Lesson 3 - Action Potential Conduction Flashcards

1
Q

what is impulse conduction?

A
  • When a patch of excitable membrane generates an action potential, this causes an influx of Na+ and depolarizes the membrane from -70 mV to +30 mV
  • Temporarily the membrane goes from “-” on the inside to “+” on the inside (influx of Na+)
  • This local reversal in potential serves as the source of depolarizing current for the adjacent excitable patch in the membrane
  • the electromagnetism allows for Na+ channels to be opened in adjacent membrane
  • Therefore, once started, an AP will propagate from its origin across the rest of the cell till the axon terminal (or it will die before that in some scenarios)
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2
Q

which cells are excitable cells and why? do most cells want to carry a signal/be excitable?

where does the AP start, travel, and end on a neuron?

do non-excitable cells also conduct currents?

A
  • Most cells are not ‘excitable’, (i.e. they do not generate APs) for the simple reason that they lack voltage- gated Na+ channels. do be excitable a neuron needs: voltage gated Na+ channels, long axons, and muscle cells
  • Most cells are not interested in carrying a signal any distance, they do not have an ‘axon’
  • An axon is a long extension of the cell body (like a wire) that carry AP away to some other location. the AP starts right at the start of the axon (axon hillock) and ends at the presynaptic axon terminal
  • These cells will however conduct passive currents, but will not generate APs
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3
Q

why or why not are excitable cells in biological tissue good conductors

A

In biological tissue if we put a voltage across membrane on one location (i.e. step change in voltage) and measure the voltage across the membrane some distance away > It doesn’t look anything like what we started with

  • this is because biological tissue, resistors and capacitors are not a good conductor
  • in contrary, a copper wire will be much better at preserving the potential
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4
Q

what does lambda measure in cable properties for signals

A

before answering we should know:
- lambda = length constant
* lambda measures how quickly a potential difference disappears (decays to zero) as a function of distance
* Thus, the conduction velocity of an AP along an axon depends on the membrane length constant, lambda
- in other words, lambda measures how far the signal/potential difference will travel before it dies

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5
Q

how do we prevent the loss of a signal along a membrane (2)

A
  • we have to improve and increase lambda
    1. lambda is increased by increasing diameter (thicker straw = more water travelled up it) (The larger the diameter > less internal resistance > less voltage is lost across that resistance as the currents travel down the membrane)
  1. lambda is increased by increasing membrane resistance (less holes or bends in a straw will be better for the water to travel up it) (The higher the membrane resistance > less current is leaked out > current is forced down the membrane)
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6
Q

what is the equation of the length constant lambda. what are the variable and the modified version of the equation

A
  • depends on:
    Ri = internal resistance
    Ro = extracellular fluid resistance
    Rm = membrane resistance

initial eq:
lambda = sqrt(Rm/(Ro+Ri))

Since the extracellular fluid resistance is not adjustable and is relatively low (Ri»>Ro), it drops from the equation and we’re left with internal resistance and membrane resistance

modified eq:
lambda = sqrt(Rm/Ri)

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7
Q

what percent voltage dropped is lambda defined until

A

lambda is defined as the distance you can travel, to the point where the voltage drops to about 37% of its original value

Ideally, you want to increase lambda as much as possible so that the depolarizing current will spread a great distance

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8
Q

what is myelination
- why is this method better for increasing membrane resistance?
- what are glial cells
- what are the two types of specialized glial cells and where are they found
- how do glial cells work

A
  • myelination: when myelin, a fatty substance, forms a sheath (composed of glial cells) around the axons of nerve cells
  • this is the most efficient means of increasing conduction velocity and membrane resistance (not by inc. diameter - harder physiologically)
  • ‘Glial’ cells are cells that assist the nervous system, they are required for nutrition and increased membrane resistance
  • Specialized ‘glial’ cells (Schwann cells of the PNS or oligodendrocytes within the CNS) wrap around successive sections of an axon

how do glial cells work - myelination in action:
- 50-100 layers wrapping around the axon making myelin sheaths > this greatly increases the membrane resistance > reduces the leakage of current out of the membrane

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9
Q

what percent of axons are myelinated and why?

A
  • about 20% of the axons are myelinated
  • this is because it takes space for the glial cells to make the sheath
  • only done to the signals that need to go very quickly or far
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10
Q

what is the difference between schwann cells and Oligodendrocyte for myelination

A

schwann cells:
- located at the PNS
- wraps around a single segment of one axon
- They wrap tightly around the axon, and during this process, most of their cytoplasm is squeezed out, leaving layers of myelin insulation (increases speed of transmission)

Oligodendrocytes:
- located at CNS
- these cells extend multiple processes that wrap around segments of several different axons at once, similar to the arms of an octopus.
- This efficient structure allows oligodendrocytes to myelinate multiple axons simultaneously in the CNS.

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11
Q

what are the regions between the portions of the myelin sheath? why are they important?

A
  • There are small gaps left between adjacent portions of the myelin sheath (a glial cell will wrap one section and next glial cell will wrap another section)
  • This small gap left between adjacent glial cells > the ‘Node of Ranvier’
  • important because this space is where the AP is and can be generated
    -> only place where we can find the voltage gated sodium channels which is required for an AP
    -> NoR allows for currents to cross and be depolarized at the membrane
  • if we didn’t have the gaps the sodium wouldn’t be able to enter the cell –> def not through the myelination
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12
Q

what disease would we acquire if we were to lose the myelinations on our axons

A
  • Multiple sclerosis (MS)
  • nervous system disease which effects brain and spinal cord
  • the damaged myelin leads to blockage and slowing down of signals
  • may lead to vision disturbances, muscle weakness, incoordination and imbalance etc.
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13
Q

what is saltatory conduction?

A
  • In myelinated axons, only the membrane exposed (NoR) at the nodes is excitable
  • Because the APs are only generated at these nodes, it means that the AP will ‘jump’ from one place to the next — in between you’re not generating any AP (Only the current is going through the myelin sheaths)
  • This ‘jumping’ mode of conduction is known as ‘saltatory conduction’
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14
Q

how many nodes can an AP’s depolarizing current travel?

what are the two processes that occur when an AP is travelling along the axon?
what is the role of the myelin here in one of the processes?

how does the current travel beyond the max number of nodes?

A
  • If we have an AP on one node, the depolarizing current that is generated at the site is strong enough and will travel down that axon for many nodes (5-10 nodes)
  • If there is sufficient strength in the current, it will bring all the following nodes to threshold potential
  • Therefore, as the AP travels along the axon there is saltatory conduction where the current jumps from one node to the next but also passive spread of the depolarizing current through the myelin sheaths
  • Myelin prevents leakage of current across membrane between nodes
  • note that even though the next ten nodes will be triggered for an AP, since the triggering happens sequentially, at a moment in time all ten nodes will be at different phases at the AP. however, it’s important to note that it is the tenth node, that when passed above threshold potential, will be the one activating the next 10 nodes.
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15
Q

what is the safety factor that is encoded in saltatory conduction?

A

You could poison some of the nodes and the depolarizing current will just skip past that and move on to the next healthy patch of membrane (i.e. you have to destroy a fair length of the membrane to stop AP in its track)

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16
Q

how do unmyelinated axons differ from myelinated axons?

how do unmyelinated axons have lower conduction velocity?

how does the concentration of voltage gated channels differ in unmyelinated axons?

are there a lot or a little unmyelinated axons?

whats a remak bundle?

A
  • The unmyelinated axons do not have this extensive wrapping around the outside > you get lots of current leakage and slows down the conductance velocity
  • Slow conduction velocity (small axon diameter and low membrane resistance)
  • Both Na+ and K+ voltage-gated channels are intermixed when its unmyelinated (instead of Na+ just being focused at the NoR like in myelinated)
  • Majority of axons are unmyelinated
  • Unmyelinated axons do have some insulation: the schwann cell and oligodendrocyte engulf the axon (5-30 axons) without winding > “Remak Bundle”
17
Q

how does axon speed and number vary between humans and cats

A
  • cats have faster axons (120 m/s) so they can catch mice
  • humans have axons at a speed of 80 m/s if myelinated and 2 m/s - thus we cannot catch mice like cats

but we have more axons than cats, so we can perform more complex functions better - like putting out cat food to catch the cat that caught the mouse

18
Q

how does the current generated from the AP know to head to the axon terminal and not go backwards?

A

we know an AP goes down an axon by jumping from node to node via saltatory conduction to the axon terminal

  • however how does it know to not go backwards as well? since a current is a free force and just travels?

AP cannot turn around and re- propagate in direction it came from because of the refractory period of an AP where the volt-gated Na+ channels are inactivated
* so at the axon terminal the AP dies out, can only go one way

19
Q

what are synapses and the two types

A

a synapse is the functional association of a neuron with another neuron or with effector organs (muscles or glands)

extracellular space which exists between adjacent cells

The synapse is defined by the presynaptic surface (the bouton, which contains the vesicles) and the postsynaptic membrane, which is the membrane of the adjacent neuron (has receptors that can bind neurotransmitters)

  • two types: electrical and chemical
20
Q

what are electrical synapses comprised of and how does it allow depolarization to cross?

when are these synapses used and whats an example?

how far apart are the adjacent membranes in this synapse?

A
  • two neurons or cells are linked together by gap junctions – think of it like two copper wires twisted together
  • Gap junction bridged by connexins which allow small ions and depolarization to cross – AP are transferred directly and does not need neurotransmitters to do that
  • these synapses are used for rapid communication and are bidirectional – can be found between neurons and glial cells
  • ex. cardiac muscle contractile cells - heart needs to act in synchrony
  • At electrotonic synapses (gap junctions), adjacent membranes are about 35Å apart
21
Q

what are and what happens in chemical synapses?

how wide is the synaptic cleft?

A
  • the depolarizing current from the action potential propagates to the axon terminal and then releases neurotransmitters in the synapse
  • neurotransmitters are released and bind to the receptors on the post synaptic membrane
  • synaptic cleft is about 200 Å wide
22
Q

what are boutons and what are they filled with?

A
  • Axons end in ‘boutons’ filled with vesicles
  • vesicle are tiny organelles, which contain neurotransmitters which is released into the extracellular fluid through exocytosis
23
Q

what is the trigger for exocytosis at the boutons? how does this work?

A
  • the trigger for exocytosis is always Ca++ ions
  • the Ca++ ions come into the bouton membrane via voltage gated Ca++ channels which open when depolarized by AP currents (threshold for opening is about -50 mV)
  • Ca++ diffuses into bouton, and triggers cascade of reactions which result in vesicle exocytosis (commonly ‘kiss & run’ type = transient OR full fusion = all transmitters are released)
  • Normally, vesicles are docked in preparation for fusion, so when the Ca++ ions enter, we have a set of vesicles which are lined-up and ready to fuse and release contents
24
Q

why do chemical synapses exist when electrical synapses are more robust?

lowkey dont get

A
  • chemical synapses are processing stations
  • it is a matter of chance that a vesicle will release its contents into the synapse (10-90% chance of 1 AP release 1 vesicle)