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CSF > Block 4 > Flashcards

Block 4 Flashcards

1
Q

Endocrine signaling

A

Cells release signals that travel long distances to other cells

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2
Q

What is an example of endocrine signaling?

A

Insulin released from pancreatic beta cells stimulates glucose uptake

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3
Q

Paracrine signaling

A

Cells release signals that affect nearby target cells

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4
Q

What is an example of paracrine signaling?

A
  1. Vascular endothelial cells secrete vasodilators/constrictors, prothrombotics, etc.
  2. Tumors promote angiogenesis via paracrine signalling of VEGF etc.
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5
Q

Juxtacrine signaling?

A

Cells communicate with the cell right next to it with membrane-bound molecules (requires cell to cell contact)

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6
Q

What is an example of juxtacrine signaling?

A

Axons growth and migration is dependent on juxtacrine signaling with its substrate

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7
Q

Autocrine signaling

A

The signal and response are generated from the same cell

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8
Q

What is an example of autocrine signaling?

A

Many squamous cell carcinomas secrete VEGF or EGFR to stimulate their own growth through autocrine signaling

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9
Q

Intacrine signaling

A

A molecules synthesized by the cell stimulates an intracellular receptor; ie signaling within the cell

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10
Q

What is an example of intacrine signaling?

A

Some breast CA cells can produce their own estrogen that stimulates growth via their own intracellular receptors

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11
Q

ACh

A

Binds to nicotinic receptor at the NMJ:

ACh -> Na+ -> depolarize -> DHP receptor (linked to ryanidine receptor) -> Ca2+ influx from SR -> contraction

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12
Q

GalphaS protein

A

G coupled protein activated by epi:
Epi -> beta adrengergic receptor -> GalphaS -> adenylate cyclase -> ATP to cAMP -> cAMP dependent protein kinase A -> phosphorylates -> changes cell function

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13
Q

GalsphaQ protein

A

G coupled protein activated by norepi:
Norepi -> alpha adrenergic receptor -> GalphaQ -> phospholipase C -> IP3/DAG -> Ca2+/activated protein kinase C -> calmodulin dependent protein kinase

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14
Q

What effect do cholera toxin (CT) and E coli toxin (ETx) have on cell signaling?

A

CT and ETx activate proteins downstream of stimulatory GPCR which causes constitutive activation of adenylate cyclase and rapid elevation of cAMP

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15
Q

How does pertussis toxin (PT) affect cell signaling?

A

PT inhibits a cAMP inhibitor also leading to constitutive activation of cAMP

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16
Q

Which hormones use intracellular nuclear receptors

A

Retinoic acid, Vitamin D, thyroid hormones, steroid hormones

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17
Q

Tamoxifan

A

Estorgen analog that does not stimulate growth veing investigated as CA tx

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18
Q

Guanylyl cyclase

A

Synthesizes cGMP

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19
Q

Adenylate cyclase

A

Synthesizes cAMP

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20
Q

NO

A

Diffuses through the membrane and activates the soluble form of guanylyl cyclase to affect smooth muscle contraction and neurotransmission

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21
Q

How does viagra work?

A

Viagra inhibits PDE5, a phosphodiesterase that breaks down cGMP; this relaxes (ie vasodilates) vascular smooth muscle and produces an erection

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22
Q

Tropomyosin

A

Blocks myosin binding site on actin to inhibit muscle contraction

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23
Q

Troponin C

A

Displaces the tropomyosin-actin complex when bound with Ca2+ so that myosin can bind and the muscle can contract

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24
Q

What is the function of structural muscle proteins?

A

Transmit movement or force to the outside of the cell as well as maintain sarcomere structure

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25
Q

What is the function of motor muscle proteins?

A

Turn the motor “on” in muscle

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26
Q

What is the structure of muscle myosin II?

A

Hexamer with a helical coiled coil chain w/ two heavy chains that each have a regulatory light chain and an essential light chain

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27
Q

What type of filaments does the A band contain?

A

Mostly thick filaments

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28
Q

What type of filaments does the I band contain?

A

Mostly thin filaments

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29
Q

What happens at the Z disk?

A

Actins attache

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30
Q

What structural proteins does skeletal muscle contain?

A

Titin, nebulin, M-line proteins, Z-disk proteins (alpha-actinin, cap-Z, 7 others), actin (connects Z disks), focal contact proteins (adherens junctions, focal adhesions), and extracellular proteins (collagen, elastin)

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31
Q

What are the 3 filaments in a sarcomere?

A

Thick filaments (myosin), thin filaments (actin, tropomyosin, troponin), titin

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32
Q

What does titin do?

A

Titin keeps myosin filaments centered during contraction, acts as a molecular ruler during myogenesis, and is involved in passive-length tension

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33
Q

What is passive length tension?

A

D/t muscles’ structure, it is able to produce some tension even when it is not contracting

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34
Q

What is muscular dystrophy?

A

These are a group of disorders involving missing proteins in the dystrophin-glycoprotein complex which leads to weak contractions, disrupted membranes, and elevated ion fluxes

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35
Q

What is titin attached too?

A

Titin is links the Z line to the thick filament

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36
Q

M line

A

Located in the middle of the A band and vertically connects thick filaments

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37
Q

Cap Z proteins

A

Cap the ends of thin filaments on the Z band

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38
Q

What determines the speed of muscle contraction?

A

The rate of product release, ie rated of Pi release

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39
Q

Slow twitch fibers

A

Type I fibers; small fatigue resistant, run on glycogen and have high mitochondria/low glycogen content and red myosin

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40
Q

Fast twitch type II A fibers

A

Intermediate-sized fatigue resistant fibers w/ red myoglobin, high mitochondria content, abundant glycogen, and oxidative metabolism

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41
Q

Fast twitch type II B fibers

A

Large-sized fatigable fibers w/ white myosin, few mitochondria, abundant glycogen, and glycolytic metabolism

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42
Q

Familial hypertrophic cardiomyopathy (HCM)

A

Single amino acid mutation usually affecting the myosin heavy chain that alters ATP hydrolysis/force production and leads to ventricular wall hypertrophy; leading cause of sudden cardiac arrest in young adults

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43
Q

Endplate potential

A

Transient depolarization d/t ACh binding at the NMJ which then becomes an AP

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44
Q

T tubules system

A

Invaginations of the sarcolemma that faciliates rapid Ca2+ release after receiving an AP

45
Q

Malignant hyperthermia

A

Genetic mutation affecting RyR1 where uncontrolled muscle contraction is triggered by exposure to anesthetics and/or depolarizing neuromuscular blockers

46
Q

RyR-2 defects

A

Decreased numbers of RyR-2 in cardiac muscle leads to decreased energy expenditure, hypertrophy and heart failure

47
Q

Troponin complex`

A

Ca2+ regulating protein w/ 3 subunits found in striated muscle (ie skeletal and cardiac but not smooth)

48
Q

Troponin-T subunit

A

Binds tropomyosin

49
Q

Troponin-I subunit

A

Inhibitory

50
Q

Troponin-C subunit

A

Ca2+ binding

51
Q

How does elevated Ca2+ concentration effect troponin?

A

At high concentrations, Ca2+ binds to troponin C which allows for Pi dissociation and consequent power stroke

52
Q

How does low Ca2+ concentration effect troponin?

A

At low concentrations, steric hindrance inhibits Pi release so there is no power stroke

53
Q

Lusitrophy

A

Myocardial relaxation

54
Q

How is cardiac troponin different from skeletal muscle troponin?

A

It has a serine residue that becomes phosphorylated during sympathetic activation which leads to decreased Ca2+ sensitivity, causing it to leave the troponin complex more rapidly which ultimately contributes to lusitrophy. Also cardiac troponin is longer

55
Q

Which step of cardiac muscle contraction is regulated?

A

The power stroke (ie dissociation of Pi)

56
Q

What kind of muscle produces the greatest force?

A

Smooth muscle d/t increased number of cross bridges

57
Q

How are thick filaments regulated in smooth muscle?

A

Phosphorylation turns thick filaments on via activation of MLCK or activation of ROK

58
Q

Myosin light chain kinase (MLCK)

A

Activated by Ca2+ induced calmodulin; phosphorylates myosin to turn it on and cause muscle contraction

59
Q

Myosin light chain phosphatase (MLCP)

A

Dephosphorylates the the light chain to turn the thick filament off in smooth muscle

60
Q

Rho A kinas (ROK)

A

Ca2+ independent inhibitor of MLCP that turns thick filaments on in smooth muscle

61
Q

How does smooth muscle generate high force

A

Myosin is kept in a tight binding state d/t the slow rated of ADP release after the power stroke

62
Q

Caldesmosome and calponin

A

Ca2+ sensing proteins in smooth muscle; turn thin filaments on if there is increased Ca2+ concentration which allows for muscle contraction if the MLC is phosphorylated

63
Q

How does smooth muscle relax?

A

Smooth muscle relaxes when there is no stimulus

64
Q

How does cGMP effect smooth muscle?

A

cGMP stimulates cGMP phosphodiesterases which lower intracellular Ca2+ and activate MLCP, which relaxes smooth muscle and increases blood flow

65
Q

How is the force of muscle contraction related to Ca2+ concentration?

A

The force of muscle contraction is directly proportional to Ca2+ concentration

66
Q

Motor unit

A

All of the myofibers innervated by a single motor neuron

67
Q

Choline acetyltransferase (CAT)

A

Catalyzes the synthesis of ACh in the presynaptic terminal

68
Q

How is the generation of APs different in skeletal muscle vs neurons?

A

D/t post-junctional folds of the skeletal muscle membrane w/ ACh receptors and vesicles all lined up, each release of neurotransmitter will generate an AP whereas in neuroaxo-dendrite synapes, many neurotransmitter releases is required to produce an AP

69
Q

How are neurotransmitters released from motor neurons?

A

An AP travels down the axon of a motor neuron which depolarizes the membrane and opens voltage-gated Ca2+ channels which then stimulates transmitter release

70
Q

What kind of ACh receptor do skeletal muscles have?

A

Nicotinic ACh receptors

71
Q

Dihydropyridine receptors (DHP)

A

An L-type Ca2+ channel in the T tubules that is physically linked to the ryanodine receptor; allows Ca2+ to diffuse into the cell following depolarization at the NMJ

72
Q

Calsequestrin

A

Ca2+ binding protein that pulls Ca2+ out of solution so SERCA can transport it back to the SR

73
Q

Myasthenia gravis

A

Autoimmune dz in which Abs are produced against the ACh receptor. Can be tx’ed with ACh esterase inhibitors that increases the concentration of ACh in the NMJ

74
Q

What are the two types of smooth muscle?

A

Single-unit and multi-unit

75
Q

Where is multi-unit smooth muscle found?

A

Ciliary muscle in the eye, piloerector muscles

76
Q

Where are single-unit smooth muscles found?

A

Organs of viscera requiring coordinated contraction

77
Q

What is the function of gap junctions in smooth muscle?

A

Gap junctions are found in single-unit smooth muscle where they facilitate coordinated contraction by allowing ions to flow from one cell the the next; ie they allow the cells to function as one just like cardiac muscle

78
Q

Where does skeletal muscle get Ca2+ from?

A

Intracellular stores it the SR

79
Q

Where does smooth muscle get Ca2+ from?

A

Intracellular or exracellular sources (through v-type Ca2+ channels)

80
Q

What does ACh do in smooth muscle?

A

ACh from parasympathetic neurons activates the muscarinic receptor in smooth muscle to cause muscle contraction via the PIP and IP3 pathway

81
Q

What does norepi do in smooth muscle?

A

Norepi from sympathetic neurons activates beta adrenergic receptors which causes smooth muscle relaxation

82
Q

What are some endocrine regulators of smooth muscle?

A

Oxytocin, CCK, api, angiotensin II

83
Q

What are some paracrine regulators of smooth muscle?

A

NO, oxygen, prostaglandins, histamine

84
Q

How does NO decrease bp?

A

NO diffuses across the membrane (bc it is a gas) and stimulates cGMP, which stimulates protein kinase G, which then decreases muscle contraction and lowers bp

85
Q

Endothelial nitric oxide synthase (eNOS)

A

Stimulated by increased Ca2+ which then synthesizes NO and causes smooth muscle relaxation; ie increases Ca2+ can also have vasodilator effects

86
Q

What effect do stretch-activated channels have on smooth muscle?

A

Stretch-activated channels open v-type Ca2+ channels which cause muscle contraction

87
Q

Protein kinase A

A

Activated by cAMP via the epi-GalsphaS signaling pathway

88
Q

Protein kinase C

A

Activated by DAG via the norepi-GalphaQ signaling pathway

89
Q

How does the PNS regulate smooth muscle?

A

The PNS stimulates contraction of smooth muscle by releasing ACh which binds to muscarinic receptors and initiates the GalphaQ signaling pathway

90
Q

How does the SNS regulate smooth muscle?

A

The SNS can stimulate contraction via norepi binding to to beta adrengergic GalphaS receptors and initiating the adenylate cyclase/cAMP pathway or it can stimulate relaxation by binding to the GalphaS alpha receptor

91
Q

What is the function of cGMP in smooth muscle?

A

cGMP (stimulated by NO) activates protein kinase G which decreases intracellular Ca2+ and thus inhibits muscle contraction

92
Q

Protein kinase G (PKG)

A

PKG decreases intracellular Ca2+ in smooth muscle either by inhibiting mobilization from intracellular stores or by inhibiting its import from extracellular stores

93
Q

How are smooth muscle APs different from skeletal muscle APs?

A

Smooth muscle has relatively few Na+ channels and the upswing of the AP depends on Ca2+ rather than Na+ (many smooth muscle just exhibit graded depolarizations rather than APs)

94
Q

What is the role of voltage gated K+ channels in smooth muscle?

A

Activated K+ channels hyperpolarize the cell, close Ca2+ channels and inhibit contraction/vasodilate. Closed K+ channels depolarize the cell, open Ca2+ channels, and contract/vasoconstrict smooth muscle

95
Q

Where does smooth muscle in the gut receive input from?

A

Stretch activated channels, blood-borne ligands (hormones), autonomic neurons, enteric neurons, inflammatory cells releasing NO

96
Q

ICC

A

Pacemaker cells in the gut

97
Q

What effect do catecholamines have on cardiac muscle?

A

Catecholamines bind to the GalphaS beta receptor and initiate the adenylate cyclase/cAMP pathway. This actiavtes phospholamban which activates the Ca2+ channel in the SR

98
Q

Phospholamban

A

Opens the Ca2+ channel in the SR after binding of catecholamines to the GalphaS beta receptor on cardiac muscle

99
Q

What is the sequence of smooth muscle contraction?

A

Ca2+ -> binds calmodulin -> binds MLCK -> phosphorylates myosin -> increases rated of actomyosin ATP hydrolysis -> contraction

100
Q

Multi-unit smooth muscle

A

Each unit is capable of contracting individually

101
Q

Single-unit smooth muscle

A

Arranged in tight contact with each other and connected by gap junctions so that contracts will be coordinated

102
Q

Time constant

A

The length if time it takes for a signal to propagate; the larger the time constant, the longer it takes to propagate

103
Q

How do K+ channel blockers tx sxs of MS?

A

Blocking K+ channels prolongs the AP

104
Q

How do local anesthetics work?

A

Block Na+ channels so sensory neurons don’t fire

105
Q

When does the power stroke of the cross bridge cycle occur?

A

After the loss of Pi but before the loss of ADP from the myosin head

106
Q

Titin

A

Protein that attaches the Z line to the thick filament and is responsible for much of the passive force produced in skeletal muscle

107
Q

Alpha-actinin

A

Protein found in both Z disks and dense bodies of smooth muscle

108
Q

Saltatory conduction

A

Propagation of APs along myelinated axons

109
Q

Active force

A

Proportional to the number of cross bridges

CSF (3 decks)

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