golf clubs the head acts as a bridge between myosin and actin
What are the two active sites on the head of a myosin molecule?
1. actin binding site 2. myosin ATPase site for binding and cleaving ATP
composed of actin, tropomyosin, and troponin
composed of actin molecules (which are globular proteins) each molecule has a binding site for a myosin head
thread-like proteins that lie end to end they wrap around the actin helix
acts as a regulatory protein for muscle contraction by covering the binding sites on actin
regulatory protein for muscle contractions
What is troponin composed of?
troponin T, troponin I, and troponin C
binds to tropomyosin
binds to actin
binds to Ca++
forms a complex with tropomyosin which can cover the actin binding sites i.e. the troponin-tropomyosin complex
Status of relaxed muscle
intracellular Ca++ is low so the troponin/tropomyosin complex covers binding sites on actin helix prevents any "crossbridging" between actin and myosin
First step of muscle contraction
increase in intracellular Ca++
Second step of muscle contraction
troponin-tropomyosin complex undergoes aconformational change that uncovers binding sites on actin helix
Third step of muscle contraction
heads of myosin molecules then attach to binding sites on actin
Fourth step of muscle contraction
Attachment of myosin head triggers conformational change in myosinthat causes head to "tilt" (power stroke) Tilting moves actin filament along myosin filament thus shortening the sarcomere. Tilting also releases ADP from myosin head
Fifth step of muscle contraction
ATP molecule now binds to myosin head. ATP binding causes head to detach from binding site on actin helix ATP is then cleaved to ADP, causing the head to return to the non-tilted conformation.
How many times does the process of muscle contraction occur?
repeatedly as long as Ca++ is present
"Walk along" theory of muscle contraction
the idea of myosin heads pulling themselves along actin fibers to contract muscles
stiffness of muscles occurring approximately 3 to 12 hours afterdeath
Rigor Mortis cause
Ca++ leaks into ICF and stimulates contraction Existing ATP is utilized but without new ATP being generated, there is no way for the myosin to detach from the actin to relax the muscle
location where motor neuron innervates each skeletal muscle fibers
Neuromuscular junction components
1. axon terminal of motor neuron 2. "Motor end plate" of muscle
Neuromuscular junction mechanism
action potential in neuron Ca++ influx into axon terminal release of acetylcholine to nicotinic receptors on motor end plate, opening ligand gated ion channels allowing large amounts of Na+ and small amounts of K+ in generating an "end plate potential"
graded potential larger than EPSP of neuron (+50 to +75 mV)
this initiate action potentials in adjacent areas of cell membrane ensures that a single action potential will cause a twitch in the muscle fiber
What are end-plates stimulated by?
Drug that blocks release of acetylcholine in neuromuscular junction
Botulinum toxin (less than 1 billionth of a gram can be lethal) paralyzes diaphragm 19,000 liters is enough to kill 3x the population of Earth
Drug that increases release of acetylcholine in neuromuscular junction
Black widow spider venom muscle spasms followed by fatigue
Drugs that block nicotinic receptors
Curare- plant extract used in poison arrows Alpha-bungarotoxin- venom in some poisonous snakes
Transverse Tubules (T-tubules)
conduct the action potential deep into fiber
extension of cell membrane, but they run perpendicular from surface deep into the center of muscle fiber.They carry action potential which stimulates sarcoplasmic reticulum
specialized ER for intracellular storage of Ca++
What is the ratio of Ca++ in the SR to the cytosol at rest?
10,000 : 1
How do T-tubules and SR interact?
causes release of Ca++ from lateral sacs of SR
Purpose of SR
releases Ca++ to initiate muscle contraction
Ca++ is pumped back into SR when at rest
found in the walls of many viscera forms ciliary and iris muscles of eye, piloerector muscles in skin, etc
Structure of Smooth Muscle
composed of small muscle fibers
each cell has a single nucleus contains actin and myosin but not organized into myofibrils
Diameter and length of smooth muscle fibers
2 to 5 um in diameter20 to 500 um in length
Why are there no striations in smooth muscle?
there are no myofibrils
Where is actin attached to in smooth muscle?
Why are smooth muscles specialized for slow prolonged contractions?
no t-tubules and poorly developed SR
Smooth Muscle Contraction
Ca++ from the ECF binds to intracellular Ca++ receptor (the receptor is “calmodulin”) Ca++/calmodulin complex activates the enzyme “myosin kinase” that then activates myosin.Once activated, the myosin then binds to actin and undergoes a power stroke
General Characteristics of Smooth Muscle Contraction
slower more prolonged strokes uses less energy forms an electrical “syncytium”
some is autorhythmic
Pharmacology relating to smooth musclem
Calcium channel blockers such as “verapamil” block the influx of Ca++ intosmooth muscle cells. Used for vasodilation, lowering blood pressure, and reducing angina
found only in heart hybrid between skeletal and smooth muscle
Cardiac muscle/skeletal muscle similarities
It contains myofibrils (so it is striated). Ca++ activates contraction by binding to troponin C.It has well-developed sarcoplasmic reticulum and t-tubules quick powerful contractions
Cardiac muscle/smooth muscle similarities
autorhythmic cells are connected via gap junctions, forming electrical syncytium
Unique to cardiac muscles
relatively short and branched muscle fibers (cells) which normally containone or two nuclei Individual cells are connected to one another by “intercalated discs
specialized cell membranes containing gap junctions and desmosomes
Cardiac action potential
long duration (250 msec) display a "plateau" which allows for a prolonged muscle contraction (300 msec)
Reason for plateau in cardiac muscle
Ca++ channels are slow to open and close steady influx of Ca++ at peak of potential causes the plateau
Want to see the other 54 Flashcards in Lecture 15 (Exam 3)?JOIN TODAY FOR FREE!