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Biology A-level > nervous coordination and muscles > Flashcards

nervous coordination and muscles Flashcards

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

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

A

Na-K pump

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30
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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31
Q

what does the Na-K pump create?

A

electrochemical gradient

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32
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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33
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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34
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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35
Q

What is an action potential?

A

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

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36
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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37
Q

What protein channels are voltage dependent?

A

voltage-gated Na+ channels

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38
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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39
Q

What happens if the voltage is raised above the threshold?

A

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

40
Q

What is the maximum voltage an axon can reach?

A

+40mV

41
Q

What happens at +40mV?

A

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

42
Q

What is the refractory period?

A

once an action potential has been generated the sodium voltage gated channels close preventing further action potential from being generated

43
Q

What are the different stages in generating an action potential?

A

resting, depolarisation, repolarisation, hyperpolarisation, resting

44
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

45
Q

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

A

nothing, the action potential and impulse are not produced

46
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

47
Q

What does a bigger stimuli cause?

A

a greater frequency

48
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

49
Q

what does the refractory period mean

A

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

50
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

51
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

52
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

53
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

54
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

55
Q

difference in membrane permeability in resting potential

A

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

56
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

57
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

58
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

59
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

60
Q

At what point can sodium and potassium ions exchange in a myelinated axon

A

Nodes of Ranvier

61
Q

Why can sodium and potassium only exchange at Nodes of Ranvier in a myelinated axon

A

because the remainder of the axon is covered by a myelin sheath that prevents ions being exchanged

62
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

63
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

64
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

65
Q

define synapse

A

junction between neurones, they do not touch and have a small gap through which neurotransmitters pass

66
Q

define the structure of a synapse

A

Presynaptic and postsynaptic neurone separated by synaptic cleft. the end of the presynaptic neurone has a synaptic knob that contains vesicles of neurotransmitters and many mitochondria

67
Q

how is a synapse unidirectional

A

-neurotransmitter is only stored in the presynaptic
-neurotransmitter receptors are only found on the postsynaptic neurone

68
Q

Spatial summation

A

several presynaptic neurones converge on one postsynaptic neurone and together release enough neurotransmitter to reach threshold and trigger an action potential

69
Q

Temporal summation

A

A single presynaptic neurone releases neurotransmitter many times over a short period releasing enough neurotransmitter to reach threshold and trigger an action potential

70
Q

describe the function of a synapse

A

Transmit information from neurone to another allowing
-a single presynaptic neurone to stimulate several postsynaptic neurones
-Several presynaptic neurones to stimulate only one postsynaptic neurone

71
Q

Explain how a cholinergic synapse functions

A

-depolarisation of presynaptic neurone
-calcium ion protein channels open allowing calcium ions to diffuse into membrane
-synaptic vesicle fuses with presynaptic membrane releasing acetylcholine into synaptic cleft and diffuse across
-Acetylcholine bind with sodium ion channel in the postsynaptic membrane
-Sodium ions enter leading to depolarisation

72
Q

explain how acetylcholine is recyled

A

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

73
Q

Explain how a synapse is involved in inhibition

A

-neurotransmitter released binds to chloride ion channels on postsynaptic neurone
-chloride ions enter the postsynaptic neurone
-Binding of neurotransmitter opens potassium ion channels and potassium ions move out
-leads to hyperpolarisation
-action potential less likely as more sodium ions needed to reach threshold

74
Q

What are the three types of muscle

A

-cardiac
-skeletal
-smooth

75
Q

What is an individual muscle fibre made up of

A

Myofibrils

76
Q

What is the organisation of structures in muscle

A

-whole muscle is made up of bundles of muscle fibres
-bundles of muscle fibres contain lots of single muscle fibres which are made of myofibrils
-Myofibrils are made of sarcomere

77
Q

What is sarcomere made from

A

Proteins actin and myosin

78
Q

What happens to sarcomeres when the muscle contracts

A

-I band gets smaller/ shortens
-H zone gets smaller and disappears
-A band stays the same
-Z lines stay the same

79
Q

What are myofibrils made from

A

sarcomere

80
Q

What do bundles of muscle fibres contain

A

Blood capillaries and nerves

81
Q

What do single muscle fibres contain

A

A nucleus, mitochondria, sarcoplasmic reticulum

82
Q

What is the structure of actin

A

thinner filament consisting of two strands twisted around one another

83
Q

What is the structure of myosin

A

thicker filament and consists of long rod shaped tails with bulbous heads that project to the side

84
Q

Why do myofibrils appear striped

A

due to their alternating light and dark coloured bands
light bands= I bands (filaments don’t overlap)
dark bands= A bands
(filaments overlap)

85
Q

what are the two types of muscle fibres

A

-slow-twitch
-fast-twitch

86
Q

slow- twitch muscle fibres

A

contract more slowly and provide less powerful contractions but over a long period

87
Q

What are the adaptations of slow-twitch muscle fibres

A

-large store of myoglobin
-rich supply of blood vessels
-numerous mitochondria to produce ATP

88
Q

fast-twitch muscle fibres

A

contract more rapidly and produce more powerful contractions but only for a short period of time

89
Q

What are the adaptations of fast-twitch muscle fibres

A

-thicker and more numerous myosin filaments
-a higher concentration of glycogen
-a higher concentration of enzymes involved in anaerobic respiration
-a store of phosphocreatine

90
Q

neuromuscular junction

A

the point where a motor neurone meets a skeletal muscle fibre

91
Q

Why are there many neuromuscular junctions along the muscle

A

to ensure the contraction of a muscle is rapid and powerful when it’s simultaneously stimulated by an action potential

92
Q

muscle stimulation

A

-impulses in the motor neurone cause acetylcholine to be released at the neuromuscular junction
-this causes opening of sodium channels and depolarisation of the sarcolemma
-depolarisation of the muscle fibre cause the release of calcium ions into the sarcoplasm which causes the events of contraction into the sarcomere

93
Q

how do muscles contract

A

-tropomyosin normally covers the myosin binding sites on the actin filament, so the myosin heads cannot bind
-stimulated muscle cells release calcium from sarcoplasmic reticulum
-calcium bind to troponin causing the tropomyosin to move exposing the myosin binding site
-myosin heads can then attach to the actin filament resulting in contraction

94
Q

how ATP is used in muscle contraction

A

-myosin heads with ADP attach to the myosin binding sites on actin filaments
-ADP dissociates causing the myosin head to change shape moving the actin filament
-ATP then binds to myosin head, causing it to detach and reset
-myosin head hydrolyses ATP to ADP allowing it to bind further along

95
Q

Relaxation of muscles

A

-when the impulses in the neuron stop, calcium ions are pumped back into the sarcoplasmic reticulum, lengthening the sarcomere
-The tropomyosin moves back to cover the myosin binding sites so the myosin heads cannot bind and pull the actin filaments
-So the actin filaments begin sliding back, causing the sarcomere to lengthen

Biology A-level (31 decks)

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