Neuro - Magnuson Flashcards
Two demyelinating diseases are MS (central) and Guillain-Barre syndrome (peripheral). How does demyelination affect AP propagation?
Persistent myelination damage leads to:
- Na+ and K+ channels distributing themselves all along the membrane
- Membrane becomes leaky = low input resistance.
- thus, length constant decreases, which means propagation decreases
- APs are not regenerated
Define local circuit current and local response
Local circuit current = charge flow that causes PASSIVE depolarization along the membrane (during AP propagation)
Local response = the depolarization that the current elicits
Name (4) things the velocity of the AP propagation depends on
1) amplitude of the AP
2) threshold potential
3) diameter of the axon–i.e. the internal resistance
4) the membrane resistance
Recording APs from a nerve trunk: how are nerve trunks stimulated? Why?
must start with a very low stimulus intensity and increase it slowly. This is because stimulator causes a field that is parallel across the peripheral nerve. APs are generated based on the interruption of that field by the cross-sectional area of that axon. The larger the diameter of the axon, the more of that field is being disrupted, the more charge trapped in that axon, and more effectively that axon will be driven threshold (b/c these things lead to higher membrane resistance and less capacitance).
So: the larger axon, the lower the threshold for APs.
What are ENGs and EMGs? What is a compound action potential? How are these related to stimulus intensity?
ENGs (electroneurograms) and EMGs (electromyograms) record APs of peripheral nerves and muscles respectively.
The summed response of ENG/EMGs is coming from a population of axons, rather than a single axon = compound action potential. B/c it is coming from a group of axons and b/c you can get more axons firing as you turn stimulus intensity up, this compound AP actually changes in amplitude (unlike an AP, which is always the same). Thus, compund AP is graded and proportional to stimulus intensity.
What is unique about the axon hillock?
it has the highest concentration of voltage Na+ channels of anywhere in the cell. This makes it the most sensitive to voltage change.
What changes to membrane resistance and internal resistance would increase the distance over which neuronal membrane can be depolarized - i.e. improve local circuit current? What else could be changed to improve local circuit current?
a GREATER membrane resistance and LOWER internal resistance. Because if the membrane is leaky (lower resistance) the AP will run a shorter distance before running out.
Could also improve efficiency of local circuit current by decreasing the capacitance (storing charge) of the membrane. The thicker the resistor, the lesser the capacitance.
Nervous system achieves both with myelination!
Compare length constants (lambda) and time constants (Tau) between myelinated and unmyelinated axons.
Myelinated axons have much longer length constants and time constants than unmyelinated axons
Why would a compressed axon have an issue with AP conduction?
as the diameter of the internal compartment increases, its resistance decreases. Means more efficient conductance of charge takes place in a larger v. smaller diameter axon. Thus, a compressed axon diameter has dramatically increased internal resistance (shorter length and time constants) and much lower efficiency of conductance in the internal compartment.
Where is the AP normally generated. Define orthodromic and antidromic conduction
Under normal circumstances, AP is generated at the axon hillock, which is CLOSE to the cell body.
- orthodomic (anterograde) propagation = from the cell body to the axon terminals
- antidromic (retrograde) = opposite; back towards the cell body
Collision
When two APs are going in opposite directions (both orthodromic and antidromic). Causes APs to stop altogether because each AP is accompanied by a path of refractory membrane following behind it that will eventually collide.
electrotonic conduction
the PASSIVE conduction that allows the AP to be moved down the axon
neuromuscular junction and end plate
neuromuscular junction: refers to CHEMICAL synapsing from neuron to muscle (as opposed to neuron to neuron)
end plate: specialization on the post-synaptic muscle membrane
Ca and transmitter release from a nerve terminal
Ca triggers the synaptic release of the transmitter from the terminal bouton. It is QUANTAL = amount of Ca influx is directly proportional to the size of the AP.
Ex. if AP amplitude is reduced, there is less Ca influx.
EPP
EPP is the depolarization of the muscle cell at the neuromuscular junction. It is ALWAYS big enough to generate an AP and spreads PASSIVELY over the muscle membrane. This opens up voltage-sensitive Na channels (pretty much same ones in neuronal membrane). And this causes Ca influx, Ca release from SR in the muscle cell, and contraction.
Reversal potential. What is the reversal potential for the end plate?
Reversal potential is the MEMBRANE potential at which the EPP (or any synaptic response) is neither depolarizing nor hyperpolarizing (e.g. net ion flow is 0).
Reversal potential of the end plate is at 0mV. 0mV is a long way from Equil potential for K+ (-86 mV). So driving force on K+ to leave the cell is HIGH. Na+ equilibrium is +60, so also a long way from that, but a little closer. Na+ is going in and balanced with K+ flow out.
If we depolarize the cell to +20, K+ flow is winning. At -65, Na+ flow is winning. Thus, reversal potential is a result of the driving force on ions and the fact that the nAchR channel is a little more permeable for Na than for K.
Neuromuscular transmission v. chemical synaptic transmission
Neuromuscular transmission
Chemical synaptic transmission
EPSP/IPSP
Excitatory or Inhibitory Post-Synaptic Response. Refers to neuron-to-neuron synapse (v. neuromuscular transmission). The goal of an EPSP is to push the membrane potential above threshold. But most EPSPs won’t be large enough to induce an AP by themselves.
IPSPs are inhibitory and open up Cl- channels. Their goal is to prevent the membrane potential at the axon hillock from exceeding threshold. Any time the Cl- channel is open, the current will flow in the direction that will drive the MEMBRANE potential to the EQUILIBRIUM potential for Cl-. Equil
synaptic integration
t
Compare neuromuscular junction v. neuron-to-neuron synapse.
Neurons receive synapses from hundreds to thousands of different presynaptic neurons. Whereas, at neuromuscular junction, there are a few different boutons on the muscle fiber and that is it! It is a 1:1 ratio for motor neuron axon: muscle fiber.
propagation of an EPSP in a dendrite to the axon hillock
EPSPs come in on the dendrite and as it is passively gets conducted towards the axon hillock, it gets smaller. (The membrane has a time and length constant. And that response will decrease in amplitude with time and distance from the synapse itself.)
What’s the requirement for an IPSP to be effective?
An IPSP can be effective as long as the equilibrium potential for Cl- is negative to threshold.
