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BIOLOGY PAPER 2 > Nervous coordination and muscles > Flashcards

Nervous coordination and muscles Flashcards

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1
Q

How do nerve cells stimulate their target cells

A

by secreting neurotransmitters directly on to them

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2
Q

what does secreting neurotransmitters directly on to target cells result in

A

rapid communication between specific parts of an organism

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3
Q

response produced by nerve cells

A

-short-lived
-restricted to a localised region of body

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4
Q

how does hormonal system transport chemicals (hormones)

A

in blood plasma to target their cells

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5
Q

what do target cells have

A

specific receptors on their cell surface membrane

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6
Q

what does a change in conc of hormones stimulate

A

specific receptors on cell surface membrane

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7
Q

results of hormonal system

A

-slower
-less specific form of communication between parts of an organism

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8
Q

response of hormonal system

A

long lasting
widespread

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9
Q

cell body

A

-contains usual organelles
-RER > production of proteins and neurotransmitters

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10
Q

what are neurones specialised to do

A

specialised cells adapted to rapidly carry electrochemical changes (nerve impulses) from one part of body to another

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11
Q

dendrons

A

-extensions of cell body which divide into dendrites
-carry nerve impulses TOWARDS cell body

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12
Q

axon

A

single long fibre that carries nerve impulses away from cell body

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13
Q

Schwann cells

A

-surround axon > protecting it and providing electrical insulation
-carry out phagocytosis
-play part in nerve regeneration
-wrap themselves around axon many times > layers of their membrane build up around it

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14
Q

myelin sheath

A

-made of membranes of Schwann cells
-membranes are rich in lipid (myelin)

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15
Q

what are neurones with myelin sheath called

A

myelinated neurones

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16
Q

nodes of Ranvier

A

-constrictions between adjacent Schwann cells where there’s no myelin sheath

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17
Q

um of constrictions of nodes of Ranvier

A
  • 2-3 um long
    -occur every 1-3mm in humans
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18
Q

sensory neurone

A

-transmit nerve impulses from receptors to an intermediate or motor neurone

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19
Q

structure of sensory neurone

A

-1 dendron thats often very long
-carries the impulse towards cell body and 1 axon that carries it away from cell body

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20
Q

motor neurone

A

transmit nerve impulses from an intermediate or relay neurone to effector

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21
Q

structure of motor neurones

A

-long axon
-many short dendrites

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22
Q

intermediate neurone

A

-transmit impulses between neurones eg sensory > motor
-have numerous short processes

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23
Q

define resting potential

A

potential difference across an axon membrane at rest (inside -65mV compared with outside)

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24
Q

How does phospholipid bilayer control Na+ and K+ across axons membrane

A

-phospholipid bilayer of axons plasma membrane prevents Na+ and K+to diffuse across it

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25
Q

How do proteins control Na+ and K+ across axons membrane

A

-channel proteins span this phospholipid bilayer
-some channels have ‘gates’ that can be open/closed so Na+ / K+ can move through them via facilitated diffusion
-some gates however remain open all the time so Na+ and K+ move unhindered through them by facilitated diffusion

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26
Q

how does sodium-potassium pump control Na+ and K+ across axons membrane

A

actively transport potassium ions into axon and sodium ions out axon

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27
Q

How a resting potential is established in neurone

A

-sodium potassium pump actively transport 3 Na+ out axons membrane and 2 K+ into axons membrane
-1 K+ moved via diffusion from high conc to lower conc through gated K+ channels that open
-Na+ channels remain firmed closed so Na+ cant move onto axon thus remain outside axon’s membrane tissue fluid
-tis makes inside less positive than outside > electrochemical gradient
-membrane more permeable to K+ than Na+ so they diffuse back out of axon further increasing potential difference across the membrane
-inside of axon less positive than outside to the value of -65mV
-polarisation of axon is created

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28
Q

Why is resting potential negative?

A

as there are more positive ions outside the cell, making the inside comparatively more negative

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29
Q

difference in membrane permeability in resting potential

A

-MORE permeable to K+ (somove out by facilitated diffusion
-LESS permeable to Na+ (closed channels)

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30
Q

What co-transport protein is involved in the maintenance of resting potentials?

A

Na-K pump

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31
Q

How many of each ion are transported each time by the Na-K pump?

A

2 x K+ INTO the cell
3 x Na+ OUT OF the cell

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32
Q

what does the Na-K pump create?

A

electrochemical gradient

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33
Q

Why is resting potentially end up negative, if both ions diffuse in/out?

A

because the membrane is more permeable to K+ ions

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34
Q

Why is the axon membrane more permeable to K+ ions?

A

-most K+ channels stay open (compared to Na+ ions which only open due to change in voltage)
-there are more K+ channels

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35
Q

How is resting potential maintained?

A

membrane more permeable to K+ ions and less permeable to Na+ ions
Na+ ions are actively pumped out and K+ ions in

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36
Q

What is an action potential?

A

an increased voltage beyond a set point, generating a nervous impulse

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37
Q

What is depolarisation and why does it occur?

A

an increase in voltage, which occurs as the membrane becomes more permeable to Na+

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38
Q

What protein channels are voltage dependent?

A

voltage-gated Na+ channels

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39
Q

How might a stimulus cause depolarisation?

A

as it may allow voltage-gated Na+ channels to open, allowing Na+ ions to diffuse in, meanwhile K+ ions still diffuse out

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40
Q

What happens if the voltage is raised above the threshold?

A

More Na+ ions can move into the cell, so voltage increases further

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41
Q

What is the maximum voltage an axon can reach?

A

+40mV

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42
Q

What happens at +40mV?

A

more K+ channels are opened, and voltage-gated Na+ channels close. This causes voltage to decrease

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43
Q

What is the refractory period?

A

where voltage goes temporarily below the resting potential

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44
Q

What are the different stages in generating an action potential?

A

resting, depolarisation, repolarisation, hyperpolarisation, resting

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45
Q

Why do action potentials move across an axon like a mexican wave?

A

as one part reaches +40mV, the voltage is enough to trigger the next part (nodes of Ranvier) of the axon to start depolarisation

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46
Q

What happens if the voltage does not pass -55mV?

A

nothing, the action potential and impulse are not produced

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47
Q

Why does a depolarisation that does not reach the threshold not cause an action potential?

A

not enough energy to open voltage gated Na+ channels

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48
Q

What does a bigger stimuli cause?

A

a greater frequency

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49
Q

Why is the all or nothing principle important?

A

makes sure animals only respond to large enough stimuli, rather than the animal becoming overwhelmed

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50
Q

what does the refractory period mean

A

action potential cannot be stimulated, as the Na+ channels are recovering

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51
Q

Why is the refractory period important?

A

-only discrete impulses are produced
-only travel forwards in one direction
-limits the number of impulse transmission

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52
Q

Why is it important that impulses are discrete?

A

so each action potential is separate and therefore information can be processed in more detail

53
Q

Why is it important that action potentials only travel forwards?

A

if it wasn’t, Na and K+ ions would spread out, preventing the threshold from ever being met and therefore preventing a response

54
Q

Why is it important that the number of action potentials are limited?

A

it prevents over reaction to a stimulus which could result in overwhelming the sense, hindering survival

55
Q

process of acton potential

A

-axon is polarised Na+ channels closed and K+ channels open
-Na+ diffuse into axon by sodium-gates channels which depolarised the axon by energy from stimulus
-reversal of electrochemical gradient causes the potential to increase to +40mV
-axon is depolarised and and increase in electrochemical gradient leads to hyperpolarisation > potential of -75mV
-axon eneters refractory period

56
Q

nature and importance of refractory period

A

-refractory period = time to restore axon at resting potential when no further action potential can be generated because Na+ channels are closed so will not happen

-ensures discrete impulses are produced (actions potentials don’t overlap)
-limits high frequency impulse transmission

57
Q

changes in membrane permeability lead to depolarisation and the generation of action potential

A

-STIMULUS > Na+ channels open, membrane permeability to Na+ increases > Na+ diffuse into axon down electrochemical gradient (causing depolarisation)
-DEPOLARISATION > if threshold potential reached, an action potential is generated > as more voltage-gated channels open (positive feedback effect) > more Na+ diffuse in rapidly
-REPOLARISATION > voltage-gated Na+ channels close> voltage-gated K+ channels open and K= diffuse out of axon
-HYPERPOLARISATION > K+ channels slow to close so there’s straight overshoot - too many K+diffuse out
-RESTING potential - restored by Na+/K+ pump

58
Q

passage of action potential in unmyelinated axon

A

1) at resting potential conc of Na+ outside axon is higher than inside and conc of K+ higher inside than outside > causes polarisation of the membrane as overall conc of + ions is greater on outside than inside
2) stimulus causes sudden influx of Na+ into axon > leading to reversal of charge > action potential and membrane is depolarised
3) localised electrical current established by influx of Na+ causes voltage-gated sodium channels to open little further along axon for new area of axon becoming depolarised > behind this new region of depolarisation Na voltage-gated channels close so K opens > K+ leave axon along electrochemical gradient so depolarisation moved along membrane
4)action potential (depolarised area) is propagated further along the axon > K+ continues to move out until axon membrane behind action potential has returned to its original charged state ( + outside, - inside) > leading to repolarisation
5)repolarisation of axon allows Na+ to actively move out again, once again returning the axon to its resting potential in readiness for new stimulus

59
Q

passage of action potential along myelinated axon

A

-fatty sheath of myelin along axon acts as electrical insulator, preventing action potential from forming
-intervals of 1-3mm there’s nodes of Ranvier where action potentials can occur
-localised circuits therefore arise between adj nodes of Ranvier and action potentials in effect jump from node to node in process of saltatory conduction

60
Q

why is an action potential passed along myelinated neurone faster than along the axon of an unmyelinated one of same diameter

A

-in an unmyelinated neurone, the events of depolarisation have to take place all the way along an axon and this takes more time

61
Q

difference between action potentials in myelinated and unmyelinated axons

A

NON-MYELINATED
-action potential passes a wave of depolarisation
-influx of Na+ in one region increases permeability of adjoining region of Na+ by causing voltage-gated Na+ channels to open so adjoining region depolarises

MYELINATED
-provides electrical insulation
-depolarisation of axons at NOR only -resulting in saltatory conduction ( local current circuits)
-so there’s no need for depolarisation along whole length of axon

62
Q

damage to myelin sheath causes what

A

-less/no saltatory conduction > so nerve impulse takes longer to reach neuromuscular junction /delay muscle contraction
-ions/depolarisation may pass > causing wrong muscle fibres to contract

63
Q

factors affecting speed at which neurones travel - myelin sheath

A

-acts as electrical insulator . prevent a.p. forming in the part of the axon covered in myelin
-it does jump from one node of ranvier to another (saltatory conduction) > increases speed of conductance from 30 ms-1 in unmyelinated neurone to 90ms-1 in similar myelinated one

64
Q

factors affecting speed at which neurones travel - diameter of axon

A
  • greater diameter the axon , faster the speed of conductance > due to less leakage of ions from a large axon (leakages make membrane potentials harder to maintain)
65
Q

factors affecting speed at which neurones travel - temp

A

-affects rate of diffusion of ions and so the higher the temp, the faster the nerve impulse
-energy for active transport comes from respiration for Na/K pump that is controlled by enzymes which function more rapidly at higher temps up to a point> after certain point they and plasma membrane proteins are denatured and impulses fail to be conducted at all

66
Q

why is temperature an important factor in cold blooded animals

A

their body temps vary in accordance with their environment

67
Q

Describe and explain the all or nothing principle

A

-There is a certain level of stimulus - threshold value - that triggers an action potential. -Below threshold no action potential or impulse (nothing), -above threshold action potential occurs but they are all the same size (all)

68
Q

why can’t the strength of a stimulus be detected by the size of the action potential

A

all action potentials are more or less the same size

69
Q

how can an organism perceive the size of a stimulus

A

-no. of impulses passing in a given time > larger the stimulus, the more impulses that are generated in a given time
-having different neurones with different threshold values > brain interprets the no. + type of neurone that pass impulses as a result of given stimulus thereby determines the size

70
Q

refractory period

A

Period of time time after an action potential when no further action potential can occur because the voltage gated sodium ion channels are closed.

71
Q

3 purposes of refractory period

A

-ensures that action potentials are propagated in one direction only > as action potentials cannot be propagated in a region that is refractory
-produced discrete impulses > due to refractory period a new action potential cannot be formed immediately behind first one > ensures a.p is separated
-limits the no, of a.p > this is due to them being separated > so this limits strength of stimulus that can be detected

72
Q

Define synapse

A

Junction between neurons, they don’t touch and have a small gap (synaptic clef) through which n.t are passed

73
Q

structure of a synapse

A

-n.t transmitted from one neurone to another
-neurones separated by small gap (synaptic cleft)
-presynaptic neurone releases n.t
-axon of presynaptic neurone ends in a swollen portion known as synaptic knob
-this processes many mitochondria and large amounts of endoplasmic reticulum
-these are required in manufacture of n.t which takes place in axon
-nt stored in synaptic vesicle

74
Q

features of synapse - unidirectionality

A

-can pass info in one direction > from presynaptic neurone to postsynaptic neurone

75
Q

summation

A

entails a rapid build up of nt in synapse by either spatial or temporal summation

76
Q

spatial summation

A

no of different presynaptic neurones together release enough n.t to exceed threshold value of posy synaptic neurone
-so together they trigger a.p

77
Q

temporal summation

A

-single presynaptic neurone releases n.t many times over a short period
-if conc of n.t exceeds threshold value of postsynaptic neurone, a new a.p is triggered

78
Q

how is it possible for impulses to travel 1 direction

A
  • neurotransmitter is only stored in the presynaptic neurone
  • neurotransmitter receptors are only found on the postsynaptic neurone
79
Q

· Explain how a synapse is involved in inhibition

A

-Inhibitory synapses make it less likely that an action potential is triggered in the postsynaptic neurone:
- The neurotransmitter released binds to chloride ion channels on post synaptic neurone
-Chloride ion channels open and chloride ions enter the postsynaptic neurone by facilitated diffusion
-Binding of neurotransmitter opens potassium ion channels and potassium ions move out of the postsynaptic neurone
-Movement of negative chloride ions in and positive potassium ions out makes the inside of postsynaptic membrane more negative and outside more positive > the membrane potential increase to -80mV (hyperpolarisation). This makes an action potential less like as more sodium ions need to enter to reach threshold.”

80
Q

Describe the functions of a synapse

A

-Transmit information from neurone to another allowing:
- single impulse along 1 neurone to initiate new impulses in a no of diff neurones at a synapse > allows single stimulus to create a no. of simultaneous responses
- no of impulses to be combined at a synapse > allows nerve impulses from receptors reacting to diff stimuli to contribute to a single response

81
Q

Explain how a cholinergic synapse functions

A

-depolarisation of presynaptic neurone
-Ca2+ channels open and Ca2+ diffuse (facilitated) into presynaptic neurone
-causes vesicles to move downwards towards presynaptic membrane and fuse to release acetylcholine into synaptic cleft
-acetylcholine diffuses across synaptic cleft
-acetylcholine binds to receptors on postsynaptic neurone
-acetylcholine binds to Na+ gate channels in membrane causing them to open
-Na+ enter postsynaptic neurone leading to depolarisation
-when it reaches a certain threshold there’s an influx of Na+

82
Q

Explain how acetylcholine is recycled

A

-Acetylcholine is hydrolysed by acetylcholinesterase into choline and ethanoic acid (acetyl)
-this prevents a continuous action potential in the postsynaptic neurone
-Choline and ethanoic acid (acetyl) diffuse back into the presynaptic neurone to be recombined into acetylcholine using ATP

83
Q

what are muscles

A

effector organs that respond to nervous stimulation by contracting and so bring about movement

84
Q

the 3 types of muscles

A

-cardiac
-smooth
-skeletal

85
Q

where is cardiac muscle found

A

heart

86
Q

where is smooth muscle found

A

wall of blood vessels and gut

87
Q

which muscles are not under conscious control

A

cardiac and smooth muscles

88
Q

skeletal muscle

A

-makes up the bulk of body muscle in vertebrates
-attached to bone and acts under voluntary control

89
Q

what are individual muscles made out of

A

-millions of tiny myofibrils
-in themselves they produce almost no force while collectively they can be extremely powerful

90
Q

in order to maximise strength how are myofibrils arranged

A

lined up parallel to each other in order to maximise its strength

91
Q

what are muscles composed of

A

smaller units bundled into progressively larger ones

92
Q

what would have happened if muscles were made up of individual cells joined end to end

A

-wont able to perform its function of contraction very efficiently
-due to junction between adjacent cells wont be a point of weakness that would reduce the overall strength of the muscle

93
Q

how do muscles overcome reduceness of the overall strength due to not being on a point of weakness

A

-separate cells have become fused together into muscle fibres
-these muscles fibres share nuclei and cytoplasm ( sarcoplasm) that’s mostly found around circumference of the fibre
-within sarcoplasm = large conc of mitochondria and endoplasmic reticulum

94
Q

what 2 protein filaments are myofibrils made of

A

-actin = thinner, consists of 2 strands twisted around one another
-myosin = thicker, consists of long rod-shaped tails with bulbous heads that project to the side

95
Q

how are myosin molecules joined together

A

tail to tail in the thick filament Z-line

96
Q

why do myofibrils appear stripped

A

due to their alternating light coloured and dark coloured bands

97
Q

name of light bands

A

I bands ( isotropic bands)

98
Q

why do I bands appear lighter

A

because the thick and thin filaments do not overlap in this region

99
Q

name of dark bands

A

A bands ( anisotropic bands)

100
Q

why do A bands appear darker

A

thick and thin filaments overlap in this region

101
Q

what is at the centre of the A band

A

-lighter coloured region called H-zone

102
Q

what is at the centre of each I band

A

line called Z-line

103
Q

what is the distance called between adjacent Z-lines

A

sarcomere

104
Q

what happens to the sarcomere when muscles contract

A

sarcomeres shorten and pattern of light and dark band changes

105
Q

another protein found in muscles

A

tropomyosin

106
Q

function of tropomyosin

A

forms fibrous strand around actin filament

107
Q

2 types of muscle fibre

A

-slow-twitch fibre
-fast-twitch fibre

108
Q

what do slow-twitch fibres do

A

-contract more slowly and provide less powerful contractions but over a longer period
-adapted to endurance work
-common in calf muscles which must contract constantly to maintain the body in an upright position

109
Q

how are slow-twitch fibres suited to their role

A

-adapted to aerobic respiration > to avoid build up of lactic acid that would cause them to function less effectively and prevent long-duration contraction

110
Q

how are slow-twitch fibres adapted for aerobic respiration

A

-large store of myoglobin > (bright red molecule that stores o2 which accounts for red colour of slow-twitch fibres)
-rich supply of blood vessels > deliver o2 and glucose for aerobic respiration
-numerous mitochondria for ATP production

111
Q

what to fast-twitch fibres do

A

-contract more rapidly and produce powerful contractions but for a short period of time
-adapted to intense exercise eg weight-lifting
-more common in muscles which need to do short bursts of intense activity eg bicep

112
Q

how are fast-twitch fibres adapted to their role

A

-thicker and more numerous myosin filaments
-high conc of glycogen
-high conc of enzymes involved in anaerobic respiration which provides ATP rapidly
-store of phosphocreatine > molecule that can rapidly generate ATP from ADP in anaerobic conditions and so provide energy for muscle contraction

113
Q

what are neuromuscular junctions

A

point where a motor neurone meets a skeletal muscle fibre

114
Q

there are many such junctions along muscle, what would have happened if there was only 1 junction

A

-take time for a wave of contraction to travel across the muscle
-not all fibres would contract simultaneously and movement would be slow

115
Q

why are rapid and coordinated muscle contraction frequently essential for survival

A

-there are more neuromuscular junctions spread throughout the muscle
-ensure contraction of a muscle is rapid and powerful when it is stimulated by action potentials

116
Q

whats a motor unit

A

all muscle fibres supplied by a single motor neurone act together as a single functional unit

117
Q

what does the arrangement of motor unit give

A

-control over the force that muscles exerts
-if only slight force needed, only few units are stimulated
-if greater force is required, a large no. of units are stimulated

118
Q

comparison of neuromuscular junction and synapse

A

-have n.t that are transported by diffusion
-have receptors that on binding with the n.t, cause an influx of Na+
-use a Na/K pump to repolarise the axon
-use enzymes to breakdown the n.t

119
Q

differences between neuromuscular junction and cholinergic synapse

A

neuromuscular junction
-only excitatory
-only links neurones to muscles
-only motor neurones are involved
-action potential ends here (end of neural pathway)
-acetylcholine binds to receptors on membrane of muscle fibre

cholinergic synapse
-may be excitatory/inhibitory
-links neurones to neurones or neurones to other effector organs
-motor, sensory and intermediate neruones may be invovled
-a new action potential may be produced along another neurone (postsynaptic neurone)
-acetylcholine binds to receptors on membrane of post-synaptic neurone

120
Q

Describe the gross structure of skeletal muscle

A

Sarcomere - myofibril - muscle fibre (cells fused end to end sharing nuclei, mitochondria and other organelles) - bundle of muscle fibres - muscle

121
Q

Describe the microscopic structure of skeletal muscle

A

-Protein filaments actin and myosin form sarcomeres.
-These overlap each other and appear striped on a micrograph.
I band - light - actin and myosin do not overlap
A band - dark - actin and myosin overlap
H zone - light - at the centre of the A band
Z line - dark - marks the ends of the sarcomere”

122
Q

· Explain how actin and myosin are arranged in a myofibril

A

-Actin - two thin strands twisted together, has binding sites for myosin heads.
-Tropomyosin wrapped around actin filament covering the myosin head binding sites
-Myosin - thick, rod shaped tails with bulbous heads to the sides
-Myosin filaments are joined tail to tail with heads protruding outwards, actin filaments are arranged in between the myosin, partially overlapping”

123
Q

Describe and explain the difference between slow-twitch and fast-twitch fibres

A

-Slow twitch - contract slowly with less power over longer periods of time. Adapted for aerobic respiration: large quantity of myoglobin (stores oxygen), rich blood supply, many mitochondria

-Fast twitch - contract rapidly, with power for a shorter period of time. Adapted by: thicker and more numerous myosin, high concentration glycogen, high concentration of enzymes for anaerobic respiration, store phosphocreatine (makes ATP from ADP in anaerobic conditions)”

124
Q

Describe the structure of a neuromuscular junction

A

-Presynaptic neurone (before synapse) and myofibril separated by a gap.
-The end of the presynaptic neurone has a synaptic knob that contains vesicles of neurontransmitter and many mitochondria.
-Myofibril has membrane folded into T tubles that are at right angles to the surface membrane and receptors for neurotransmitter.

125
Q

Explain what is meant by antagonistic muscles and how they operate

A

-Muscles can contract but they cannot extend, for this reason they are found in pairs.
-One muscle contracts and in order to return it to its original position the paired muscle contracts.

126
Q

Describe and explain how the sliding filament theory causes muscles to contract and relax

A

-Ca ions bind and move tropomyosin uncovering myosin head binding site on actin;
-This allows myosin heads to attach to actin filaments forming cross bridges;
-Myosin heads change angle causing actin to slide relative to myosin shortening the sarcomere;
-Binding of ATP causes myosin head to detach from actin;
-Hydrolysis of ATP releases energy which causes recocking of the myosin head;

127
Q

· Summarise the evidence that supports the sliding filament mechanism of muscle contraction

A

-Myofibrils appear darker where the actin and myosin filaments overlap.
-When muscle contraction occurs sliding filament theory suggests that there will be less light areas.
-This is evident from: I band narrower, H zone narrower, Z lines closer together.
-A band remains constant evidence the length of the myosin filament does not change.

128
Q

Describe the energy supply during muscle contraction

A

-Energy required for recocking myosin heads and actively transporting Ca ions into endoplasmic (sarcoplasmic) reticulum.
-Provided by hydrolysis of ATP to ADP and Pi.
-ATP provided by aerobic and anaerobic respiration.
-Phosphocreatine regenerates ATP during anaerobic respiration. It is stored in muscle and supplies phosphate to ADP

BIOLOGY PAPER 2 (15 decks)

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