muscles and bones biology Flashcards
muscle contraction - steps
neurotransmitter release –> postsynaptic ligand –> depolarization –> Ca2+ release from sarcoplasmatic reticulum –> troponinin C to tropomyosin system –> displacement of myosin on the actin filament –> myosin binds and hydrolyses ATP
muscle contraction - neurotransmitter release is caused by
action potential depolarization opens presynaptic voltage-gated Ca2+ channels, inducing neurotransmitter release
muscle contraction - postsynaptic ligand leads to
muscle cell depolarization in the motor end plate
muscle contraction - depolarization process
it starts from ligand binding –> depolariztion travels along muscle cell and down the T - tubule
muscle contraction - depolarization result to –>
depolarization of the voltage-sensitive dihydropyridine receptor, mechanically coupled to the ryanodine receptor on the sarcoplasmic reticulum –> conformation change
–> Ca2+ release from sarcoplasmic reticulum
muscle contraction - Ca2+ action (and mechanicals changes)
released Ca2+ binds to troponin C causing a conformation change that moves tropomyosine out of the myosin-binding groove on actin filaments
muscle contraction - myosin action
myosin release bound ADP and inorganic PO4(3-) –> displacement of myosin on the actin filament (power stoke) –> binding a new ATP causes detachment of myosin head from actin filament –> hydrolysis –> high energy position (cocked) for the next cycle
sarcomere anatomy - M line
M line: middle line
sarcomere anatomy - H band
myosin between myosin heads (in the middle of the sarcomere)
sarcomere anatomy - A band
all myosins (in the same sarcomere) (thick filaments)
sarcomere anatomy - I band
from the end of the myosins of the one sarcomere to the end of the myosins of the next sarcomere
sarcomere anatomy - Z lines
the lines of sarcomere
transverse (T) tubules?
extensions of plasma membrane part of juxtaposed with terminal cisternae (part of sarcoplasmic reticulum)
Terminal cisternae are
enlarged areas of the sarcoplasmic reticulum surrounding the transverse tubules
T tubules and Terminal cisternae - numbers
in skeletal muscle: 1 T + 2 terminal cisternae (triad)
in cardiac muscle: 1 T + 1 terminal cisternae (diad)
contraction - appearance of bands
- shortening of H band + I band + sarcomere
- A band remains the same length
H band after contraction
shorter
A band after contraction
same
I band after contraction
shorter
sarcomere band after contraction
shorter
muscle contraction - postsynaptic ligand binding leads to muscle cell depolarization in the
motor end plate
muscle depolarization travels muscle cell and down the
T-tubule
muscle cells - T-tubule receptor
dihydropyridine receptor
muscle cells - sarcoplasmic reticulum receptor
ryanodine receptor
Types of muscle fibers
- type 1 muscle
2. type 2 muscle
sarcomere - thick filaments
myosin
sarcomere -thin filaments
actin
types 1 vs type 2 - functional characteristic
type 1 - slow twitch
type 2 - fast twitch
types 1 vs type 2 - colour (why)
type 1 - red (increased mit and myoglobin)
type 2 - white (decreased mit and myoglobin)
types 1 vs type 2 - metabolism (why)
type 1 - oxidative phosph (increased mit and myoglobin)
type 2 - anaerobic glyc (increased mit and myoglobin)
muscle fibers with sustained contraction
type 1
muscle fibers - weigh training results in
hypertrophy of fast-twitch (2) muscle fibers
fast twitch muscle fibers - type?
2
slow twitch muscle fibers - type?
1
Osteoblasts action
build bone by secreting collagen and catalyzing mineralization
bone mineralization is process in which
crystals of calcium phosphate are produced and laid down within the bone’s fibrous matrix
Osteoblasts - differentiate from
mesenchymal stem cells
Osteoblasts - differentiate from (where)
mesenchymal stem cells
in periosteum
osteoclasts appearance
multinucleated cells
osteoclasts action
dissolve bone by secreting acid and collagenases
osteoclasts - differentiate from
monocytes
macrophages
parathyroid hormone action on bone
- low, intermittent levels –> anabolic effects (building bone) on osteoblasts and osteoclasts (indirect)
- chronically increased PTH (1ry hyperparath) –> catbolic effect (osteitis fibrosa cystica
estrogen action on bone
- inhibits apoptosis in osteoblasts
2. induce apoptosis in osteoclasts
bone - estrogen deficiency –>
excess cycles of remodeling –> bone resorption leads to osteoporosis
bone - multinucleated cells
osteoclasts
bone - monocytes and macrophages are differentiate to
osteoclasts
bone - mesenchymal stem cells are differentiate to
osteoblasts
bone formation - types
- endochondral ossification
2. Membranous ossification
bone formation - membranous ossification - which bones
bones of calvarium and facial bones
bone formation - endochondral ossification - which bones
bones of axial and appendicular skeleton and base of the skull
bone formation - membranous ossification - mechanism
woven bone formed directly without cartilage. Later remodeled to lamellar bone
bone formation - endochondral ossification - mechanism
Cartilaginous model of bone is first made by chondrocytes. Osteoclasts and osteoblast later replace with woven bone and then remodel to lamellar bone
woven bone is also called
fibrous bone
in adults woven bone occurs after
fractures and in Paget disease
smooth muscle contraction process
membrane depolarization –> L-type voltage gated Ca2+ channe –> increased intracellular Ca2+ –> increased Ca2+-calmodoulin complex –> activation of MLCK –> Myosin - p (+ actin) –> contraction (via cross bridging)
MLCK
myosin-light-chain- kinase
MLCK (myosin-light-chain- kinase) action
myosin+actin –> myosin-P+actin
Smooth muscle cell - vasodilator
Nitric oxide (NO)
Ca2+ vs NO on smooth muscle contraction
Ca2+ –> contraction
NO –> relaxation
NO associated relaxation of smooth muscles - process
NO –> activation of Guanylate cyclase –> increased cGMP (from GTP) –> activation of MLCP –> Myosin+actin (no Pi) –> relaxation
MLCP
myosin-light-chain-phosphatase
MLCP (myosin-light-chain-phosphatase) action
Myosin-P+actin –> Myosin+actin
MLCP vs MLCK according action and results
MLCP –> Myosin-P+actin –> Myosin+actin –> relaxation
MLCP –> myosin+actin –> myosin-P+actin –> contraction
NO synthase - action
L-arginine –> NO
