Cell membranes and synaptic activity Flashcards

1
Q

What autoimmune disease is associated with demyelination of central axons (CNS)?

A

[multiple sclerosis]

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2
Q

What does it mean, ‘membrane potential’?

A

[refers to a separation of charge across the membrane; due to differences in permeability between ions. This separation yields a ‘potential’ measured in volts that represents potential energy in letting this charge separation disappear]

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3
Q

Do all cells have a membrane potential?

A

[Yes….it’s not just neurons… but neurons are best at exploiting membrane potential for signaling purposes.. also, only neurons and muscle cells produce action potentials - large, local, quick shifts in membrane potential]

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4
Q

Is it true that the ‘resting potential’ is only due to K+ current?

A

[true for glial cells, not for neurons. K+ conductance is high at rest, but Cl- conductance is about 1/3 of that, Na+ conductance is about 1/25 of K+. Because the Nernst potential for Cl- is nearly the same as the resting potential, it’s influence is minimal. However, because the Nernst potential for Na+ is so far away from the resting potential, it is a factor for the resting potential ]

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5
Q

Which ion is most responsible for the ‘resting potential’?

A

[K+]

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6
Q

Which ion’s permeability causes the massive depolarization observed in the action potential?

A

[Na+]

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7
Q

Which ion is necessary for release of neurotransmitter at the synapse?

A

[Ca++]

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8
Q

What is the duration of an action potential?

A

[1 msec]

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9
Q

How much does the membrane potential shift during an action potential?

A

[100 mV]

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10
Q

What constrains the voltage limits on an action potential?

A

[Maximum depolarization is constrained by the Nernst potential for Na+ (~50 mV), maximum hyperpolarization is constrained by the Nernst potential for K+ (~-90 mV)

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11
Q

What is a good approximation of the ‘resting’ potential?

A

[-70 mV]

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12
Q

What does the Nernst potential represent?

A

[For a single ion, it describes the membrane potential at which the inward and outward current would be zero; equal # of that ion flow in and out across the membrane]

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13
Q

If neurons are so permeable to K+, why isn’t the Nernst potential for K+ also the ‘resting potential’?

A

[the membrane is also permeable to Na+ and Cl- both of which depolarize the resting potential from Keq (especially Na+)]

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14
Q

If the membrane at rest, is so permeable to Cl-, how come no one cares about Cl-?

A

[we’re not bigots. The fact is the Nernst potential for Cl- is close to the observed membrane potential…so, moving a few Cl- ions across the membrane will not change much in that regard. However, in synaptic transmission, increasing Cl- conductance does have impact because it negates the influence other ions normally have when they cross the membrane. This effect is known as shunting… it effectively short-circuits the influence of other ions]

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15
Q

At the ‘resting’ potential, does opening a K+ channel generate an outward or inward current?

A

[outward, K+ ions will leave, hyperpolarizing the cell…trying to bring it to the Nernst potential for K+)]

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16
Q

Name the ‘bag’ that holds neurotransmitter for release?

A

[vesicle]

17
Q

What is the refractory period?

A

[minimal time between action potentials, constrained by availability of voltage-gated Na+ channels]

18
Q

What is the time constant?

A

[the time a membrane drop to 1/e (37%) of its charged up membrane potential. It is equal to the membrane resistance X membrane capacitance. The “membrane time constant” of a neuron is simply a way of measuring how quickly a neuron’s voltage level decays to its “resting state” after it receives an input signal.]

19
Q

What constrains axonal conduction velocity?

A

[the time it takes to charge up and discharge the membrane; in general, want to minimize Rm, Cm and Ri…. The squid’s giant axon is non-myelinated, and speeds up conduction by minimizing Ri. Myelination speeds conduction because although the fat increases Rm, this is more than offset by the drop in Cm]

20
Q

What is a good guess for the absolute refractory period for a myelinated axon?

A

[ 0.5 msec]

21
Q

What is the relative refractory period?

A

[a 2nd action potential can occur, but requires more stimulation and its amplitude is decreased because it doesn’t have the full complement of voltage-gated Na+ channels available and some VG K+ channels have opened which also decreases size; in myelinated axons, relative refractory period is ~4-5 msec]

22
Q

What does the Na+/K+ ‘pump’ do?

A

[maintains the membrane potential over time, but does require energy, ATP]

23
Q

Name 3 properties of the Na+/K+ pump?

A

[it requires ATP to operate, it hyperpolarizes the membrane potential (~ 4-6 mV), and this hyperpolarization is due to a net outward current: 3 Na+ ions out for every 2 K+ ions in]

24
Q

Identify the two major types of neurotransmitter receptors?

A

[ionotropic, metabotropic]

25
Q

What is the neurotransmitter/receptor associated with the neuromuscular junction?

A

[acetylcholine, nicotinic cholinergic receptor (ionotropic, mixed cation, Na+/K+)]

26
Q

What is the major inhibitory neurotransmitter, and what amino acid is it made from?

A

[GABA, glutamate]

27
Q

What is the reversal potential?

A

[The point at which there is no net flow of ions through a receptor channel]

28
Q

Which receptor produces a strong outward current?

A

[GABA-B, metabotropic, increases K+ conductance]

29
Q

What is the most common neurotransmitter in CNS?

A

[glutamate, an amino acid]

30
Q

Does activating AMPA glutamate receptors produce an EPSP or IPSP?

A

[EPSP, ionotropic, mixed cation, Na+/K+]

31
Q

How do local anesthetics work?

A

[block voltage-gated Na+ channels, usually for 20 min-hr, depending on drug design]

32
Q

How do most anesthetics work?

A

[enhance GABA-A receptors (shunts membrane), e.g., propofol]

33
Q

What is an analgesic?

A

[an agent that blocks pain]

34
Q

What is an anesthetic?

A

[an agent that blocks pain AND causes loss of consciousness]

35
Q

What does ‘botox’ do?

A

[Botulism toxin destroys the machinery for exocytosis associated with synaptic release. In large quantities, it kills. In discrete doses it is a useful drug for treating focal dystonia (a muscle disorder of continuous and focal muscle cramps) such as torticollis. A single dose will provide local block for 4-6 months, and then another injection can be used. It has also been used to treat uncontrollable sweating, but, by far its major use is cosmetic, to relax the muscles to provide ‘youthful’ looks to the face.