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Physiology > Synapse and muscle > Flashcards

Synapse and muscle Flashcards

1
Q

At what location is action potential from one nucleus transmitted to another nucleus

A

At the synapses

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2
Q

When are neurotransmitters released?

A

when vesicles fuse with the presynaptic membrane

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3
Q

What is the outcome of The released neurotransmitters diffusing and binding to receptors on the postsynaptic membrane

A

excitatory or inhibitory effects at the postsynaptic membrane.

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4
Q

2 ways to get rid of neurotransmitters?

A

Break it down

reabsorb it.

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5
Q

Do bound receptors result in depolarization?

A

yes

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6
Q

4 entry and exit mechanism of calcium

A

Calcium pump
Ligand gated calcIUM cHANEL,
voltage gate calcium
Na/ca exchanger

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7
Q

what is the transporter for Ca+ pump

A

Calmodulin.

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8
Q

What is the mode of action for Ligand-gated channel

A

Ligand gated channel: Fastest

Example, nicotinic AChR, ligand gated cation (Na+ and K+) channel found at NMJ

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9
Q

What is the mode of action for Direct-G-Protein Coupling

A

Direct G-protein coupling:
Example, muscarinic AChR M2, e.g. parasympathetic innervation of heart. Direct coupling of G-protein receptor to ion channel with no need for a 2nd messenger

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10
Q

What neurotransmitter is released from the presynaptic terminal

A

Ach

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11
Q

The postsynaptic membrane contains a nicotinic receptor (T/F)

A

T

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12
Q

How is Ach formed and stores in the presynaptic

A

Choline acetyltransferase catalyzes the formation of ACh from acetyl coenzyme A (CoA) and choline in the presynaptic terminal. ■ ACh is stored in synaptic vesicles with ATP and proteoglycan for later release

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13
Q

What is the mode of action for second messenger coupling

A

Second messenger coupling: Slowest
Example, muscarinic AChR M1, e.g. innervation of sweat glands. Second messenger triggers ion channel after numerous steps

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14
Q

A synaptic transmission results in 2 outcomes namely:

A

Excitatory(Depolarizing) and inhibitory(Hyperpolarizing) changes.

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15
Q

What are the excitatory changes?

A

(excitatory postsynaptic potential; EPSP) Depolarizing changes: is produced:
Transmitter substances go into the synaptic cleft and cause an increase in permeability of sodium and potassium in the postsynaptic cleft. more sodium in and potassium out due to the electrochemical gradient. This causes a depolarization. this occurs in the postsynaptic cell.
ACh, norepinephrine, epinephrine, dopamine, glutamate, and serotonin.

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16
Q

What are the inhibitory changes

A

Transmitter substances increase the permeability of the postsynaptic membrane to cl-.
The resultant Ionic current flow is in the direction that hyperpolarizes the postsynaptic cell.ISPS
γ-aminobutyric acid (GABA) and glycine

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17
Q

What Ions produce EPSP

A

Na+ or ca++ ions

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18
Q

What ions produce IPSP

A

cl- or K+ ions

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19
Q

what is a one to one synapse arrangement

A

An action potential in the presynaptic element (the motor nerve) produces an action potential in the postsynaptic element (the muscle)

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20
Q

What is a Many to one synapse arrangement

A

An action potential in a single presynaptic cell is insufficient to produce an action potential in the postsynaptic cell. Instead, many cells synapse on the postsynaptic cell to depolarize it to threshold. The presynaptic input may be excitatory or inhibitory

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21
Q

what is spatial summation

A

occurs when two excitatory inputs arrive at a postsynaptic neuron simultaneously. Together, they produce greater depolarization

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22
Q

Temporal summation

A

occurs when two excitatory inputs arrive at a postsynaptic neuron in rapid succession. Because the resulting postsynaptic depolarizations overlap in time, they add in stepwise fashion

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23
Q

How does presynaptic inhibition happen?

A

In presynaptic inhibition, an inhibitory fiber of one nerve cell has a synapse on an excitatory axon of another neuron before the latter communicates with the motor neuron

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24
Q

How does postsynaptic inhibition happen

A

the inhibitory and excitatory fibers both synapse directly with the target neuron

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25
Q

IPSP does not occur at the neuromuscular junction T/f?

A

T

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26
Q

2 pathways after the major motor pathways

A
  1. upper motor neuron

2. Lower motor neuron

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27
Q

Major motor pathways

A 
cerebral cortex
Midbrain
pons 
medulla
spinal cord
Motor end plate
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28
Q

What is the functional unit of the muscle

A

Myofibril

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29
Q

How is the action potential generated at the NMJ

A

At the neuromuscular junction, the axon of a motor nerve- synapses with skeletal muscle at a site known as the -motor endplate. Stimulation of a motor nerve results in the release of acetylcholine from vesicles at the presynaptic membrane; acetylcholine diffuses and binds to postsynaptic receptors, producing depolarization of the sarcomere and leading to an action potential

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30
Q

what gets depolarized in the muscle for an action potential to be generated

A

sarcolemma

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31
Q

What is the NMJ

A

The synapse between a nerve and muscle is termed the Neuromuscular junction (NMJ)

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32
Q

Synaptic vesicles contain what?

A

Neurotransmitter ACH

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33
Q

Single vesicles are called?

A

Quanta

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34
Q

what’s the function of Acetylcholinesterase?

A

between the pre and postsynaptic
membranes there is the basal membrane that contains the enzyme Acetylcholinesterase (AChE) that hydrolizes (breaks down ) ACh to choline and acetic acid terminating its action.

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35
Q

If acetylcholinesterase is inhibited, what will happen

A

muscle will contract and will not relax.

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36
Q

How does the Ach receptor channels function

A

The postsynaptic membrane has membrane folds on top of which there are the ACh receptor ion channels (AChR) at a huge density ready to be activated by Ach.

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37
Q

How is EPP generated

A

The EPP (or EJP, excitatory junction potential) is an EPSP on a muscle fiber. EPP is caused by the opening of Ach receptors, and propagation on the muscle membrane is electrotonic, i.e. it decreases with distance in contrast to the action potential in nerve & muscle that propagates actively.

This is because AChR channels are only found at the end plate while voltage-gated Na channels are found all along the membrane in muscles.

EPP has a reversal potential (membrane voltage at which it changes direction) at ~0 mV. This is because the AChR channel is permeable to both Na+ and K+ and an equilibrium between the Nernst potential of these ions and their relative flux is reached at ~0mV with equal Na+ entering and K+ leaving the cell

38
Q

Differences btwn EPP and AP

A

Graded,Ligand gated, rapid depo overshoot to 0+mv, charge carriers Na and k+, passive repolarization and one large chanel./Ap- Voltage-gated, rapid depo with an overshoot to +40mv.Na+ os charge carrier for Depo, Repolarization due to increase gk+.Two independent channels,all or none

39
Q

What is the action of Curare on ACHr

A

Blocks it.

40
Q

What is the effect of Botulinum toxin on Ach

A

it inhibits the release of Ach

41
Q

When is the EPP depo initiated

A

When the Cation channel is opened.

42
Q

If there is a voltage-gated Chanel on a cell that is doing something it is the?

A

L type…its depolarizes quickly and slow to inactivate

43
Q

what ion causes a muscle to contract

A

Calcium

44
Q

What’s the triad in the muscle contraction

A

T-tubule, sarcoplasmic reticulum, terminal cisternae

45
Q

Action potential enters the surface of the muscle fiber via the?

A

T-tubule

46
Q

What is the mechanism of action of Calsequestrin

A

Binds ca and decreases calcium concentration in SR allowing more calcium to be pumped

47
Q

explain excitation-contraction coupling.

A

When an action potential in a motor neuron results in the release of acetylcholine at the neuromuscular junction, binding of acetylcholine on the sarcolemma opens a cation channel, permitting influx of Na + . An action potential is produced and spreads into the transverse tubules, resulting in the release of Ca 2+ stored in the sarcoplasmic reticulum, initiating cross-bridge formation and muscle contraction. Ca 2+ is resequestered into the sarcoplasmic reticulum by Ca 2+ -ATPase to terminate the contraction.

The triad allows coupling of the invading depolarization from the action potential (in the T- tubule) and the release of Ca2+ from the SR .

This is the base of excitation-contraction coupling.
Calsequestrin keeps high Ca 2+ in the SR and the Ca-ATPase pumps it back! Note it is ATP dependent!!!!

48
Q

What ensures calcium release from the SR

A

The depolarization activates the L type Ca channel (DHP receptor) that activates in turn the calcium release site (Ryanodine receptor) to release of Ca2+ from the SR.
Please note that Ca flux through the Ca channel is not relevant to the process. The Ca release from the SR results from a physical interaction between the DHP and Ryanodine Receptors

49
Q

N-type

A

presynaptic

50
Q

L-type

A

postsynaptic

51
Q

What’s the ratio of Na: ca exchanger during ca influx and muscle contraction

A

NCX (3Na+/1Ca++ exchanger) is found on the sarcolemma/T tubule
this ratio causes depolarization

52
Q

types of muscles

A

skeletal, cardiac, smooth muscles.

53
Q

characteristics of skeletal muscles

A

strong,quick,discontinuous,voluntary contractions

54
Q

cardiac muscles

A

Strong,quick,continous,involuntary contractions

55
Q

smooth muscles

A

weak,slow,involuntary contractions

56
Q

How does muscle contract with calcium and Troponin in play?

A

Muscle contraction, initiated by the binding of Ca2+ to the TnC unit of troponin, which exposes the myosin-binding site on actin (cross-hatched area). In a second step, the myosin head binds to actin and the ATP breaks down into ADP, yielding energy, which produces a movement of the myosin head. As a consequence of this change in myosin, the bound thin filaments slide over the thick filaments. This process, which repeats itself many times during a single contraction, leads to a complete overlapping of the actin and myosin and a resultant shortening of the whole muscle fiber. I, T, C are troponin subunits

57
Q

what does calcium bind to During muscle contraction

A

TNC unit of Troponin.

58
Q

What is the relationship between length and tension during muscle contraction/stimulation

A

Relationship of The force generated when skeletal is stimulated- is related to the size of the motor units stimulated (A) , the number of motor units activated and the frequency of stimulation of the muscle fibers (B) , and the resting length of muscle fibers (C) .

59
Q

What is isometric contraction

A

the muscle tension developed is less than its opposing load. The muscle cannot shorten and lift the object with that load. Thus the muscle cannot change a prefixed length!!
We can change it, however, to measure how much force can be developed at different lengths upon nerve stimulation.

The tension generated by the sarcomers is used to pull on the tendons. No change in length is seen

60
Q

What is Isotonic contraction

A

The muscle tension developed is greater than its opposing load. The muscle shortens and lifts an object without changing strength. The tension that is generated is used to shorten the muscle.

In an experimental setting stimulation of the nerve innervating the
Muscle produces an isometric contraction first followed by the Isotonic contraction.
Two types of isotonic contraction. Concentric (muscle shortening) and Eccentric (muscle lengthening)

61
Q

What’s the relationship between the velocity of muscle shortening and the magnitude of the load

A

The velocity of muscle shortening is inversely proportional to the magnitude of the load.

62
Q

Moment to moment regulators of the skeletal muscle tension involves what which system

A

nervous system

63
Q

The most effective way to regulate muscle strength is by?

A

Repetitive action potential in the innervating axon

64
Q

during the illustration showing the time sequence of muscle action potential, intracellular Ca2+ rise and decline and the force during one twitch. A considerable delay occurs between calcium rise and twitch and the force does not reach maximum

A

This is due to the need to fully extend the series elastic element i.e. the connective tissue, tendon and the mass of the fiber themselves

65
Q

What is Tetanus

A

Ca2+ rise and the force developed upon repetitive high-frequency stimulation of the nerve. Giving the muscle maximal strength.

66
Q

Repetitive stimulation of a muscle increases its tension by ?

A

Twitch summation

67
Q

If a muscle fiber is stimulated very rapidly, it cannot relax between stimuli. The twitches merge into a smooth, sustained, maximal contraction called

A

Tetanus

68
Q

What causes twitch summation

A

Sustained elevation of calcium in the cytosol

69
Q

Intermittent stimulation frequency results in ?

A

Incomplete tetanus

70
Q

What is a motor unit?

A

is the ensemble of muscle fibers that receive innervations by the same alpha motor neuron and therefore will twitch at the same time when an action potential is produced by that neuron

71
Q

Strength of contraction is regulated by?

A

the number and the size of the activated Motor Units.

72
Q

What is the innervation ratio

A

The ratio of muscle fibers to nerve fibers in a motor unit

73
Q

FYI:The lower the IR, the more fine or exact the control of movement

A

T

74
Q

How do you Increase tension?

A

Tension is increased by increasing the number of motor units and by changing the type of motor unit from type 1 to type 2

75
Q

Types of Motor units are

A

Fast and slow

76
Q

Muscle fibres in motor units are classified as?

A

Oxidative or Glycolytic

77
Q

What are the oxidative fibers made up of

A

Red with a high concentration of myoglobin

78
Q

What specifies the type of muscle fibre?

A

The lower motor neuron

79
Q

Troponin concentration is still used to detect MI T/f

A

T

80
Q

After trauma what happens to heal a wound

A

progenitor cell activation and proliferation.
Chemotaxis fusion to the injured site
Fusion to produce new Myofibres(Hyperplasia)
Fusion to damaged Myofibres(Hypertrophy)

81
Q

What’s the function of Golgi tendon organ

A

This structure collects information about differences in tension among tendons and relays data to the central nervous system, where they are processed and help to coordinate fine muscular contractions. The Golgi tendon organs monitor tension in a muscle

82
Q

What’s the function of the muscle spindle

A

Muscle spindles participate in the nervous control of body posture and the coordinate action of opposing muscles. Muscle spindles monitor changes in muscle length.

83
Q

Characteristics of Multiunit smooth muscle

A

cells respond independently

large arteries, airways, piloerector

84
Q

Characteristics of unitary smooth muscle

A

cells respond in unison, has lots of Gap

Gi Uterus bladder

85
Q

Components of smooth muscle is?

A

Actin and Myosin

86
Q

What produces contraction in smooth muscles

A

Sliding of actin and myosin filaments when intracelliular ca is elevated

87
Q

what is Caveolae?

A

are invaginations in the cell membrane and are a site of Ca 2+ flux

88
Q

What is the process of contraction in smooth muscles

A

Intracellular calcium ion (Ca ++) concentration increases when Ca ++ enters the cell through calcium channels in the cell membrane or the sarcoplasmic reticulum (SR). The Ca ++ binds to calmodulin to form a Ca ++-calmodulin complex, which then activates myosin light chain kinase (MLCK). The MLCK phosphorylates the myosin light chain (MLC) leading to contraction of the smooth muscle. When Ca ++ concentration decreases, due to pumping of Ca ++ out of the cell, the process is reversed and myosin phosphatase removes the phosphate from MLC, leading to relaxation

89
Q

Explain Excitation-Contraction Coupling of Smooth Muscle

A

Binding of a ligand to the sarcolemma results in elevation of free intracellular Ca 2+ , through either depolarization of the cell membrane and opening of Ca 2+ channels, or activation of the enzyme phospholipase C. In the latter case, cleavage of inositol trisphosphate by phospholipase C produces IP 3 , which binds to sites on the sarcoplasmic reticulum, causing release of stored Ca 2+ . In either case, Ca 2+ binds to the protein calmodulin, which activates myosin kinase, initiating actin–myosin interaction. The contraction cycle continues as long as Ca 2+ is elevated. The latch state occurs when myosin is dephosphorylated by myosin phosphatase. In this state, contraction can be maintained without further ATP hydrolysis

90
Q

In addition to innervation, smooth muscle is activated by the following

A

Hormones & other chemical signals
Stretch
Neighboring cells

Smooth muscles also has a “latch-state”, in which it remains contracted with very minimal energy expenditure

91
Q

What’s the difference btw cardiac and skeletal muscles

A

The striated appearance of cardiac muscle is associated with the arrangement of the contractile proteins actin and myosin into sarcomeres, as in skeletal muscle. A notable difference between these types of muscles is that cardiac muscle utilizes extracellular Ca 2+ as well as intracellular stores to initiate contraction. Another difference is that transverse tubules of cardiac muscle form dyads with the terminal cisternae of the sarcoplasmic reticulum, as opposed to the triads found in skeletal muscle. In addition, unlike skeletal muscle, cardiac muscle fibers are connected by gap junctions at intercalated disks between the cells, allowing the spread of depolarization from cell to cell, producing synchronous contraction of muscle

92
Q

what are the changes in the length of filament as the muscle contract

A

The physical lengths of the actin and myosin filaments do not change during contraction. Therefore, the A band, which is composed of myosin filaments, does not change either. The distance between Z disks decreases, but the Z disks themselves do not change. Only the I band decreases in length as the muscle contracts.

Physiology (11 decks)

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