Talbot - Excitable Cells and Muscle Contraction Flashcards
what are 5 types of excitable cells
neurons, cardiac, smooth, skeletal muscle and beta pancreatic cells
what does it mean to be an excitable cell
capable of developing an action potential across a plasma membrane with voltage-gated channels
what is the plasma membrane called in muscles
sarcolemma
what are muscle cells called and how many nuclei do they have
myofiber with many nuclei (*syncytium - mass of cytoplasm containing many nuclei)
what makes up a myofiber
myofibrils
what are myofibrils made of
end-to-end sarcomeres (created striations)
what are the two domains in skeletal muscle
sarcolemma and sarcoplasmic reticulum (SR)
what 3 types of channels are located in the sarcolemma
invaginations called T-tubules with Cl- channels (ClC-1) and Na+ and K+ channels
where is Ca2+ stored in the muscle
in the sarcoplasmic reticulum
what are the 2 domains within the sarcoplasmic reticulum
longitudinal elements and terminal cisternae (end sacs)
what makes up a triad in the sarcoplasmic reticulum
1 T-tubule + 2 terminal cisternae of SR regions
how is the resting membrane potential different in skeletal muscle from neuronal
it is more negative or more hyperpolarized (-90mV vs -70mV)
why is the resting membrane potential more negative in skeletal muscle than neurons
increased K+ gradient (higher [K+]) and increased Cl- gradient (lower [Cl-]) = higher permeability to Cl- than most cells
what is the difference in action potentials for skeletal muscles and neurons
the skeletal muscle does not hyperpolarize - the Vm is much closer to Ek than neuronal (the K+ channels allow for repolarization)
are skeletal muscles neurogenic action potentials or myogenic action potentials
neurogenic - they need a neurotransmitter (acetylcholine) to induce action potential
are cardiac muscles neurogenic action potentials or myogenic action potentials
myogenic - they can spontaneously produce an action potential
how are cardiac muscles connected
they are branched and the myocytes connect through intercalated discs
what are the 2 types of connections in the cardiac intercalated discs
gap junctions and desmosomes
why are the gap junctions important in cardiac muscle
they allow direct electrical coupling (AP jumps to neighboring cells) of myocytes and rapid conduction of AP’s
why are desmosomes important in cardiac muscles
allow force transfers between cells and keep them from pulling apart when heart contracts
what are 3 types of cardiac muscle cells
autorhythmic, conduction, and contractile
what are autorhythmic cells
pacemaker or nodal cells found in SA and AV nodes - spontaneously depolarize to generate AP
what are contractile cells
the main cell type in cardiac muscle - striated and get depolarized through gap junctions
what is unique about the action potentials in autorhythmic cells
don’t maintain a stable resting potential - has pacemaker potential instead and AP is longer than neuron or skeletal muscle
what channel does the autorhythmic cell have that is permeable to Na and K
If channels -> creates a slow net depolarization
what type of Ca channels are in the autorhythmic cells
Fast Ca2+ channels *only type of cell where depolarization is carried by Ca and not Na
what is different about contractile action potentials
they have slow L-type Ca2+ channels that open in response to depolarization and keeps membrane depolarized creating a plateau phase (fast K channels have closed prolonging the phase)
what is different about EC coupling in cardiac cells vs skeletal muscle cells
DHP receptors and ryanodine receptors in SR are not physically coupled
what is tetanus in skeletal muscles
state of prolonged muscle contraction that occurs when high frequency of incoming AP’s keeps membrane depolarized - allowing continued efflux of Ca2+ from SR
what is excitation-contraction (EC) coupling
mechanism that allows the excitation of muscle membrane (production of AP) to induce release of Ca2+ from SR = muscle contraction
how is Ca2+ released during the EC coupling in skeletal muscle
the depolarization is sensed by DHP receptors in T-tubule - conformational change in DHP - physically pushes on ryanodine (RyR) receptor inducing it to open and Ca2+ enters cytoplasm
where are acetylcholine receptors located on the muscle cell and what are they called
at the motor end plate - ACh receptor or nicotinic AChR
what is a sarcomere
contractile unit of muscle (skeletal and cardiac) actin, myosin, and other accessory proteins
what 2 binding proteins are located on actin filaments
tropomyosin and troponin complex (Tn T, Tn I, and Tn C)
what does tropomyosin do
runs along side of 2 strands of actin and physically blocks myosin binding sites “steric hindrance” in the absence of Ca2+
what does troponin do
the Tn C subunit binds to Ca2+ to pull tropomyosin off myosin binding sites
what are the + end and - end binding proteins on actin
+ end = tropomodulin
- end = CapZ and alpha actinin
what is neculin accessory protein
an actin stabilizing protein - helps set the length of actin
what is titin accessory protein
runs Z-disc to middle of thick myosin filament - helps set length of myosin and helps pull sarcomere back to resting length at end of contraction
what is myomesin accessory protein
stabilizes the sarcomere - visible as M line
what is the A band
length of myosin filament - dark region in middle of sarcomere, may overlap actin
what is the I band
region of actin that does not overlap myosin - light region - spans 2 sarcomeres A-band to A-band
what is the H band/zone
lighter region in middle of A band - myosin does not overlap actin (only myosin)
what is the Z disc/line
end of sarcomeres - point of actin attachment
what happens during the sliding filament muscle contraction
myosin heads walk along actin pulling Z-discs closer to each other - shortens H zone and I band increasing amount of overlap
are actin and myosin touching/interacting when muscle is at rest
no
what is happening to the myosin head when muscle is at rest
has bound and hydrolyzed ATP and still has the ADP and Pi non-covalently bound to it = high energy phase - “cocked” myosin head
what induces myosin head to release Pi and ADP and attach to actin
Ca2+ (released from SR) exposing the myosin binding sites on actin
what is the myosin low energy conformation
rigor - myosin head is “stuck” on actin and cannot release without ATP present
how is contraction different in smooth muscles
+ ends of actin attach to dense bodies and terminate at protein plaques - actin only has tropomyosin (no troponin) - and maintains contraction longer
where is single unit (unitary) smooth muscle located
walls of visceral organs and blood vessels - use gap junctions
where is multi-unit smooth muscle located
trachea, iris, ciliary body, piloerector of skin and some blood vessels
which type of smooth muscle is myogenic and which is neurogenic
single unit = myogenic
multi-unit = neurogenic
what is the depolarization phase carried out by in smooth muscle
Ca2+
