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Physiology > Chapter 1- Skeletal and Smooth Muscle > Flashcards

Chapter 1- Skeletal and Smooth Muscle Flashcards

1
Q

resting membrane potential

A

-the potential difference across the membrane of excitable cells (like nerve and muscle) at rest
-established by diffusion potentials created by concentration differences of ions across the membrane
-Ions with highest permeabilities or conductances at rest -> greatest contribution to resting membrane potential
-lowest permeabilities -> little or no contribution
-resting membrane mostly- range of −70 to −80 mV.
-At rest- far more permeable to K + and Cl − than to Na + and Ca 2+ due to the resting membrane potential

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2
Q

action potential

A

-phenomenon of excitable cells like nerve and muscle
-rapid depolarization (upstroke) -> repolarization -> resting
-transmission of information in the nervous system and muscle
-3 characteristics:
-stereotypical size and shape
-propagation
-all-or-none response

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3
Q

depolarization

A

process of making the membrane potential less negative

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4
Q

hyperpolarization

A

process of making the membrane potential more negative

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5
Q

inward current

A

flow of positive charge into the cell

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6
Q

outward current

A

flow of positive charge out of the cell

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7
Q

threshold potential

A

-membrane potential at which the action potential is inevitable
-less negative than the resting membrane potential -> inward current is required to depolarize the membrane potential to threshold

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8
Q

refractory period

A

period when another normal action potential cannot be elicited in an excitable cell

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9
Q

Stereotypical size and shape

A

-Each action potential for a cell type looks identical
-depolarizes to the same potential
-repolarizes back to the same resting potential

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10
Q

propagation

A

-action potential at one site causes depolarization at near sites
-brings adjacent sites to threshold

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11
Q

all or nothing response

A

An action potential either occurs or does not occur

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12
Q

action potential steps

A
  1. resting membrane potential
  2. upstroke of the action potential
  3. repolarization of the action potential
  4. hyperpolarization afterpotential (undershoot)
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13
Q

action potential: step 1: resting membrane potential

A

-At rest- −70 mV
-K + conductance/permeability is high
-K + channels almost fully open -> K + diffuse out down its concentration gradient -> creates K + diffusion potential -> drives the membrane potential towards K + equilibrium potential
-At rest, Na + conductance is low, -> resting membrane potential is far from the Na + equilibrium potential, and Na + is far from electrochemical equilibrium

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14
Q

action potential: step 2: upstroke of the action potential

A

-inward current -> causes depolarization to threshold (approx −60 mV)
-rapid opening of Na+ activation gates of t
-Na + conductance increases higher than K + conductance
-inward Na + current -> membrane potential further depolarized toward Na + equilibrium potential of +65 mV.

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15
Q

action potential: step 3: repolarization

A

-upstroke is terminated
-repolarizes to resting level
-1. inactivation gates on Na + channels respond to depolarization by closing -> terminates upstroke
-response is slower than the opening of the activation gates
-2. depolarization opens K + channels and increases K + conductance higher than occurs at rest
-closing of the Na + channels + greater opening of the K + channels -> K + conductance much higher than the Na + conductance
-> outward K + current results -> repolarized.

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16
Q

hyperpolarization afterpotential (undershoot)

A

-K + conductance is higher than at rest
-membrane potential is driven even closer to the K + equilibrium potential (hyperpolarizing afterpotential)
-then K + conductance returns to resting
-membrane potential depolarizes slightly back to the resting
-ready, if stimulated, to generate another action potential

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17
Q

voltage-gated Na + channel

A

-responsible for upstroke
-in order for Na + to move through the channel -> both gates on the channel must be open
-activation gates open quickly in response to depolarization
-inactivation gates close in response to depolarization, but slowly
-Regulated by changes in
membrane protentional
-Open during depolarization

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18
Q

repolarization

A

Repolarization back to resting causes inactivation gates to open
-Na + channels return to closed and are ready for another action potential

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19
Q

refractory period

A

-excitable cells are incapable of producing action potentials
-absolute refractory period- closure of inactivation gates of the Na + channel in response to depolarization. These inactivation gates are in the closed position until the cell is repolarized back to the resting membrane potential and the Na + channels have recovered to the “closed, but available” state.
-relative refractory period- overlaps with hyperpolarizing afterpotential, action potential can be elicited, but only for greater than usual depolarization. Higher K + conductance than is present at rest. Because the membrane potential is closer to the K + equilibrium potential, more inward current is needed to bring the membrane to threshold for the next action potential to be initiated.

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20
Q

accommodation

A

-when a cell is depolarized slowly or is held at a depolarized level -> threshold potential may pass without an action potential having been fired
-occurs because depolarization closes inactivation gates on the Na + channels.
-If depolarization occurs slowly enough -> Na + channels close and remain closed
-upstroke of the action potential cannot occur because there are not enough Na + channels to carry inward current

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21
Q

propagation process

A

-spread of local currents from active regions to adjacent inactive regions
-Action potentials are initiated in the initial segment of the axon, nearest the nerve cell body
-propagate down the axon by spread of local currents

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22
Q

conduction velocity

A

speed at which information can be transmitted in the nervous system
-increasing conduction velocity:
-increasing the size of the nerve fiber
-myelinating the nerve fiber

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23
Q

synaspe

A

-information is transmitted from one cell to another
-electrical or chemical

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24
Q

electrical synapse

A

-allow current to flow from one cell to next via low resistance pathways -> gap junctions
-found in cardiac muscle
-some types of smooth muscle
-very fast conduction in these tissues

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25
Q

chemical synapse

A

-gap between presynaptic and postsynaptic -> synaptic cleft
-Information transmitted across synaptic cleft with neurotransmitters
-neurotransmitter diffuses across synaptic cleft
-not unidirectional

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26
Q

postsynaptic cell

A

-change in membrane potential on postsynaptic is either excitatory or inhibitory
-depends on neurotransmitter
-excitatory -> depolarization of postsynaptic cell
-inhibitory -> hyperpolarization of postsynaptic cell
-unidirectional (from presynaptic cell to postsynaptic cell).

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27
Q

motoneurons

A

-nerves that innervate muscle fibers
-motor unit- single motoneuron and the muscle fibers it innervates
-vary in size
-may activate a few or thousands of muscle fibers
-small motor units are involved in fine motor activities (e.g., facial expressions)
-large motor units are involved in gross muscular activities (e.g., quadriceps muscles used in running)

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28
Q

neuromuscular junction

A

synapse between a motoneuron and a muscle fiber

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28
Q

neurotransmitter

A

-substance that is released from the presynaptic terminal and binds to receptors on the postsynaptic terminal
-released by the presynaptic cell on stimulation
-response of the postsynaptic cell must mimic the in vivo response
-ACh
-biogenic amines
-amino acids
-neuropeptides.

28
Q

ACh

A

-only neurotransmitter used at the neuromuscular junction
-released from all preganglionic and most postganglionic neurons in the parasympathetic nervous system
-released from all preganglionic neurons in the sympathetic nervous system
-released from presynaptic neurons of the adrenal medulla

29
Q

Norepinephrine, epinephrine, and dopamine

A

-biogenic amines
-They share a common precursor: tyrosine
-share a common biosynthetic pathway
-the neurotransmitter secreted depends on which portion of the enzymatic pathway are present in a particular type of nerve or gland

30
Q

serotonin

A

-biogenic amine
-is produced from tryptophan
-produced in serotonergic neurons -> brain and GI

31
Q

histamine

A

-biogenic amine
-synthesized from histidine
-catalyzed by histidine decarboxylase
-present in hypothalamus
-also present in nonneural tissue like mast cells of GI

32
Q

glutamine

A

-amino acid
-major excitatory neurotransmitter
-central nervous system
-significant role in spinal cord and cerebellum

33
Q

glycine

A

-amino acid
-inhibitory neurotransmitter
-found in the spinal cord and brain stem

34
Q

GABA

A

-amino acid
-inhibitory neurotransmitter
-distributed widely in CNS in GABAergic neurons

35
Q

nitric oxide (NO)

A

-short-acting
-inhibitory neurotransmitter
-gastrointestinal tract and central nervous system

36
Q

neuropeptides

A

function as neuromodulators, neurohormones, and neurotransmitters

37
Q

purines

A

-ATP and adenosine
-neuromodulators in ANS and CNS
-ex. ATP is synthesized in the sympathetic neurons that innervate vascular smooth muscle

38
Q

skeletal muscle

A

-voluntary or reflex control
-each cell is innervated by a branch of a motoneuron
-Action potentials are propagated along the motoneurons-> release of ACh -> depolarization of the motor end plate -> initiation of action potentials in the muscle fiber

39
Q

excitation-contraction coupling

A

events occurring between the action potential in the muscle fiber and contraction of the muscle fiber
-mechanism that translates the muscle action potential into the production of tension

40
Q

muscle fiber

A

-muscle fiber- single unit
-is multinucleate
-contains myofibrils

40
Q

myofibrils

A

-surrounded by SR
-invaginated by transverse tubules (T tubules)
-contains interdigitating thick and thin filaments
-thick and thin filaments are arranged longitudinally and cross sectionally in sarcomeres

41
Q

sarcomeres

A

-repeating units of sarcomeres -> striated muscle (skeletal and cardiac)

42
Q

thick filaments

A

-contain myosin
-myosin has 6 polypeptide chains (one pair of heavy chains and two pairs of light chains)
-heavy-chain myosin- α-helical structure -> tail
-four light chains and the N terminus of each heavy chain form two globular heads on the myosin
-globular heads have actin-binding site -> cross-bridge formation -> binds and hydrolyzes ATP (myosin ATPase)

43
Q

actin

A

-globular protein
-in globular form- G-actin
-In thin filaments- G-actin is polymerized into two strands that are twisted into an α-helical structure -> form filamentous actin, called F-actin
-has myosin-binding sites
-at rest, the myosin-binding sites are covered by tropomyosin so that actin and myosin cannot interact

44
Q

tropomyosin

A

-filamentous protein
-along each actin filament
-At rest it blocks the myosin-binding sites on actin
-during contraction it must be moved out of the way so that actin and myosin can interact

45
Q

troponin

A

-complex of three globular proteins (troponin T, troponin I, and troponin C) located at regular intervals along the tropomyosin filaments.
-Troponin T (T for tropomyosin)- attaches troponin complex to tropomyosin.
-Troponin I (I for inhibition)- along with tropomyosin, inhibits the interaction of actin and myosin by covering the myosin-binding site on actin.
-Troponin C (C for Ca 2+ ) is a Ca 2+ -binding protein that plays a central role in the initiation of contraction -> When Ca 2+ increases -> Ca 2+ binds to troponin C -> conformational change in troponin complex
-conformational change moves tropomyosin out of the way -> permits the binding of actin to the myosin heads

46
Q

A bands

A

-in the center of the sarcomere
-contain the thick (myosin) filaments
-appear dark under polarized light
-Thick and thin filaments may overlap in the A band
-areas of overlap -> potential sites of cross-bridge formation

47
Q

I bands

A

-located on either side of the A band
-appear light under polarized light
-contain the thin (actin) filaments, intermediate filamentous proteins, and Z disks
-no thick filaments

48
Q

Z disk

A

-darkly staining structures
-run down the middle of each I band
-delineating the ends of each sarcomere

49
Q

bare zone

A

-center of each sarcomere
-no thin filaments
-no overlap of thick and thin filaments or cross-bridge formation

50
Q

M line

A

-bisects the bare zone
-contains darkly staining proteins that link the central portions of the thick filaments together.

51
Q

cytoskeleton proteins

A

-establish the architecture of the myofibrils
-ensure thick and thin filaments are aligned correctly and at proper distances with respect to each other

52
Q

transverse cytoskeleton proteins

A

-link thick and thin filaments
-form a “scaffold” for the myofibrils
-link sarcomeres of adjacent myofibrils

53
Q

dystrophin

A

-anchors myofibrillar array to the cell membrane
-actin-binding protein

54
Q

longitudinal cytoskeleton proteins

A

include two large proteins called titin and nebulin

55
Q

transverse (T) tubules

A

-extensive network of muscle cell membrane (sarcolemmal membrane)
-invaginates deep into muscle fiber
-responsible for carrying depolarization from muscle cell surface to interior of the fiber

56
Q

sarcoplasmic reticulum (SR)

A

-internal tubular structure
-site of storage and release of Ca 2+ for excitation-contraction coupling.

57
Q

action potential in the skeletal muscle fiber

A

-temporal relationships between action potential -> the increase in intracellular Ca 2+ (released from SR) and contraction of the muscle fiber
-action potential precedes the rise in Ca 2+ concentration which precedes contraction.

58
Q

steps of contraction

A

-action potential propagated to T tubules that carry the depolarization from the surface to the inside
-depolarization of T tubules -> confirmation change in voltage-sensitive dihydropyridine receptors
-open Ca release channels (ryanodine receptors) on SR
-Ca is released from SR -> increase of Ca in ICF
-Ca 2+ binds to troponin C on the thin filaments -> confirmation change in troponin complex
-Troponin C binds Ca (cooperative binding increases affinity for binding to the next Ca)
-tropomyosin moves -> myosin-binding sites on actin are exposed
-cross bridge cycling- myosin binds actin
-relaxation- Ca concentration low

59
Q

cross bridge cycling

A

-myosin binds actin - rigor state
-ATP bind to myosin -> conformational change
-myosin releases actin
-ATP hydrolyzed to ADP
-myosin binds actin again -> power stroke
-releases ADP -> unbinds actin
-repeat

60
Q

smooth muscle

A
  • has thick and thin filaments but not organized into sarcomeres -> non striated
    -produce motility + maintain tension
    -Unitary smooth muscle- gap junctions allow for fast electrical activity
    -Multiunit smooth muscle- little or no coupling between cells
    -combination of unitary/multiunit- found in vascular smooth muscle.
61
Q

Multiunit smooth muscle

A

-little or no coupling between cells
-present in iris, ciliary muscles of the lens, and vas deferens
-each muscle fiber behaves as a separate motor unit
-innervated by postganglionic fibers of parasympathetic and sympathetic nervous
-regulate function.

62
Q
A

-Ca 2+ enters during action potential via voltage-gated Ca 2+ channels
-Ca 2+ binds calmodulin -> activates myosin-light-chain kinase -> phosphorylates myosin
-Myosin~P binds actin -> form cross-bridges, -> tension
-Ca also enters via :
-ligand-gated Ca 2+ channels in sarcolemmal membrane
-IP3 -gated Ca 2+ channels in the SR membrane

63
Q

48-year-old woman with insulin-dependent diabetes mellitus reports to her physician that she is experiencing severe muscle weakness. She is being treated for hypertension with propranolol, a β-adrenergic blocking agent. Her physician
immediately orders blood studies, which reveal a serum [K+] of 6.5 mEq/L (normal, 4.5 mEq/L) and elevated BUN (blood urea nitrogen). The physician tapers off the dosage of propranolol, with eventual discontinuation of the drug. He adjusts her insulin dosage. Within a few days, the patient’s serum [K+] has decreased to
4.7 mEq/L, and she reports that her muscle strength has returned to normal

A

-hyperkalemia with muscle weakness
-Because her insulin dosage is insufficient -> caused K+ to move out of cells into blood (insulin promotes K+ uptake into cells)
-Propranolol β-blocker (antagonist) (“iprils”) -> shifts K+ out of cells and into blood
-Elevated BUN -> suggest renal failure -> kidneys unable to excrete the extra K+ that is accumulating in her blood
-renal physiology and endocrine physiology
-resting potential of muscle depends on concentration gradient for K+ (Nernst equation)
-At rest, K+ diffuses out -> creating a K+ diffusion potential
-K diffusion potential responsible for the resting membrane potential -> cell interior negative
-The larger the K+ concentration gradient, the greater the negativity in the cell
-if blood [K+] is elevated -> concentration gradient is less -> resting
membrane potential is less negative -> hyperpolarization
-closes the inactivation gates on Na+ channels -> no action potentials can be generated
-Without action potentials in the muscle, there can be no contraction

64
Q

hyperkalemia treatment

A

-shift K+ back into the cells
-increase insulin dosages and discontinue propranolol
-reduce blood [K+] to normal -> resting membrane potential of her skeletal muscle cells to normal –> Na+ inactivation gates on will be open at the resting membrane potential (as they should be)-> normal action potentials

65
Q

32-year-old woman had her first episode of blurred vision 5 years ago. She had trouble reading the newspaper and the fine print on labels. Her vision returned to normal on its own, but 10 months later, the blurred vision recurred, this time with other symptoms including double vision, and a
“pins and needles” feeling and severe weakness in her legs. She was too weak to walk even a single flight of stairs. She was referred to a neurologist, who ordered
a series of tests. Magnetic Resonance Imaging (MRI) of the brain showed lesions typical of multiple sclerosis. Visual evoked potentials had a prolonged latency that was consistent with decreased nerve conduction velocity. Since the diagnosis, she has had two relapses and she is currently being treated with interferon beta.

A

-multiple sclerosis
-action potential jump from one node of Ranvier to the next in myelinated axons -> saltatory conduction
-latency and signals going to wrong tissues
-Multiple sclerosis- demyelinating disease of CNS
-decrease in membrane resistance -> current “leaks out” across the membrane -> currents decay (decreased length constant)
-may be insufficient to generate an action potential when they reach the next node of Ranvier
-increased nerve diameter and myelination -> increase length constant

66
Q

18-year-old college woman comes to the student health service complaining of progressive weakness. She reports that occasionally her eyelids “droop” and that she tires easily, even when completing ordinary daily tasks such as brushing her hair. She has fallen several times while climbing a flight of stairs. These symptoms improve with rest. The physician orders blood studies, which reveal elevated levels of antibodies to ACh receptors. Nerve stimulation studies show decreased responsiveness of skeletal muscle on
repeated stimulation of motoneurons. The woman is diagnosed with myasthenia gravis and is treated with the drug pyridostigmine. After treatment, she
reports a return of muscle strength.

A

-autoimmune
-cant do repeated actions, muscles that constant are contracted -> droop
-antibodies are produced to ACh receptors on the motor end plates of skeletal muscle
-> severe muscle weakness
-ACh receptors are on motor end plates -> neuron to skeletal muscle
-ACh released normally but ACh binding to motor end plates is impaired Because ACh cannot bind
-depolarization of the motor end plate (EPP) will not occur
-normal action potentials cannot be generated in the skeletal muscle
-Muscle weakness and fatigability ensue

67
Q

myasthenia gravis treatment

A

-Because pt improved with pyridostigmine (a long-acting AChE inhibitor) ->confirmed dx
-AChE on the motor end plate normally degrades ACh (i.e., AChE terminates the action of ACh)
-By inhibiting ACh-degradative enzyme with pyridostigmine -> ACh levels in the neuromuscular junction are maintained at a high level, prolonging the time available for ACh to activate its receptors on the motor end plate
-Thus a more normal EPP in the muscle fiber can be produced even though many of the ACh receptors are blocked by antibodies

68
Q

ligand gated channels

A

-Hormones
-2nd messengers
-neurotransmitters
-can go nerve to nerve or nerve to MUSCLE

Physiology (24 decks)

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