Lectures 1.4-1.5 Flashcards

1
Q

How does ion diffusion across a semi-permeable cell membrane lead to a membrane potential?

A

ion channels facilitate diffusion of ions across the lipid bilayer. A diffusion potential arises when diffusion of ions leads to an unequal number of charges on the inside versus the outside of the cell.

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2
Q

equilibrium potential

A

the membrane potential where the net flow through any open channels is 0

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3
Q

Goldman-Hodgkin-Katz equation

A

describes the membrane potential for biological membranes

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4
Q

properties of action potentials

A

rapid, transient, self-propagating electrical excitation in the plasma membrane of an excitable cell.

  • All-or-none
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5
Q

what ion currents contribute to depolariation and repolarization phases of an action potential ?

A

Na+ flows through voltage-gated channels causing an inward positive current (depolarization) and K+ flows through voltage-gated channels causing an outward positive current (repolarization)

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6
Q

what is the function of voltage gated ion channels during an action potential?

A

an inward current depolarizes membrane potential to threshold. this depolarization triggers voltage-gated Na+ channels to open, as Na+ floods into the cell, it is further depolarized and causes more voltage-sensitive Na+ channels to open.

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7
Q

how do axon diameter and myelination affect action potential conduction velocity?

A
  • increased axon diameter increases conduction velocity by decreasing internal resistance
  • myelination increases conduction velocity
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8
Q

how do refractory periods contribute to action potential conductance?

A

they limit the rate of action potential firing and help to ensure unidirectional propagation

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9
Q

how do refractory periods arise?

A

inactivation gates of the Na+ channels are closed and no action potential can occur until the channel is in the resting closed conformation with the inactivation gates open

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10
Q

local potential

A

small change in the resting membrane potential of a neuron at one point in the cell

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11
Q

depolarization

A

an instance where the membrane potential becomes more positive than the resting potential

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12
Q

diffusion potential

A

the potential difference generated across a membrane because of a concentration difference of an ion. It can be generated only if the membranes is permeable to the ion. The size of the diffusion potential depends on the size of the concentration gradient

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13
Q

membrane repolarization

A

the period where the membrane potential returns back to resting potential

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14
Q

threshold potential

A
  • the membrane potential at which the action potential is inevitable.
  • when a local potential leads to depolarization above the threshold potential, an action potential arises
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15
Q

axon hilock

A

the section of axon adjacent to the cell body that has a high density of voltage-gated Na+ channels

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16
Q

voltage-gated K+ channels

A

depolarization causes K+ channels to open slowly and increases K+ conductance

  • repolarization is caused by outward K+ current
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17
Q

internode

A

flattened plasma membrane that is wrapped around the axon to form a segment of biochemically specialized sheath

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18
Q

nodes of ranier

A

regions of axon between internodes of myelin (location of most membrane channels)

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19
Q

saltatory conduction

A

when the action potential jumps from node to node

  • action potentials travel faster as it is not passing through the entire axon
  • metabolic energy is conserved
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20
Q

Multiple Sclerosis

A

demyelinating disease that affects the central nervous system

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21
Q

relative refractory period

A

onset is at the end of the absolute refractory period and continues until membrane potential returns to resting levels

  • an action potential can be elicited only by very large inward currents
  • need more inward current than normal because the K+ conductance is higher than at rest and the membrane potential is closer to the K+ equilibrium than it is to the resting membrane potential
22
Q

absolute refractory period

A

the period during which another action potential cannot be elicited no matter how large the stimulus

  • comprises the entire duration of the action potential
  • due to the closed inactivation gates of the Na+ channels
23
Q

synapse

A

a junction between two nerve cells, consisting of a minute gap across which impulses pass by diffusion of a neurotransmitter.

  • Chemical synapses can be excitatory (open cation channels that cause Na+ influx/depolarization) or inhibitory (open ligand gated Cl- or K+ channels to suppress firing and make it harder to depolarize the membrane)
24
Q

neuromuscular junction

A

chemical synapse formed by the contact between a motor neuron and a muscle fiber

  • depolarization of nerve terminal opens Ca2+ channels triggering release of neurotransmitter acetylcholine into synaptic cleft
25
Q

neuromuscular junction

A

chemical synapse formed by the contact between a motor neuron and a muscle fiber

  • depolarization of nerve terminal opens Ca2+ channels triggering release of neurotransmitter acetylcholine into synaptic cleft
  • acetylcholine binds to receptors in muscle cell plasma membraneopening Na+ channels and allows Na+ influx
  • depolarization causes action potential
  • depolarization causes Ca2+ channels to open and Ca2+ releases into sarcoplasmic reticulum causing muscle to contract.
26
Q

Neurotransmitter

A

a chemical substance that is released at the end of a nerve fiber by the arrival of a nerve impulse and, by diffusing across the synapse or junction, causes the transfer of the impulse to another nerve fiber, a muscle fiber, or some other structure.

27
Q

acetylcholine receptor

A

binds to acetylcholine on in the muscle cell plasma membrane and causes cation selective channels to open and allows Na+ influx into the muscle cell

28
Q

acetylcholine esterase

A

enzyme that hydrolyzes ACh and decreases ACh concentration in cleft to terminate the signal from the presynaptic cell

29
Q

voltage-gated calcium channels

A

opens due to depolarization of muscle plasma membrane. Releases Ca2+ into the sarcoplasmic reticulum thus causing muscle to contract

30
Q

Stages of eukaryotic cell

A

G1 (Gap 1), S (DNA Synthesis), G2 (Gap 2), M (Mitosis)

G0 (nondividing/terminally differentiated cells) most cells in the body

31
Q

properties of cyclin-dependent kinase

A
  • regulates the cell cycle
  • Cdk activity is needed for progression of cell cycle
  • two components: Cdks and cyclin
  • Cdk is only active when bound o a cyclin molecule
32
Q

what are the four mechanisms by which cdks is activated?

A
  • only active when bound to a cyclin molecule
  • Cdk and cyclin synthesis regulated by cellular growth factors
  • regulated by phosphorylation (kinases and phosphotases)
  • other regulatory proteins (inhibitors) bind to Cdks and inhibit activity
33
Q

what happens at cellular checkpoints?

A

the cell cycle is stopped if an essential processe is not complete

34
Q

G1/S checkpoint

A
  • DNA damage activates p53 (a transcription factor that regulates genes such as p21)
  • p21 concentration in the cell increases
  • p21 binds and inhibits cdk2/cyclinE
  • Rb is not phosphorylated and E2F is not activated so cells do not enter S phase
35
Q

How do cdks and checkpoint proteins regulate entry into S phase?

A
  • Regulated through phosphorylation of Rb
  • active CDK2-Cycling E phosphorylates Rb
  • Reduces binding to E2F
  • E2F activates synthesis of proteins required for DNA synthesis (S phase)
36
Q

name the steps in DNA damage checkpoint activation

A

essentially make a kinase cascade:

  • sensor proteins bind to DNA damage and recruite transducer kinases
  • transducer kinases amplify signal by phosphorylating effector kinases
  • transducer and effector kinases phosphorylate protein effectors which modulate cell processes and stop the cell cycle
37
Q

differences between DNA and RNA molecular makeup

A
chemical difference: 2' H vs. 2' OH
structural difference: RNA is base labile
Named different ("deoxy" before DNA names)
38
Q

base pairing

A
  • G-C, A-T; (RNA = A-U)
  • hydrogen bonds: 3 in G-C and 2 in A-T
  • base pairs have similar geometry
  • base pairing causes DNA to form antiparallel helix
39
Q

Hoogsteen pairing

A
  • T bonds with AT
  • C+ bonds wih GC
  • Most stable at low pH when C is protonated
  • Allows formation of 3 and 4 strand DNA
40
Q

L=T+W

A

Linking number = Twist + Writhe

41
Q

A form

A

RNA-DNA duplexes

42
Q

Z form

A

left-handed helix that forms from methylation and negative supercoiling
- forms from alernative purine/pyrimidine sequences

43
Q

Hairpins

A

forms from palindromes

- usually in ssDNA and RNA

44
Q

Cruciforms

A

formed from palindromes

- usually in dsDNA

45
Q

What allows specific DNA sequences to be identified in the lab (molecular diagnostics)?

A

Denatured DNA can anneal to form double stranded DNA

46
Q

Linking Number

A

number of times the two strands are linked together

  • sum of twist and supercoils
  • cannot change w/o breaking one or both strands of DNa
47
Q

topoisomers

A

DNA that differs only in topology (L)

48
Q

topoisomerases

A

enzymes that interconvert topoisomers

49
Q

twist number

A

number of watson-crick turns in a DNA molecule

  • only depends on number of turns in double helix
  • b-form= twist is +1 for every 10.4 bp
  • most DNA is B form so T= bp length of DNA / 10.4
50
Q

Writhing Number

A

supercoiling of the double helix

  • dependent on the path through space
  • number of times the double helix crosses itself in 3D
  • DNa with no supercoils is called relaxed DNA (lowest energy form)
51
Q

Writhing Number

A

supercoiling of the double helix

  • dependent on the path through space
  • number of times the double helix crosses itself in 3D
  • DNa with no supercoils is called relaxed DNA (lowest energy form)
52
Q

Why is controlling DNA topology important?

A

controlling topology is essential for maintaining and expressing genetic information. It affects DNA behavior.