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Neurobiology > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

movement of electric charge movement of electric charge (ions)

A

electrical current

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2
Q

force exerted on a charged particle

A

electrical potential

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3
Q

relative ability of an electric charge to migrate from one point to the next

A

electrical conductance

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4
Q

relative inability of a charge to migrate

A

electrical resistance

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5
Q

Ohm’s Law

A

V (voltage) = I (current) * R (resistance)

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6
Q

Equation for conductance

A

g (conductance) = 1/R

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7
Q

difference between membrane potential (Vm) and the equilibrium potential of a particular ion (Eion )

A

driving force

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8
Q

ionic current

A

conductance X driving force (Gion[Vm-Eion])

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9
Q

What are the currents of Na, K and Cl at rest?

A
  • Ina is inward (negative)
  • Ik is outward (positive)
  • Icl is approximately zero
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10
Q

What changes during an action potential?

A
  • membrane permeability to Na and K
  • conductance
  • ionic currents
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11
Q

___ current is depolarizing. ___ ions move in and ___ ions move out.

A

inward
positive
negative

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12
Q

___ current is hyperpolarizing. ___ ions move out and ___ ions move in.

A

outward
positive
negative

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13
Q

Depolarizing current shows a ____ deflection on a current vs. time chart.

A

downward

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14
Q

What does tetrodotoxin do?

A

Blocks sodium current

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15
Q

What does tetraethylammonium do?

A

Blocks potassium current

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16
Q

activated by the influx of Na +, counteracts the effect of that cation by allowing the discharge of K + (resets the membrane potential)

A

K+ delayed rectifier channels

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17
Q

During resting potential, potassium channels are ____, and permeability to potassium is ____. Resting membrane potential is near ___.

A

always open
highest
Ek

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18
Q

During depolarization, permeability to Na+ _____. Membrane potential _____.

A

increased

rises

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19
Q

Voltage-gated Na+ channels open in response to ________.

A

depolarization above threshold (~-50mV)

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20
Q

The voltage-gated Na+ channel is a single long polypeptide with __ domains each with __ transmembrane alpha-helices. It is ___ more permeable to Na+ than K+ due to ____.

A

4
6
12x
hydration (potassium is too big when hydrated)

21
Q

The __ alpha-helice in sodium channels is the voltage sensor. It twists away from the inside when the cell is depolarized to ___. The twists causes the channel to open and ____. Vm ___ as a result.

A

S4
-40mV
Na+ to rush in
rises

22
Q

Following depolarization, Na+ channels become ____. K+ channels, on the other hand, only ___.

A

inactivated

close

23
Q

the period immediately following the firing of a nerve fiber when it cannot be stimulated no matter how strong the stimulus; due to the increase in K+ permeability

A

absolute refractory period

24
Q

What de-inactivates the sodium channels?

A

repolarization

25
Q

What happens during the rising phase of an action potential?

A
  • voltage-gated sodium channels open
  • potassium channels close
  • sodium influx
26
Q

What happens during the falling phase of an action potential?

A
  • sodium channels inactivate
  • potassium channels open
  • cell becomes more negative
27
Q

4 polypeptide subunits joined to form a pore

A

voltage-gated potassium channels

28
Q

What is an afterhyperpolarization?

A

voltage-gated K+ channels take a few msec to return to the closed state; efflux of K+ from the cell is higher than at rest; membrane potential becomes more negative than at rest

29
Q

a period during which you can trigger an AP by applying a larger than normal stimulus; some (but not all) Na+ channels have been reset

A

relative refractory period

30
Q

What is spatial buffering of potassium and why is is important?

A

repolarization of neurons tends to raise potassium concentration in the extracellular fluid; potassium ions are taken up at one region of the astrocyte and then distributed throughout the cytoplasm of the cell, and further to its neighbors via gap junctions.

31
Q

How does lidocaine work?

A

blocks sodium channel pore (from inside), blocks action potentials in sensory axons so that pain signals do not reach the brain

32
Q

How does scorpion toxin work?

A

It blocks sodium channel inactivation –> muscle stiffness

33
Q

How are action potentials propagated?

A

Na+ channels locally open in response to stimulus generating an action potential; resulting current flows passively along the length of the axon

34
Q

Why doesn’t the action potential travel backwards?

A

upstream Na+ channels inactivate, K+ channels open –> temporary hyperpolarization; also delay in sodium channel reopening

35
Q

What is membrane resistance (Rm)?

A

of channels open for ions to cross the membrane

36
Q

How is membrane resistance related to the surface area of membrane and conduction speed?

A
  • increased SA –> increased leaky channels –> decreased resistance
  • increased resistance –> increased conduction speed
37
Q

How is internal (axial) resistance (Ri) related to axon volume?

A

increased diameter –> increased volume –> decreased resistance

38
Q

How is internal (axial) resistance (Ri) related to conduction speed?

A

decreased resistance –> increased speed

39
Q

What does myelin do?

A

acts as insulation to decrease current loss through leak channels

40
Q

How do the Nodes of Ranvier work?

A

voltage-gated sodium channels present in nodes only; action potential “recharges” as it propagates

41
Q

action potential “jumps” from node to node

A

saltatory conduction

42
Q

damage or loss of myelin over time

A

demyelination

43
Q

myelin never forms correctly

A

dysmyelination

44
Q

slowly progressive CNS disease; characterized by patches of demyelination in the CNS

A

multiple sclerosis

45
Q

What are the symptoms of MS?

A
  • weakness and clumsiness
  • stiffness and gait disturbances
  • visual disturbances
  • mental disturbances, including lack of judgment, emotional liability, sudden weeping or laughter
46
Q

What is the epidemiology of MS?

A
  • affects mainly Caucasians
  • average age of onset is 28 - 30 years
  • female:male ratio = 2:1
  • chronic illness leading to cumulative disability
  • complex disorder (combination of genes and environment)
  • mediated by autoimmune processes
47
Q

What causes MS?

A
  • myelin proteins recognized as foreign by T cells
  • lymphocytes and macrophage cross BBB and destroy oligodendrocytes
  • molecular mimicry (?): antigen initiates an immune response, antibodies cross-react with a self protein that “mimics” the antigen
48
Q

Is is possible to recover from MS?

A
  • occasional re-myelination
  • some demyelinated axons express higher than normal densities of sodium channels in demyelinated regions (restore conduction –> remission)
  • degeneration of axons is irreversible; permanent loss of function
49
Q

How is MS treated?

A
  • no cure
  • enhance endogenous remyelination
  • limit damage to oligodendrocytes
  • transplant exogenous myelin-forming cells (stem cells)

Neurobiology (9 decks)

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