NMP Duke final Flashcards
Types of Sleep
normal sleep + REM sleep
Normal sleep
Stage 1
β-waves
Normal sleep
Stage 2
α-waves
Normal sleep
Stage 3
θ-waves; considered; light sleep; broken into stages I and II
Normal sleep
Stage 3
part 1
α with θ; the θ waves characteristic of light sleep are taking over the awake brain
Normal sleep
Stage 3
part 2
θ with spindles (spindles are alpha bursts; its like the awake doesn’t want to let go)
Normal sleep
Stage 4
δ-waves; considered deep sleep; broken into stages III and IV
Normal sleep
Stage 4
part 3
δ with spindles; deeper sleep is setting in but
α still tries to burst in
Normal sleep
Stage 4
part 4
δ
A person gets more out of sleep if they go through these stages _____________
in order
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)
REM sleep
AKA
paradoxical sleep, or
β-wave sleep
REM sleep
occurs every
90 mins
REM sleep
duration
2-3 minutes, up to 30 mins (rarely longer than 10 mins)
REM sleep
β-waves come heavily from
striate cortex
During REM sleep what tract is activated by the PPN?
lateral reticulospinal tract
During activation of the reticulospinal tract by the PPN, what is happening?
inhibiting extensors, so you’re paralyzed during REM
How does the PPN regulate REM?
first sending to the LG; PPN→LG→Striate cortex
area 17
Regulation of Wakefulness vs. Sleep Centers
AKA
flip-flop circuit
Narcolepsy
a sudden loss of muscle tone
that is often accompanied by the onset of sleep
Orexin / hypocretin
produced primarily in lateral and tuberal (medial) hypothalamus; it is responsible for
wakefulness
narcoleptic people often show decreased
levels of orexin
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
pre-optic nucleus
(anterior medial hypothalamus)
induces
non-REM sleep
pre-optic nucleus
action
It sends GABA-ergic axons to inhibit both the
lateral/tuberal hypothalamus and the ascending chemical pathways.
third major sleep center
PAG
PAG
action
sends GABA-ergic axons to the ascending pathway, but not to the orexin-producing hypothalamus
PAG
result
it induces REM sleep, like the PPN
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
The PPN is the beginning of what pathway?
pontogeniculocalcarine pathway
the PPn activates what cells in the medulla?
n. gigantocellularis
n. gigantocellularis
messages what?
the lateral reticulospinal tract which inhibits extensors mm. = paralysis during REM sleep
skeletal muscle Ach receptors? AKA
nicotinic
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.
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
What is DHP?
voltage-sensitive, integral membrane protein w/ cytosolic domain that contacts a ryanodine
recetpor on the SR(sarcoplasmic reticiulum)
Ryanodine Receptor is?
protein embedded in SR membrane. A true Ca2+
channel: comes in tetrads too
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!
What are the steps of AP—>skeletal muscle contraction?
- AP enters skeletal muscle
- AP enters T-tubule & reaches DHP receptor
- DHP changes conformation
- DHP cytosolic domain causes a Ryanodine conformation change too
- Ryanodine opens
- Ca2+ pours out of SR into cell
- Ca2+ binds to Troponin at TnC
- Troponin changes conformation
- Tropomyosin is moved out of the way
- Myosin can bind to actin
- Skeletal muscle contraction
What must be pumped back into the SR?
Ca2+
As Ca2+ levels decrease, what can change conformation?
troponin
What sits in the groove in troponin blocking myosin from binding?
tropomyosin
What happens when myosin isn’t binding to troponin?
muscle relaxation
How long is the delay from Ca2+ peak to muscle contraction?
200ms
how do we turn “all-or-none:” AP’s into graded contractions?
1) Temporal Summation
2) Organization of Skeletal Muscle
3) Length/tension Relationships
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.
What leads to tetany?
Extremely high level of APs.
All the myofibrils that are fired by the same motor neuron =
motor unit
T or F
All motor units are the same size.
F
The heavier the weight (force) against the muscle _____
the slower the velocity of contraction
not many myosin heads can get a hold of the actin filaments =
weak contraction
White muscle AKA
Fast-Twitch Glyoclytic
Red muscle AKA
Slow-Twitch Oxidative
Which type of muscle runs glycolysis for main source of energy?
White
Which type of muscle is highly vascular?
Red
Which type of muscle is for endurance?
Red
Which type of muscle has lots of myoglobin?
Red
Which type of muscle produces lots of lactic acid?
White
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)
What is a powerful phosphorus storing molecule important in skeletal muscle?
creatine
Smooth Muscle has no ______ (part of the sarcomere)
Z-lines
What does smooth muscle have instead of Z-lines?
dense bodies
What is smooth muscle’s normal state?
contracted
What does Ca2+ bind to in smooth muscle?
calmodulin (instead of troponin)
Active calmodulin turns on what in smooth muscle?
myosin light chain kinase
What is the purpose of myosin light chain (MLC) Kinase?
1) phyosphorylating and activating a myosin chain
2) increasing the myosin’s ATPase activity
MLC phosphatase function
removing ATP from the myosin
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
how does Phospholipase C work?
cleaves phospholipid to DAG & IP3
; IP3 diffuses to SR, turns on a receptor at SR, allowing Ca2+ release
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
T or F
Repeated stimulus generates the same temporal
summation in Smooth that we saw in Skeletal muscle.
T
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
Myofibril
def
myofibrils are bundles of myofilaments
Sarcoplasmic Reticulum
def
smooth ER surrounding myofibril
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)
Actin
units/stains
up to 3000 units per myofibril; stains lightl
Myosin
units/stains
up to 1500/myofibril; contains crossbridges; stains dark
T-tubules
invaginations of the cell membrane; important in upcoming pathways (AP travels to here)
Sarcomere
basic contractile unit of muscle; extends from Z-disc to Z-disc; resting length = 3.2-3.5μm
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
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
The light stain creates
the I-band
the I-band =
actin that is not overlayed by myosin = straddles 2 sarcomeres
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
The dark stain creates
the A-band
the A-band =
all of myosin + the part of actin overlayed by myosin
H-band =
portion of myosin not overlaying actin; this band shortens during contraction
Alternating sequence of actin/myosin creates
a light-dark-light-dark pattern = striped or “striated”
mm.
one actin filament =
2 F-actins + 2 tropomyosins, and many
troponin triplets
F-actin contains
myosin binding sites
Tropomyosin
two of these filaments run along grooves in the F-actin; they cover the myosin binding sites
What covers the myosin binding sites?
tropomyosin
Troponin
a triplet of proteins that sit on top of tropomyosin
What are the three subunits of troponin?
- TnCa
- TnT
- TnI
TnCa
has affinity for
Ca2+
TnT=
sits on tropomyosin
TnI =
intermediate/intercalated sits between troponin triplets and the myosin head
Myosin
(thick filament)
contains
2 heavy + 2 light chains;
Myosin forms crossbridges with the capability of
latching onto actin
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
What causes shortening of the H-band?
myosin heads pulling the actin closer together
The sarcomere contracts to what length during max contraction?
3.2-3.5μm down to 2.0-2.2μm
The pulling in of actin by the myosin heads is a process known as….
ratcheting
When a skeletal muscle is excited Ca2+ binds
TnCa, causing it to reconfigure
When TnCa reconfigures it causes what?
tropomyosin to be moved out of the way, exposing the myosin binding sites on the F-actin
