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biosci 107 > Muscles and Neurons > Flashcards

Muscles and Neurons Flashcards

1
Q

Explain the structure of a nerve cell

A

a soma (cell body) and two types of processes: dendrites and usually a single axon.

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2
Q

Inputs from other neurons (synaptic inputs) are received on the

A

dendritic tree and the soma.

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3
Q

What is the difference between an action potential and a synaptic potential?

A

Synaptic potential goes towards the soma, while action potentials go away from the soma

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4
Q

In communication, what are the two types of signals?

A

Electrical signals Chemical signals

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5
Q

Where does electrical signalling happen?

A

dendrites, cell body, axon

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6
Q

Where does chemical signalling happen?

A

synapses

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7
Q

What is the membrane potential?

A

voltage across the cell membrane

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8
Q

What is the membrane potential range in mV for a cell?

A

between –100 and +50 mV

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9
Q

What is the resting membrane potential value?

A

Its value is usually between –50 and –70 mV (typically -65 mV).

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10
Q

True or false: Almost all cells in the body have a negative resting membrane potential.

A

True

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11
Q

Only x, y and some z can suddenly respond with a transient change of this potential (ie. with an action potential) in response to a stimulus – so they are excitable !

A

Only neurons, muscle fibres and some endocrine cells can suddenly respond with a transient change of this potential (ie. with an action potential) in response to a stimulus – so they are excitable !

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12
Q

How are the intracellular potentials measured today ?

A

The microelectrode recording technique and The patch-clamp technique (additional feature of being able to measure current)

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13
Q

What is the RMP definition?

A

Electrical potential difference (50 to 70 mV) across the cell membrane which results from separation of charge. There is more negative charges inside the cell in comparison to the extracellular fluid.

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14
Q

The RMP is due to what three factors?

A

a) Unequal concentrations of Na+ and K+ inside and outside the cell b) Unequal permeability of the cell membrane to these ions [c) Electrogenic action of the Na-K pump – only a small contribution !]

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15
Q

What is the Approximate concentrations of K+ and Na+ ions inside and outside neurons?

A

OUTSIDE [Na+] 150 mM [K+] 5 mM INSIDE [K+] 100 mM [Na+] 15 mM 

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16
Q

Explain Ca2+ ion’s affect on the RMP:

A

Ca2+ ions do not affect the RMP as the membrane is not permeable to these ions at rest

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17
Q

Explain Cl2- ion’s affect on the RMP:

A

Cl- ions also do not contribute to the RMP as their distribution is usually ’passive’ (i.e. in most neurones there are no active Cl- pumps).

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18
Q

How do large ions affect RMP?

A

There are many negatively charged proteins inside the cell. However, since the cell membrane is not permeable to these large ions, they do not affect the RMP !

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19
Q

State the Na/K pump ratio:

A

3 Na+ out 2 K+ in

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20
Q

How is unequal permeability of the cell membrane to different ions (including Na+ and K+) explained ?

A

Two main types of ion channels (ie. channels which have selective permeability to ions) in neurons: a) Non-gated (‘leak’) channels - open at rest b) Gated channels (voltage-gated, ligand-gated*, or mechanically-gated) -usuallyclosed at rest

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21
Q

In cell membrane of neurons, there are many leak __ channels, but very few leak___ channels.

A

In cell membrane of neurons, there are many leak K+ channels, but very few leak Na+ channels.

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22
Q

At rest: PK+ / PNa+ ≈ where p means membrane permeability

A

40 / 1

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23
Q

Explain The concept of the ‘Equilibrium potential’

A

An intracellular potential at which the net flow of ions is zero, in spite of a concentration gradient and permeability!

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24
Q

The equilibrium potential can be calculated for each ion by the ‘Nernst equation’ What is this equation?

A

Eion = 61.5 mV x log ([ion]o / [ion]i)

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25
Q

The Nernst equation applies only to a situation when…

A

…a cell membrane is permeable only to one ion ! (ie. has leak channels only for one specific ion).

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26
Q

Glia cells have leak channels only for

A

K+ ions

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27
Q

The higher the permeability of the cell membrane to a particular ion,

A

the greater the ability of this ion to shift the RMP towards its equilibrium potential.

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28
Q

What is an example of the rule that ‘The higher the permeability of the cell membrane to a particular ion, the greater the ability of this ion to shift the RMP towards its equilibrium potential’

A

At rest, in neurons the membrane permeability is much higher to K+ than to Na+; therefore the RMP is closer to the equilibrium potential for K+

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29
Q

Define the action potential:

A

The action potential is a very brief (lasting a few milliseconds in axons, longer in cell bodies) fluctuation in membrane potential caused by a transient opening of voltage-gated ion channels (mainly Na+ and K+) which spreads, like a wave, along parts of the neuron.

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30
Q

Explain hyperpolarization

A

If it becomes more negative (eg. changes from -70 to -75 mV) (the potential inside the cell moves closer to EK+ , and away from ENa+)

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31
Q

Explain depolarization

A

If it becomes less negative (eg. changes from -70 to -60 mV) (the potential inside the cell moves away from EK+ and closer to ENa+)

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32
Q

What are the three key stages of the action potential?

A
  1. Fast depolarisation to about +30mV (‘reversal of polarisation’, or ‘overshoot’) after the membrane potential reaches threshold; 2. Repolarisation; 3. After -hyperpolarisation (AHP).
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33
Q

Information is coded in the _____ of action potentials.

A

Information is coded in the frequency of action potentials.

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34
Q

Briefly explain Depolarisation to threshold

A

Occurs by a stimulus (physical or chemical) Voltage-gated Na+ channels start to open near threshold (PK>PNa)

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35
Q

Briefly explain Stage 1: Fast depolarisation

A

Voltage-gated Na+ channels open very fast PNa>>>PK fast depolarisation to ≈ +30mV

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36
Q

Briefly explain Stage 2: Repolarisation

A

Na+ channels inactivate and voltage-gated K+ channels open PK>>>PNa

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37
Q

Briefly explain Stage 3: After- hyperpolarisation

A

Voltage gated K+ channels remain open for a while and then close PK>>>PNa then PK>>PNa

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38
Q

What is the absolute refractory period?

A

Fast depolarisation and Repolarisation

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39
Q

What is the relative refractory period?

A

after-hyperpolarisation

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40
Q

What counts as a stimulus?

A

physical (eg. electric current, light) or chemical (a drug or synaptic excitation)

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41
Q

Explain the ionic processes occurring during depolarisation

A

When MP reaches the threshold, there is a sudden activation (opening) of voltage-gated Na+ channels ( PNa+↑ ) - At this moment PK+ / PNa+ → 1 : 20 (before was 40 : 1); therefore MP shifts towards the ENa+ (ie. towards +60 mV) - Opening of voltage-gated Na+ channels is only short lasting, as these channels quickly inactivate !

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42
Q

Explain the ionic processes occurring during repolarisation

A
  • depolarisation is followed by a transient opening of voltage-gated K+ channels, leading to repolarisation and AfterHyperPolarization (MembranePotential shifts towards EK+) Inactivation of voltage-gated Na+ channels and activation of voltage-gated K+ channels (since PK+/PNa+ becomes ≈ 100 : 1)
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43
Q

Explain Unmyelinated axons:

A

small diameter; transmission of APs slow, continuous

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44
Q

Explain Myelinated axons:

A

larger diameter, transmission of APs fast, saltatory

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45
Q

Explain the passive spread of current: (3 steps)

A
  1. (Subthreshold) depolarisation at one region of the membrane (local) 2. Passive current flow (inside and outside the axon) (in a circular motion going from inside to outside, from outside to inside) 3. Depolarization of adjacent parts of membrane
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46
Q

How far does the passive spread of current spread from the initial point?

A

Approximately 1mm

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47
Q

Speed of AP transmission in unmyelinated axons:

A

1m/s

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48
Q

Why is speed of AP transmission in unmyelinated axons relatively slow?

A

‘Passive’ current flow between two adjacent points is fast, but AP must be regenerated at every point on the membrane. This takes time and therefore conduction velocity is slow.

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49
Q

Speed of AP transmission in myelinated axons:

A

20 to 100 m /sec

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50
Q

Myelin sheath formed in CNS:

A

by oligodendrocytes

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51
Q

Myelin sheath formed in PNS:

A

by Schwann cells

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52
Q

Myelination is discontinuous; interupted at

A

nodes of Ranvier

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53
Q

Myelination increases passive spread of current, how?

A

Due to the insulating properties of myelin, there is less current dissipation as it flows along the axon !

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54
Q

Passive conduction occurs in both directions – True or false

A

True

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55
Q

How does Myelination increases action potential conduction velocity? (i.e. explain ‘saltatory conduction’)

A

Myelination increases speed of AP conduction by increasing efficiency of passive spread. Thus, AP need not be regenerated at every part of cell membrane. APs are generated only at nodes of Ranvier (current flows passively between nodes).

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56
Q

Can AP’s travelling in opposite directions pass each other?

A

No they cannot as once an AP has passed a membrane it will be in the refractory period preventing further excitation. They will cancel each other – the process known as ‘collision’

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57
Q

AP transmitted from the cell body is in the what direction?

A

‘orthodromic’ direction

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58
Q

AP evoked by electrical stimulation of the axon, is transmitted in the what direction?

A

‘antidromic’ direction

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59
Q

How are APs generated in sensory neurons ?

A

First it evokes a graded depolarisation, known as ‘the receptor potential’. ● The receptor potential spreads passively to more distally located ‘trigger zone’ where APs are generated. ● APs then spread along the axon (myelinated or unmyelinated) towards the CNS.

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60
Q

How is Information about the strength of the stimulus coded in sensory neutrons?

A

the amplitude of the receptor potential and the frequency of APs.

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61
Q

How is a message transmitted from one excitable cell to another excitable cell?

A

a) Through chemical synapses - most often b) Through electrical synapses (eg. in the retina). Much less common !

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62
Q

Explain how synaptic transmission occurs from presynaptic membrane to post synaptic membrane:

A

presynaptic action potential reaches presynaptic knob there is an increased presynaptic Ca2+ permeability and thus a Ca2+ influx Then a release of a neurotransmitter by exocytosis occurs across the synaptic cleft to the post synaptic membrane then the neurotransmitters react with the post synaptic receptors which activates synaptic channels and causes a post synaptic action potential

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63
Q

What is an example of a neurotransmitter in a neuromuscular junction?

A

acetylcholine (ACh)

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64
Q

Endplate potential always triggers an action potential - t or f

A

true

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65
Q

What are the 2 main types of chemical synapses in the CNS?

A

Excitatory synapses and Inhibitory synapses

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66
Q

Explain Excitatory synapses

A

depolarisation of the postsynaptic membrane, called the Excitatory Postsynaptic Potential ( EPSP )

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67
Q

Explain Inhibitory synapses

A

hyperpolarisation of the postsynaptic membrane, called the Inhibitory Postsynaptic Potential (IPSP )

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68
Q

What are the neurotransmitters of excitatory synapses?

A

mainly glutamic acid (glutamate) or ACh

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69
Q

What are the Ionic mechanism of EPSPs?

A

transient opening of channels selective for Na+, K+ and sometimes Ca2+

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70
Q

What are the neurotransmitters of inhibitory synapses?

A

mainly GABA (gamma-aminobutyric acid) or glycine

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71
Q

What are the Ionic mechanism of IPSPs?

A

transient opening of K+ or Cl- channels

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72
Q

What are the two groups of Classification of neurotransmitters?

A

Small molecule neurotransmitters (‘Classical’ neurotransmitters) Neuropeptides (‘Neuromodulators’)

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73
Q

Give examples of Small molecule neurotransmitters

A
  • Amino acids: glutamate, GABA, glycine - Acetylcholine (ACh) - Amines: serotonin (5-HT), noradrenaline, dopamine - ATP (Adenosine triphosphate)
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74
Q

Are small or large molecule neurotransmitters faster?

A

small, as it acts directly on postsynaptic receptors, while large neurotransmitters have an indirect ( ‘metabotropic’) action on postsynaptic receptors, or modulatory action on the effects of other neurotransmitters

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75
Q

What are examples of neuropeptides?

A

Neuropeptide Y (NPY), Substance P, Kisspeptin, Endorphins

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76
Q

What are the Factors determining synaptic action?

A

A) Type of neurotransmitter / neuromodulator B) Type of neurotransmitter receptor expressed in the postsynaptic membrane C) The amount of neurotransmitter receptor expressed in the postsynaptic membrane – ’Synaptic plasticity: LTP or LTD’

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77
Q

What are the 4 main subtypes of glutamate receptors?

A

AMPA, NMDA, Kainate and metabotropic glutamate receptor

78
Q

What happens if too much glutamate is released?

A

Too much glutamate release leads to excessive depolarisation and overactivation of neurons. Long-term opening of NMDA receptors causes excessive Ca2+ entry that damages neurons- the process known as excitotoxicity.

79
Q

What are three ways neurotransmitters are inactivated?

A

Re-uptake (for most of the aminoacids and amines) and re-cycling ! Diffusion away from the synapse Enzymatic degradation in the synaptic cleft (eg. Acetylcholine esterase degrades ACh ) Involvement of specific neurotransmitter transporters in the presynaptic membrane or adjacent glia cells; eg. ‘glutamate transporter’

80
Q

The membranes of neurons at rest are very permeable to _____ but only slightly permeable to _____.

A

K+; Na+

81
Q

The concentrations of which two ions are highest outside the cell.

A

Na+ and Cl–

82
Q

What are the three main types of muscle?

A
  1. Skeletal: attached to bones and is responsible for movement; 2. Cardiac: forms the bulk of the heart mass and its contraction ejects blood from the organ; 3. Smooth: mainly lines hollow organs and blood vessels, and regulates their dimensions.
83
Q

Explain the characteristics of Skeletal Muscle

A

• Under voluntary control • Striated • Single long cylindrical cells • Multiple peripheral nuclei

84
Q

Explain the characteristics of Cardiac Muscle

A

• Located only in the heart • Striated • Branched cells with 1-3 central nuclei • Connected via intercalated discs • Involuntary control

85
Q

Explain the characteristics of Smooth Muscle

A

• Involuntary • Found in the wall of internal organs (gut, blood vessels etc) • Spindle shaped, uninucleated cells • Not striated

86
Q

voluntary muscle being under control of the ______ and involuntary muscle under control of the ________.

A

voluntary muscle being under control of the somatic nervous system and involuntary muscle under control of the autonomic nervous system.

87
Q

Skeletal muscle is Attached to bones via

A

tendons

88
Q

How long can a muscle cell be?

A

35cm

89
Q

How wide can a muscle cell be?

A

0.1mm

90
Q

Draw the structure of a muscle fibre

A
91
Q

Thick filaments:

A

run the entire length of an A band

92
Q

Thin filaments:

A

run the length of the I band and partway into the A band

93
Q

Zdisc

A

coin-shaped sheet of proteins that anchors the thin filaments and connects myofibrils to one another

94
Q

H zone

A

lighter mid region

where filaments do not

overlap

95
Q

M line

A

line of protein myomesin that holds adjacent thick filaments together

96
Q

T tubules

A

deep invaginations continuous with the sarcolemma (cell membrane) and circle each sarcomere at each of the junctions of the A and I bands. Allows action potentials to be carried deep within the muscle cell

97
Q

Sarcoplasmic reticulum

A

The calcium storage site. The terminal cisternae of the SR lie close to the T-tubules.

98
Q

Explain the protein structure of myosin

A

Each myosin has 2 subunits each with a globular head and a tail, the two tails intertwine to form a helix

  • The heads have a binding site for actin
  • The head is an enzyme that hydrolyses ATP (an ATPase)
99
Q

Explain the protein structure of thin filaments

A

Composed primarily of globular actin proteins

The filaments are composed of a double stranded helical actin chain (polymers).

Troponin and tropomyosin are regulatory proteins associated with actin in skeletal and cardiac muscle

100
Q

Explain what happens when muscle contracts

A

The sarcomere shortens as the thin filaments are pulled over the thick filaments: -The Z-line is pulled toward the M-line

-The I band and H zone become narrower

101
Q

Explain the 4 steps of the The cross bridge cycle

A

Cross-bridge formation

Powerstroke

Detachment

Energization of myosin head

102
Q

Explain 1. Cross-bridge formation

A

-Myosin binds to the actin binding site to form a crossbridge

as ATP has been hydrolyzed to ADP and Pi

  • Note: crossbridges can only occur in the presence of calcium when the myosin binding site on actin is exposed.
103
Q

Myosic heads are what type of enzyme specifically?

A

The myosin heads are an ATPase, or an enzyme that hydrolyses ATP to ADP and Pi.

104
Q

Explain the process of the 2) Power STroke

A

ADP is released

  • The myosin head rotates to its low energy state (about 45° to the actin) pulling with it the thin filament
  • The result is the shortening of the sarcomere
105
Q

Explain 3) Detacthment

A
  • A new ATP molecule binds to the myosin
  • The actin-myosin bind is weakened and the myosin

detaches

106
Q

Explain the 4. Energization of the myosin head

A
  • Myosin head hydrolyzes the ATP to ADP + Pi
  • The myosin head moves back to its “high energy” confirmation (about 90° to the actin)
107
Q

How is calcium in skeletal muscle regulated?

A

In skeletal muscle opening of calcium channels in the SR allows the movement of calcium ions into the cytosol.

Active transport pumps (Ca2+ ATPase) are constantly moving Ca2+ from the cytoplasm back into the sarcoplasma reticulum

108
Q

Describe the difference between Isometric vs isotonic

A

Isotonic (e.g. bicep curl)

Shortening

Tension constant

Velocity variable

Isometric (holding textbook)
No shortening

Length constant

Tension variable

109
Q

When does the ball part of the channel block the channel?

A

Between depolarization and repolarization

110
Q

WHat is the subthreshold voltage?

A

Before depolarization occurs, the voltage of the inside of the membrane must get more positive and if it reaches a certain threshold point an action potential will start, but if not (a subthreshold -55mV) , the action potential wont occur.

111
Q

Where does electrical synapses occur? Give an example

A

Through gap junctions

112
Q

What is the difference between spatial summation and temporal summation?

A

Spatial summation is when two neurons join at a point and their APs add together

While temporal summation is when one neuron’s multiple APs send it in high frequency and they add together

113
Q

What is the time it takes for calcium 2+ to diffuse across synaptic cleft?

A

0.5ms

114
Q

WHat is an example of enzymes that degrade neurotransmitters?

A

Acetylcholerase

Mono amine oxidase

115
Q

How do u remeber excitatory neurotrasmitters?

A

‘Get excited about it ay mate’

ACh and glutamate

116
Q

How do u remember inhibitory neurotransmitters?

A

‘Dont get down about the glycine GABA”

GABA and Glycine

117
Q

What is the triad?

A

The T tubule and two Sarcoplasmic reticulum around it

118
Q

Ca2+ binds to ___ which holds ______ in place

A

Ca2+ binds to troponin which holds tropomyosin in place

119
Q

What is the sarcolemma?

A

The layer around all the bundles of myofibrils

120
Q
A
121
Q

Explain the length tension relationship

A

During an isometric contraction –

At the level of the sarcomere the maximum force (tension developed) is dependent on the degree of actin and myosin overlap

122
Q

Draw the lenght tension relationship graph

A
123
Q

At lengths <____ filaments collide and interfere with each other reducing force developed

A

At lengths <2.0 μm filaments collide and interfere with each other reducing force developed

124
Q

At lengths>_____active forces decline as the extent of overlap between filaments reduces, reducing the number of cross bridges

A

At lengths>2.2μm active forces decline as the extent of overlap between filaments reduces, reducing the number of cross bridges

125
Q

Maximal force between

A

Maximal force between 2.0 – 2.2 μm

126
Q

WHat is passive force?

A

As muscle is stretched the connective tissue around the muscle cells resists the stretch = passive force.

127
Q

How do you find out total tnsion?

A

Total tension is the sum of the active tension dependent on the sarcomere length and the passive tension

128
Q

Under normal conditions, this is maximal at a sarcomere length of

A

Under normal conditions, this is maximal at a sarcomere length of 2.0 – 2.2 μm (2.0 – 2.2 x 10-6 m).

129
Q

it is important to appreciate that during injuries, the possible range of sarcomere lengths may

A

increase.

130
Q

The active force _____ as the extent of overlap between the filaments reduces, which ____ the number of possible cross bridge interactions along the sarcomere;

A

The active force declines as the extent of overlap between the filaments reduces, which reduces the number of possible cross bridge interactions along the sarcomere;

131
Q

Definea motor unit

A

A motor unit consists of a motor neuron and all the muscle fibers it innervates.

132
Q

Explain this step ‘1. ACh released into neuromuscular junction’

A
  • An action potential travels down the motor neuron
  • At the axon terminal Ca2+ channels open, and Ca2+ enters the axon terminal
  • This triggers the vescicles containing ACh to fuse with the terminal membrane, releasing ACh into the neuromuscular junction (synaptic cleft)
133
Q

Explainthis step: 2. Activation of ACh receptors

A
  • The binding of ACh to the receptors on the muscle end plate causes opening of the ligand (ACh) gated ion channels.
  • Opening of these channels allows movement of predominantly Na+ into the muscle cell making it less negative (end plate potential)
134
Q

Why are the effects of Ach are short lasting?

A

the enzyme acetylcholinestarase rapidly breaks down Ach

135
Q

Explain this step: 3. A Muscle Action Potential is triggered

A
  • If sufficient ligand gated channels are opened the end plate potential reaches threshold
  • Voltage gated Na+ channels open and an action potential is triggered
  • The action potential is then propagated along the sarcolemma into the T tubule system
136
Q

WHat is the difference between a skeletal muscle AP and a nerve cell AP?

A

Skeletal muscle has a resting membrane potential of -90mV (which is more negative than the RMP of nerve cells)

137
Q

Explain this step: 4. Calcium is released from the SR

A
  • The action potential is conducted down the t‐ tubules coming in close contact with the sarcoplasmic reticulum.
  • This results in voltage gated Ca2+ channels in the sarcoplasmic reticulum opening.
  • Ca2+ is then released into the cytosol
138
Q

Explain this step: Ca2+ binds with troponin

A

• When Ca2+ concentrations reach a critical threshold the myosin binding sites on the actin filament are exposed allowing the cross‐bridge cycle to occur

139
Q

Explain this step: Contraction ends when Ca2+ levels fall

A
  • Calcium is actively pumped back into the sarcoplasmic reticulum via Ca2+‐ATPase pumps
  • Troponin moves back covering the myosin binding site
140
Q

What is the role of creatine phosphate?

A

For brief periods (<15s) creatine phosphate can act as an ATP “store”

Creatine phosphate + ADP = creatine + ATP

Anaerobic

141
Q

Explain the difference in type 1 and type 2 muscle fibres and their uses:

A

Type 1 is used for more aerobic activity, it has a small diameter and have high mitochondria and have good blood supply therefore look red. use by marathon runners.

Type 2 are used in powerlifters. They are larger in diameter and have less mitochondria as they mostly use anaerobic glycolysis

142
Q

WHat is the regulation of force Dependent on?

A
  • Rate of stimulation of individual motor units
  • The number or motor units recruited
143
Q

How long is the AP in a muscle fibre?

A

2ms

144
Q

Explain the action of slow twitch vs fast twicth fibres:

A

Type 1 (“slow twitch”):

• Units with neurons innervating the slow efficient aerobic cells (maintaining posture, walking)

Type 2 (“fast twitch”):

• Units with the neurons innervating the large fibres that fatigue rapidly but develop large forces (jumping, weight lifting)

145
Q

The efflux of calcium from the SR causes the myoplasmic calcium levels to ____ from about ____________.

Calcium is then pumped back into the SR by a ___ _____, which uses ATP as an energy source (_____).

A

The efflux of calcium from the SR causes the myoplasmic calcium levels to increase from about 10–7M to 10–5M.

Calcium is then pumped back into the SR by a calcium pump, which uses ATP as an energy source (Ca-ATPase).

146
Q

What is the eznyme called that transfers Pi from Creatine-Pi to ADP to give ATP?

A

creatine phosphokinase

147
Q

Explain the role of adenylate kinase

A

ATP may also be formed from two molecules of ADP by adenylate kinase to give one molecule of ATP and one of AMP. (anaerobically)

148
Q

Explain temporal sumation in terms of calcium levels in muscles

A

Since the duration of the action potential is much shorter than that of the calcium transient, additional action potentials can be initiated before the calcium levels return to resting levels (and the muscle has not relaxed).

This leads to the calcium levels remaining elevated and continuing force development. This effect is called temporal summation of the calcium transients and the force continues to rise until a higher steady level is achieved, called a tetanus.

Hence, the amount of force developed by a muscle depends both on the rate of stimulation of individual fibres as well as the number of fibres activated.

149
Q

Draw a table comparing Type 1, Type 2A and type 2B muscle fibres on:

Max. ATPase Rate

SR Pumping Capacity

Diameter

Mitochondria/ Myoglobin/ Blood Supply

Glycolytic capacity

A
150
Q

Thus, physical training can alter the composition of a muscle to match the demands placed upon it, by both changing

A

innervation patterns as well as the production of new muscle fibres (by division of existing fibres).

151
Q

Sustained use leads to muscle ____ while a reduction in activity (due to a loss of innervation or sloth) leads to muscle _____.

A

Sustained use leads to muscle hypertrophy while a reduction in activity (due to a loss of innervation or sloth) leads to muscle atrophy.

152
Q
A
153
Q

Atrial cells are about ____μm long and ___μm in diameter with a central nucleus.

A

Atrial cells are about 100 μm long and 10 μm in diameter with a central nucleus.

154
Q

Do ventircular msucles have t-tubules?

A

Yes

155
Q

Do atrial cells have t tubules?

A

no

156
Q

Ventricular cells are larger (typically __ μm long and __ μm in diameter)

A

Ventricular cells are larger (typically 100 μm long and 30 μm in diameter)

157
Q

______ prevent ventircular cells from separating during contraction

A

Desmosomes prevent cells from separating during contraction

158
Q

Contain _________that allow the action potentials to be carried from one cell to the next

A

Contain gap junctions that allow the action potentials to be carried from one cell to the next

159
Q

How long is the Ventricular myocyte action potential?

A

• Long lasting! >100ms

160
Q

Draw the ventricular myocyte action potential graph

A
161
Q

Explain this graph

A

0 – rapid depolarisation due to fast voltage‐gated Na+ channel

2 – plateau phase due to slow voltage gated Ca2+ channel (L‐type Ca2+ channel)

3 – repolaristation due to closing of Ca2+ channels and opening of K+ (outward) channels

162
Q

The heart has numerous ______ and large amounts of ________

A

The heart has numerous mitochondria and large amounts of myoglobin

163
Q

Each cell has ______ nuclei and growth occurs mainly through _______ with relatively little cell division (after birth).

A

Each cell has one to three nuclei and growth occurs mainly through hypertrophy with relatively little cell division (after birth).

164
Q

Explain cardiac muscle contraction

A
  • Depolarization opens voltage‐gated fast Na+ channels in the sarcolemma
  • Reversal of membrane potential from –90 mV to +30 mV
  • Depolarization wave opens slow (L‐ type) Ca2+ channels in the sarcolemma (DHPR)
  • Ca2+ surge prolongs the depolarization phase (plateau)
  • Ca2+ influx balanced by a Na+/Ca2+ exchanger
  • Ca2+ influx triggers opening of Ca2+‐ sensitive channels in the SR (RyRa), which liberates bursts of Ca2+ (i.e. calcium induced calcium release)
  • E‐C coupling occurs as Ca2+ binds to troponin and sliding of the filaments begins (same as in skeletal muscle)
  • Duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscle
  • Calcium pumped out via SR Ca‐ATPase (SERCA) and extruded via Na+/Ca2+ exchanger
165
Q

What does myogenic mean?

A

Cardiac muscle is myogenic – it initiates contractions without nervous input.

166
Q

Action potentials are initiated in a group of specialised cells in the _____ _______ called the __________.

The action potential spreads throughout the atria and then via specialised conducting cells called _________ to the ventricles.

A

Action potentials are initiated in a group of specialised cells in the right atria called the sino-atrial node.

The action potential spreads throughout the atria and then via specialised conducting cells called Purkinje fibres to the ventricles.

167
Q

Regation of Cardiac Output (CO) formula?

A

CO = stroke volume x Heart rate

168
Q

Stroke volume (SV) reflects the tension developed by the cardiac muscle fibres in one contraction. Can be increased by:

A
  • ‐ increased stretch of ventricles (length)
  • ‐ increased rate of firing (heart rate/HR)
  • ‐ certain hormones (e.g. Noradrenaline)
169
Q

Explain this graph

A

1 Pacemaker potential: This slow depolarization is Mostly due to opening of Na+ channels.

2 Depolarization: At threshold, Ca2+ channels open. Explosive Ca2+ influx produces the rising phase of the action potential .

3 Repolarization is due to Ca2+ channels inactivating and K+ channels opening.

170
Q

Explain Autonomic innervation of the heart.

A
171
Q

How does epinephrin work?

A

Increases rate of spontaneous depolarization = increase heart rate

172
Q

How does ACh work on the heart?

A

Decrease rate of spontaneous depolarization and decreases MDP = decrease heart rate

173
Q
A
174
Q

Why does Increasing heart rate increases contractile force (stroke volume)?

A

due to less time available for Ca2+ to be pumped out of cell

175
Q

How does norandrenaline affect stroke volume?

A

Acts via β receptors on L‐ Type channels resulting in more calcium entering the cell.

‐Also acts on Ca2+ pump in SR so SR increases its Ca2+ stores

Net result = bigger/shorter contraction

176
Q

Noradrenaline released by

A

sympathetic nerves

177
Q

Smooth muscle cells are very _______ (typically ____ μm long and ______ in diameter) with a ___ central nucleus and tapered at the ends.

A

Smooth muscle cells are very long and thin (typically 100–400 μm long and 5–10 μm in diameter) with a single central nucleus and tapered at the ends.

178
Q

They may be connected to each other by ‘________’ or by ____ junctions and groups of cells may be ____ connected.

A

They may be connected to each other by ‘dense bodies’ or by gap junctions and groups of cells may be electrically connected.

179
Q

What are the 2 Arrangements of smooth muscle in the walls of hollow organs

A

Longitudinal layer of smooth muscle

Circular layer of smooth muscle

180
Q

Are there t tubules in smooth muscle?

A

No T‐tubules – caveolae instead (act to increase surface area)

181
Q

What are the roles of dense bodies in smooth muscle?

A

Dense bodies act like z‐lines to “anchor” actin to sarcolemma

182
Q

No Troponin – the regulatory protein is instead

A

calmodulin

183
Q

How can smooth muscle be contracted?

A

neural, hormonal or spontaneous (myogenic)

  1. Myogenic with slow waves of depolarisation (e.g. gut)
  2. Neurally induced contraction (e.g ciliary and iris muscles)
184
Q
A
  1. Calcium ions (Ca2+) enter the cytosol from the ECF via voltage‐ dependent or voltage‐ independent Ca2+ channels, or from the scant SR.
  2. Ca2+ binds to and activates calmodulin.
  3. Activated calmodulin activates the myosin light chain kinase enzymes.
  4. MLCK activates the myosin ATPases.
  5. Activated myosin forms cross bridges with actin of the thin filaments and shortening begins in the usual fashion.
185
Q

Explain Activation of Myosin by mysosin light chain kinase (MLCK)

A

Calmodulin binds with the myosin light chain kinase phosphoralating the light chains (e.g. LC20) located on the neck of the myosin, in turn activating the ATPase on the myosin

186
Q

How to turn on and off MLCK (Myosin light chain kinase) ?

A

– activated by calmodulin‐Ca2+

Phosphatase required to de‐phosphoralate the myosin light chain

187
Q

In smooth muscle Contraction ends when

A

a myosin light chain phosphatase dephosphoraltes the myosin light chain.

188
Q

Does Ca@= affect length of contraction?

A

Ca++ concentration does not determine the length of the contraction.

189
Q

Smooth muscle contraction is ____ regulated

A

Smooth muscle contraction is enzyme regulated

190
Q

When you stretch smooth muscle it will generally

A
  1. Initially contract, effectively resisting the stretch

‐stretch activated calcium channels
2. Slowly relax, adapting to the change in length

‐ via calcium dependent K+ channels

191
Q
A

biosci 107 (7 decks)

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