Lecture 6-8 Flashcards
Myocyte
muscle cell
Sarcoplasmic Reticulum
ER in muscle cells that stores calcium
Striated and Non-striated Muscles
S- skeletal and cardiac
Non- smooth
Muscle Fibers
long, thin cell with multiple nuclei and myofibrils
Myofibrils
consist of many sarcomeres surrounded by sarcoplasmic reticulum and t-tubule system
Sarcomere
functional unit of muscle
smallest part of muscle that can still perform its function
Contractile Protein Structure
thick and thin filaments
Thick Filaments
myosin
heavy chains w/ globular heads that bind actin and have ATPase activity
Thin Filaments
Actin- 2 strands of F actin in a helix
Tropomyosin
Troponin Complex
F Actin
made of G actin
has myosin binding sites
Tropomyosin
double stranded helix around actin
covers myosin binding site
Troponin Complex
binds to tropomyosin
Troponin T
binds complex to tropomyosin
Troponin I
Holds tropomyosin in myosin binding site
Troponin C
binds calcium, uncovers myosin binding site
Dystrophin
connects sarcomere to sarcolemma and ECM
mutations cause muscular dystrophy
Nebulin
holds thin filaments apart from each other
Alpha- Actinin
holds thin filaments to z-disc
Titan
spring that runs through heavy chain and connects it to z-disc
M Line
bisects sarcomere and bare zone
right down the middle
Bare (H) Zone
only heavy chains
center, no heads
A Band
thick and thin filaments
dark striation
I Band
only thin filaments
light striation
Z-Disc
borders- connects individual sarcomeres
bisects I band
Terminal Cisternae
ends of sarcoplasmic reticulum
has RyR receptor
RyR Receptor
RyR, calcium release channel
Triad
t-tubule and SR (2 terminal cisternae)
Changes of DHPR
changes RyR shape due to tight packing in t-tubule system
Calcium Binding Proteins
keep free Ca low in SR
Calcium reuptake and release
reuptake- longitudinal sections
release- terminal areas
Cross Bridge Cycling
myosin binds actin and pulls it toward M line
Sliding Filament Theory
actin and myosin slide past each other, pulling z-discs together
force transferred to CT around fiber
entire muscle eventually shortens and moves bones
Cross Bridge Cycling at rest
tropomyosin cover binding site on actin
myosin has bound ATP and is cocked; has high affinity for actin
Cross Bridge Cycling- calcium binding
Ca binds TnC, moves tropomyosin off actin’s myosin binding pocket
myosin - ATP to ADP and binds actin
Cross Bridge Cycling- power stroke
myosin releases ADP and ratchets, pulling actin toward M line
Cross Bridge Cycling- reloading
myosin binds ATP and releases actin; recocked
Cross Bridge Cycling- Relaxation
Ca stays in SR by SERCA, no Ca to bind
tropomyosin covers actin binding site
contraction stops
Tetanus
recruiting multiple units or stim same unit multiple times to get mvmt
Isotonic Contraction
enough force is generated to move weight
force velocity relationship
Isometric Contraction
same length
not enough force to move weight
length tension relationship
Smooth Muscle
no control no sarcomere operate effectively when stretched fatigue resistant make resting tone- stay partially contracted
Single Unit
Smooth M cells linked by gap junction little inn some can make own AP contract together
Multi Unit
Smooth M
each cell has own inn
function as distinct muscle cell
E-C Coupling in Smooth M
Ca enters cytoplasm- depolarization
cytoplasm releases Ca from SR
Ca binds to Calmodulin, which activates MLCK
MLCK
controls cross bridge cycling in smooth muscle
Calcium Entry into Smooth M
2nd Messenger Gated Channels
NT activate Gq receptors which make IP3
IP3 channels open on SR
IP3 dependent Ca opens other Ca channels
Cross Bridge Cycling in Smooth M
Ca binds and activates calmodulin
calmodulin activates MLCK
MLCK phosphorylates myosin, increasing its ATPase activity
Relaxation in Smooth M
when MLCK is no longer active
low ICF Ca
myosin dephosphorylated by myosin phosphatase
Phasic Contractions
spike of Ca, single contraction, relaxation
Tonic Contractions
spike of Ca, maintain force
latch state
Latch State
allows for resting muscle tone to be generated at lower metabolic cost
Length- Tension Relationship of Smooth M
cant overstretch smooth m
can generate max force at any length
no sarcomeres allow for proper alignment at all preload
Force- Velocity Relationship of Smooth M
velocity of contraction increases with more myosin phosphorylated
Hypercalcemia
threshold more negative
less excitable
Hypocalcemia
threshold less negative
more excitable
Cardiac Muscle
gap junctions at intercalated disk contract on its own longer AP fatigue resistant- more mitochondria RMP -90mV
Cardiac M AP Phase 4
RMP same as other cells
K leak channels
Cardiac M AP Phase 0
Upstroke
Na channels open
Cardiac M AP Phase 1
early repolarization
K channels open
Cardiac M AP Phase 2
Plateau
Ca channels open
SR dump
Cardiac M AP Phase 3
late repolarization
K channels open
Absolute Refractory Period of Cardiac M
200 msec
prevents tetany
Opening RyR channels in cardiac m
need ECF Ca
phase 1 and 2
Effective Refractory Period
no conducted potential can generate AP
Relative Refractory Period
AP can fire if a greater than norm stim is provided
shorter plateau
Supranormal Period
cell is more excitable than normal
not yet reach RMP
Frank Starling Law
heart generates more force when preload is increased
Cardiac Pacemakers
electrical conduction system of heart Sinoatrial Node no SR unstable RMP depolarize at set rate
Phases of Cardiac Pacemakers
4- Unstable RMP; K close, Na and Ca open
0- Fire AP; Ca open
3- Repolarize- K open
PNS Synapses of SA Node
M2 receptors
increase K, decrease Na and Ca
SNS Synapses of SA Node
B1 receptor
increase Na and Ca
