Flashcards in NMP Duke final Deck (105):
Types of Sleep
normal sleep + REM sleep
θ-waves; considered; light sleep; broken into stages I and II
α with θ; the θ waves characteristic of light sleep are taking over the awake brain
θ with spindles (spindles are alpha bursts; its like the awake doesn't want to let go)
δ-waves; considered deep sleep; broken into stages III and IV
δ with spindles; deeper sleep is setting in but
α still tries to burst in
A person gets more out of sleep if they go through these stages _____________
Physiologic Properties of Deep Sleep
↓ 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)
paradoxical sleep, or
2-3 minutes, up to 30 mins (rarely longer than 10 mins)
β-waves come heavily from
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
Regulation of Wakefulness vs. Sleep Centers
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
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
(anterior medial hypothalamus)
It sends GABA-ergic axons to inhibit both the
lateral/tuberal hypothalamus and the ascending chemical pathways.
third major sleep center
sends GABA-ergic axons to the ascending pathway, but not to the orexin-producing hypothalamus
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?
the PPn activates what cells in the medulla?
the lateral reticulospinal tract which inhibits extensors mm. = paralysis during REM sleep
skeletal muscle Ach receptors? AKA
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?
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
What must be pumped back into the SR?
As Ca2+ levels decrease, what can change conformation?
What sits in the groove in troponin blocking myosin from binding?
What happens when myosin isn't binding to troponin?
How long is the delay from Ca2+ peak to muscle contraction?
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 =
T or F
All motor units are the same size.
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 =
White muscle AKA
Red muscle AKA
Which type of muscle runs glycolysis for main source of energy?
Which type of muscle is highly vascular?
Which type of muscle is for endurance?
Which type of muscle has lots of myoglobin?
Which type of muscle produces lots of lactic acid?
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?
Smooth Muscle has no ______ (part of the sarcomere)
What does smooth muscle have instead of Z-lines?
What is smooth muscle's normal state?
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.
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
myofibrils are bundles of myofilaments
smooth ER surrounding myofibril
make up the myofibril of a muscle fiber/cell; there are 2 kinds and they are always in a 2:1ratio (actin:myosin)
up to 3000 units per myofibril; stains lightl
up to 1500/myofibril; contains crossbridges; stains dark
invaginations of the cell membrane; important in upcoming pathways (AP travels to here)
basic contractile unit of muscle; extends from Z-disc to Z-disc; resting length = 3.2-3.5μm
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
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 =
actin that is not overlayed by myosin = straddles 2 sarcomeres
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 =
all of myosin + the part of actin overlayed by myosin
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"
one actin filament =
2 F-actins + 2 tropomyosins, and many
myosin binding sites
two of these filaments run along grooves in the F-actin; they cover the myosin binding sites
What covers the myosin binding sites?
a triplet of proteins that sit on top of tropomyosin
What are the three subunits of troponin?
has affinity for
sits on tropomyosin
intermediate/intercalated sits between troponin triplets and the myosin head
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....
When a skeletal muscle is excited Ca2+ binds
TnCa, causing it to reconfigure