytosis, how would this affect release of small molecule vs. peptide neurotransmitters?
Blocks release of small molecule neurotransmitters (no vesicle recycling) but not peptides (secretory granules are ‘one and done’)
If AMPA receptors are permeable to both Na+ and K+, why does activating them cause depolarisation?
At rest, membrane is only permeable to K+. Even if you increase permeability to both Na+ and K+, Na+ permeability is ‘proportionally’ higher than at rest
OR
The receptor’s reversal potential is 0mV, so opening the channel moves the membrane potential closer to 0
What would happen if GABA opens a GABAA receptor and the membrane potential is below chloride’s Nernst potential?Would you get net inflow or outflow of chloride ions?
outflow,
If You’re below chlorides nerst potential, opening chlorides conductance will depolarize the cell, below chlorides nersts potential, the negative potential pushing chloride out overwhelms the inflow.
Why is atropine used to treat nerve gas poisoning?
Nerve gas increases Ach by blocking acetylcholinesterase, atropine blocks muscaranic acetylcholine receptors.
Why is an excitatory synapse on the soma more effective in evoking action potentials in the postsynaptic neuron than an excitatory synapse on the tip of a dendrite?
The EPSP decays as it propagates from the tip of the dendrite to the soma.
