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Flashcards in NMP Duke final Deck (105):
1

Types of Sleep

normal sleep + REM sleep

2

Normal sleep
Stage 1

β-waves

3

Normal sleep
Stage 2

α-waves

4

Normal sleep
Stage 3

θ-waves; considered; light sleep; broken into stages I and II

5

Normal sleep
Stage 3
part 1

α with θ; the θ waves characteristic of light sleep are taking over the awake brain

6

Normal sleep
Stage 3
part 2

θ with spindles (spindles are alpha bursts; its like the awake doesn't want to let go)

7

Normal sleep
Stage 4

δ-waves; considered deep sleep; broken into stages III and IV

8

Normal sleep
Stage 4
part 3

δ with spindles; deeper sleep is setting in but
α still tries to burst in

9

Normal sleep
Stage 4
part 4

δ

10

A person gets more out of sleep if they go through these stages _____________

in order

11

Physiologic Properties of Deep Sleep
(Stage 4)

↓ respiratory rate (10-8 bpm)
↓ muscle tone
↓ sympathetic tone (can drop by 10 -30%)
↓ metabolic rate (MR)

↑parasympathetic tone (↓HR, ↑ GI motility/secretions, relaxed sphincters, sexual arousal)

12

REM sleep
AKA

paradoxical sleep, or
β-wave sleep

13

REM sleep
occurs every

90 mins

14

REM sleep
duration

2-3 minutes, up to 30 mins (rarely longer than 10 mins)

15

REM sleep
β-waves come heavily from

striate cortex

16

During REM sleep what tract is activated by the PPN?

lateral reticulospinal tract

17

During activation of the reticulospinal tract by the PPN, what is happening?

inhibiting extensors, so you're paralyzed during REM

18

How does the PPN regulate REM?

first sending to the LG; PPN→LG→Striate cortex
(area 17)

19

Regulation of Wakefulness vs. Sleep Centers
AKA

flip-flop circuit

20

Narcolepsy

a sudden loss of muscle tone
that is often accompanied by the onset of sleep

21

Orexin / hypocretin

produced primarily in lateral and tuberal (medial) hypothalamus; it is responsible for
wakefulness

22

narcoleptic people often show decreased

levels of orexin

23

If both (ascending chemical pathways
(wakefulness), and PPN (REM))are stimulated, why don't we have wakefulness and REM and the same time?

The asecnding pathways actually inhibit the PPN
so if orexin is firing, the net result is wakefulness because orexin's stimulative effect on the PPN
is negated

24

pre-optic nucleus
(anterior medial hypothalamus)
induces

non-REM sleep

25

pre-optic nucleus
action

It sends GABA-ergic axons to inhibit both the
lateral/tuberal hypothalamus and the ascending chemical pathways.

26

third major sleep center

PAG

27

PAG
action

sends GABA-ergic axons to the ascending pathway, but not to the orexin-producing hypothalamus

28

PAG
result

it induces REM sleep, like the PPN

29

What happens when the PAG is on?

he ascending chemical pathways are shut down


the PAG shuts off wakefulness centers, prevents them from turning off the PPN, and it leaves the production of orexin on, so PPN is stimulated even more = REM sleep

30

The PPN is the beginning of what pathway?

pontogeniculocalcarine pathway

31

the PPn activates what cells in the medulla?

n. gigantocellularis

32

n. gigantocellularis
messages what?

the lateral reticulospinal tract which inhibits extensors mm. = paralysis during REM sleep

33

skeletal muscle Ach receptors? AKA

nicotinic

34

Skeletal muscle AP----->generic description

The AP comes down, releases ACh, & new AP is initiated in the skeletal muscle. This means we have fired the sarcolemma.

35

The AP comes down, releases ACh, & new AP is initiated in the skeletal muscle. The AP runs along the membrane until it hits an invagination. What invagination?

T-tubules with sodium channels and DHP receptors

36

What is DHP?

voltage-sensitive, integral membrane protein w/ cytosolic domain that contacts a ryanodine
recetpor on the SR(sarcoplasmic reticiulum)

37

Ryanodine Receptor is?

protein embedded in SR membrane. A true Ca2+
channel: comes in tetrads too

38

What happens when the AP hits the DHP?

It changes conformation.
The cytosolic loop causes the ryanodine to change conformation too, causing an opening of Ca2+ channels of the SR = Ca2+ release into the cell!

39

What are the steps of AP--->skeletal muscle contraction?

1. AP enters skeletal muscle
2. AP enters T-tubule & reaches DHP receptor
3. DHP changes conformation
4. DHP cytosolic domain causes a Ryanodine conformation change too
5. Ryanodine opens
6. Ca2+ pours out of SR into cell
7. Ca2+ binds to Troponin at TnC
8. Troponin changes conformation
9. Tropomyosin is moved out of the way
10. Myosin can bind to actin
11. Skeletal muscle contraction

40

What must be pumped back into the SR?

Ca2+

41

As Ca2+ levels decrease, what can change conformation?

troponin

42

What sits in the groove in troponin blocking myosin from binding?

tropomyosin

43

What happens when myosin isn't binding to troponin?

muscle relaxation

44

How long is the delay from Ca2+ peak to muscle contraction?

200ms

45

how do we turn “all-or-none:” AP’s into graded contractions?

1) Temporal Summation
2) Organization of Skeletal Muscle
3) Length/tension Relationships

46

What is temporal summation?

stair-step effect called treppe, allows stronger contraction

One (1) AP only results in a muscle twitch,
but now those elastic fibers have all the slack
out of them.

47

What leads to tetany?

Extremely high level of APs.

48

All the myofibrils that are fired by the same motor neuron =

motor unit

49

T or F
All motor units are the same size.

F

50

The heavier the weight (force) against the muscle _____

the slower the velocity of contraction

51

not many myosin heads can get a hold of the actin filaments =

weak contraction

52

White muscle AKA

Fast-Twitch Glyoclytic

53

Red muscle AKA

Slow-Twitch Oxidative

54

Which type of muscle runs glycolysis for main source of energy?

White

55

Which type of muscle is highly vascular?

Red

56

Which type of muscle is for endurance?

Red

57

Which type of muscle has lots of myoglobin?

Red

58

Which type of muscle produces lots of lactic acid?

White

59

Where does energy come from when you start exercising quickly?

1) Existing ATP
2) High Energy Phosphates
3) As creatine decreases, glycolysis increases
4) Red muscle (aerobic)

60

What is a powerful phosphorus storing molecule important in skeletal muscle?

creatine

61

Smooth Muscle has no ______ (part of the sarcomere)

Z-lines

62

What does smooth muscle have instead of Z-lines?

dense bodies

63

What is smooth muscle's normal state?

contracted

64

What does Ca2+ bind to in smooth muscle?

calmodulin (instead of troponin)

65

Active calmodulin turns on what in smooth muscle?

myosin light chain kinase

66

What is the purpose of myosin light chain (MLC) Kinase?

1) phyosphorylating and activating a myosin chain
2) increasing the myosin's ATPase activity

67

MLC phosphatase function

removing ATP from the myosin

68

What ways allow increased Ca2+, which
increases calmodulin binding?

1) AP turns on voltage-sensitive Ca2+ channels
2)Second messengers (IP3) release Ca2+
3) Phospholipase C
4) Ryanodine Channels

69

how does Phospholipase C work?

cleaves phospholipid to DAG & IP3
; IP3 diffuses to SR, turns on a receptor at SR, allowing Ca2+ release

70

Three Ways to get rid of Ca2+

1) Pump it back across the SR for storage
2) Pump it out of the cell using Ca2+-ATPase
3) Pump it out of cell using cotransport
mechanism; Na+ gradient to couple Ca2+
movement across membrane; but it takes 3 Na+ for each 1 Ca2+. This produces slight depolarization

71

T or F
Repeated stimulus generates the same temporal
summation in Smooth that we saw in Skeletal muscle.

T

72

Muscle fibers
definition

refers to an entire muscle cell; in neurons, the
axon is elongated, but the whole cell is in skeletal mm.; cells are multinucleated ≈ 35/mm; up to 40mm long; each muscle fibercontains many myofibrils

73

Myofibril
def

myofibrils are bundles of myofilaments

74

Sarcoplasmic Reticulum
def

smooth ER surrounding myofibril

75

Myofilaments
def

make up the myofibril of a muscle fiber/cell; there are 2 kinds and they are always in a 2:1ratio (actin:myosin)

76

Actin
units/stains

up to 3000 units per myofibril; stains lightl

77

Myosin
units/stains

up to 1500/myofibril; contains crossbridges; stains dark

78

T-tubules

invaginations of the cell membrane; important in upcoming pathways (AP travels to here)

79

Sarcomere

basic contractile unit of muscle; extends from Z-disc to Z-disc; resting length = 3.2-3.5μm

80

Z-disc

the boundaries of a sarcomere; they used to be called "Z-line" but because the myofibril is 3D in
nature, like a long slender cylinder, it wraps around, making a disc; it is the anchor for actin filaments

81

Actin

arranged in pairs; filaments are anchored to Z-disc via titin; actin filaments of adjacent sarcomeres
extend toward each other, but do not meet (assuming the muscle is at rest);stains light

82

The light stain creates

the I-band

83

the I-band =

actin that is not overlayed by myosin = straddles 2 sarcomeres

84

Myosin

overlays adjacent actin filaments; contains crossbridges, that hang down and span the gap between actin and myosin; the crossbridge is golf
- club shaped and contains an arm and a head; stains dark

85

The dark stain creates

the A-band

86

the A-band =

all of myosin + the part of actin overlayed by myosin

87

H-band =

portion of myosin not overlaying actin; this band shortens during contraction

88

Alternating sequence of actin/myosin creates

a light-dark-light-dark pattern = striped or "striated"
mm.

89

one actin filament =

2 F-actins + 2 tropomyosins, and many
troponin triplets

90

F-actin contains

myosin binding sites

91

Tropomyosin

two of these filaments run along grooves in the F-actin; they cover the myosin binding sites

92

What covers the myosin binding sites?

tropomyosin

93

Troponin

a triplet of proteins that sit on top of tropomyosin

94

What are the three subunits of troponin?

1. TnCa
2. TnT
3. TnI

95

TnCa
has affinity for

Ca2+

96

TnT=

sits on tropomyosin

97

TnI =

intermediate/intercalated sits between troponin triplets and the myosin head

98

Myosin
(thick filament)
contains

2 heavy + 2 light chains;

99

Myosin forms crossbridges with the capability of

latching onto actin

100

during excitation of the muscle, the myosin heads do what?

binds to sites on F-actin because (tropomyosin is moved out of the way) and pull inward, bringing actin molecules closer together; hence, the shortening of the H-band

101

What causes shortening of the H-band?

myosin heads pulling the actin closer together

102

The sarcomere contracts to what length during max contraction?

3.2-3.5μm down to 2.0-2.2μm

103

The pulling in of actin by the myosin heads is a process known as....

ratcheting

104

When a skeletal muscle is excited Ca2+ binds

TnCa, causing it to reconfigure

105

When TnCa reconfigures it causes what?

tropomyosin to be moved out of the way, exposing the myosin binding sites on the F-actin