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27 Cards in this Set

  • Front
  • Back
describe the embryological development of muscle

how do satellite cells happen?
myoblasts fuse to form an extremely large muscle fiber--->multinucleate muscle

those that remain are reserved for tissue replacement--->Satellite cells
what is the membrane of skeletal muscle called?
sarcolemma
describe the order of muscle, from lowest to highest beginning with the structural unit of muscle.
myofilament

myofibril

myofiber

fasicle

multiple fascicles

gross anatomical structure
what is the composition of a myofibril?
comprised of myofilaments arranged in sarcomeres!!!

the fundamental contractional unit
describe how myofibrils are kept in register with each other
desmin, an IF, binds actin binding protein on Z disc of each sarcomere

plectin assembles desmin filaments into a network between myofibrils
CLINICAL

how is dystrophin and laminin-2 involved in skeletal muscle?

what are muscular dystrophies
dystrophin is a big proteins that formers the perimeter of myofibril complex. it is bound to an IMP call dystroglycan complex 2 which is linked to laminin-2. larmin-2 is anchored to ECM

when muscle contracts this complex keeps muscle cell from tearing its cell membrane

A DEFECT in any of these parts makes muscle cell fragile--->disoriented----->ruptures sarcolemma----->rush of calcium into cell----------->degeneration of skeletal muscle cell
HY

describe contraction
calcium ions bind to troponin, which induces underlying tropomysin complex to allosterically change and expose active binding sites

myosin heads bind at these sites and pivot. ATP binds heads and is hydrolyzed, resulting in myosin detaching from thin filaments and return to original posiiton
how is muscle relaxed?
calcium ions actively transported into sarcoplasmic reticulum and tropomyosin re-covers active sites
what composes a triad? why are they important?
triad: two terminal cisternae + one T-tubule. it runs thru the muscle btw surrounding myofibrils

these structures allow for smooth, instantaneous transmission of an action potential (which results in depolarization of sarcolemma) from the cell surface to all points within the cell. thus calcium will induce smooth coordinated contraction
what property of NMJ + motor endplates increases muscle response?
collaterals: magnify influence of one stimululs by forming NMJ with more than one myofiber
a muscle spindle is made of two types of fibers. NAME THEM (and describe them)!
extrafusal fibers (the ones that do the work)

intrafusal fibers (monitor level of contraction and/o load bearing capacity)
what shape denotates a smooth muscle cell?

how are they connected to each other? how does this contribute to concerted movement
fusiform (tapered cell with tapered, centrally located nuclei)

no striations

connected by adhering and gap junctions. signal comes from gap. force of contraction is integrated across large pop. of cells via adhering junctions=====>conglomerate behaves like a single cell (functional syncytium)
how do smooth muscles get their calcium?
cavaolae vesicles regulate the release of calcium from the sER, the functional equivalent of t-tublules

regulate the rele
describe the sequence of events in NM transmission
1. nerve impulse depolarizes nerve terminal

2. depolarization opens calcium channels

3. calcium enters and facilitates fusion of synaptic vesicle membrane with nerve terminal membrane

4. ACh is released from synaptic vesicles (exocytosis)

5. ACh binds to receptors on post-synaptic membrane (muscle)

6. ACh-receptor binding opens cation channels (Na and K)

7. Ion flow (+++ moves inside) causes depoarization of end plate membrane (EPP)

8. EPP triggers AP in rest of muscle cell

9. AChE hydrolyzes ACh into Acetate + choline
describe the functional unit of a nicotinic Ach receptor
multimeric, five protein subunits--->ligand-gated ion channel

the alpha subunit contains the ACh binding sites, after binding (it takes two, babe) the subunits change configuration and become an open channel
how is acetylcholine synthesized? where does this occur? how do substrates get to this place?
choline acetyltransferase occurs in the pre-synaptic terminal

choline enters cell from the cleft via a Na+/choline transporter (thus choline entering the cell is dependent of [Na])
CLINICAL

what do eserine (physostigmine) and neostigmine do?
they are anticholinesterases

initially enhance muscle contracting by inhibiting the action of AChE, but if too much is present then muscles experiences a tetanus and then relaxes into a non-responsive state as AchR receptors become unresponsive to AcH
CLINICAL

what does curare do?
block transmission by binding to postsynaptic receptor and preventing ACh from binding; thus reduces muscle depolarization below threshold (no muscle AP)

this induces muscle relaxation (used during surgery)
are EPP propogated?

do they have refractory period?

are activated end plate membranes permeable to anions?
NO

NO

NO
CLINICAL

what is the functional result of botulsim?

myasthenia gravis?
botulism: too little ACh released

MG: reduction in AChR
how do anticholinesterase drugs affect the EPP?
increase the magnitude and prolong the the depolarization
what is the effect of high Mn++, Co++ or Ni++ on presynaptic terminal?
they block calcium entry, thus block transmission
CLINICAL

how are hypercalcaemia and hypocalcaemia caused and what is the result of each?
hyper: serum [Ca] higher than normal--->muscle weakness

hypo: serum [Ca] lower than normal--->muscle become hyperexcitable and individual muscle fibers may randomly, spontaneously twitch (hypocalcaemic tetany)
differentiate epi, peri and edomysium. how is each sheath made?
endo: surrounds individual muscle fibers

peri: surrounds fascicles (bundles)

epi: surrounds the whole thing

fibroblasts make them
CLINICAL

describe how the following toxins affect the axon/NMJ:

tetanus

diptheria

tetrodotoxin

botulinum

black widow spider

alpha-bungarotoxin (snakes)
tetanus: blocks release of inhibitatory NT (leads to muscle spasms/cramps)

diptheria: interferes with schwann cells

tetrodo: blocks voltage-dependent sodium channels

botulinum: prevents AcH vesicle fusion in presynaptic membrane

black widow: promotes fusion of Ach vesicles in an uncoordinated way that results in painful muscle tetany

alpha-bungarotoxin: irreversible binds to Ach receptor on muscle membrane (prevents muscle contraction)
describe the hierarchy of muscle from individual cells
A fascicle is a group of muscle cells. Recall that a myofiber is one muscle cell. Myofilaments are the structural components of myofibrils, both of which are intracellular muscle components. A myotube is a muscle development term. In the embryo and fetus skeletal muscle cells are formed by myoblasts which increase in number and then fuse. This primitive skeletal muscle cell containing the cytoplasm and the nuclei of the myoblasts is called a myotube. Recall that adult skeletal muscle cells can be regenerated by satellite cell division to create a population of myoblasts which then fuse to form a myotube. By adding the correct amount of myosin and actin and organizing into multiple myofibrils, an adult skeletal muscle cell can be formed just like occurs in development.
differentiate the relative size of myofilaments, myofibers and myofibrils
Recall that a myofilament is either thick, composed mainly of myosin, & is around 15 nm, or thin, composed mainly of actin, & is around 7 nm. Myofibrils average 1.0 micron in diameter. Myofibers are all larger. Human muscle cells are between 50 - 100 microns in diameter.