Nervous coordination and muscles Flashcards

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1
Q

Synapse definition

A

The point where one neurone connects with another or an effector

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2
Q

2 types of synapse

A

Excitatory and inhibitory

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3
Q

Excitatory synapse

A

depolarise the postsynaptic membrane, so a new action potential is more likely to be triggered

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4
Q

Inhibitory synapse

A

hyperpolarise the postsynaptic membrane, to make it less likely a new action potential will be triggered. A larger influx of Na+ would then be needed to generate an action potential.

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5
Q

How do inhibitory synapses cause hyperpolarisation?

A

The presynaptic neurone releases a neurotransmitter which causes chloride ion channels to open, so chloride ions move into the postsynaptic neurone and make the inside of the postsynaptic neurone more negative - increased membrane potential.

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6
Q

Structure of a synapse

A

Synaptic cleft = gap
Presynaptic and postsynaptic neurones
Synaptic knob - end of pre-s. Contains many mitochondria and ER to make neurotransmitter.
Synaptic vesicles - where neurotransmitter is stored.
Calcium ion channels - in pre-s membrane
Sodium ion channels with neurotransmitter receptors - in post-s

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7
Q

Features of synapses

A

Unidirectionality - information is only passed in 1 direction, from the presynaptic to the postsynaptic neurone.
Summation

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8
Q

Temporal summation

A

multiple action potentials arrive at the presynaptic knob in quick succession. The same presynaptic neurone releases neurotransmitter many times in a short period. Neurotransmitter builds up in the synaptic cleft and its concentration exceeds the threshold value.

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9
Q

Spatial summation

A

many presynaptic neurones connect to the same postsynaptic neurone. Each presynaptic neurone releases a small amount of neurotransmitter, and together this is enough to reach the postsynaptic neurone threshold and generate an action potential.

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10
Q

Cholinergic synapse - process

A

1) The arrival of an action potential at the end of the presynaptic neurone causes calcium ion channels to open
Calcium ions diffuse into the synaptic knob.

2) The Ca2+ influx causes synaptic vesicles in the presynaptic neurone to fuse with the pre-s membrane, releasing acetylcholine into the synaptic cleft.
3) acetylcholine diffuses across the synaptic cleft and binds to receptor sites on sodium ion protein channels on the postsynaptic membrane. This causes the Na+ channels to open, so Na+ diffuse into post-s.
4) this causes depolarisation, and if the threshold is reached, a new action potential is generated in the postsynaptic neurone.
5) Acetylcholine esterase hydrolyses acetylcholine into choline and ethanoic acid, which diffuse back across the synaptic cleft into the presynaptic neurone.
6) ATP from mitochondria is used to recombine choline and ethanoic acid to make acetylcholine. Na+ channels close in the absence of acetylcholine.

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11
Q

What is a neuromuscular junction?

A

The point where a motor neurone reaches a muscle fibre.

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12
Q

Why can information pass in one direction only at synapses?

A

The neurotransmitter is produced in the presynaptic neurone only.
Receptor proteins for the neurotransmitter are only found on the postsynaptic membrane. The neurotransmitter diffuses down a concentration gradient.

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13
Q

Motor neurone structure

A

Cell body - contains organelles, including a lot of RER for production of proteins and neurotransmitters.
Dendrons - extensions of cell body which branch into dendrites. They carry nerve impulses from the previous neurone to the cell body.
Axon - long fibre which carries nerve impulses from the cell body to the next neurone.
Schwann cells - layers of cells around myelin sheath which secrete myelin. They protect and insulate the axon.
Myelin sheath - formed of the lipid myelin, insulates the axon.
Nodes of Ranvier - gaps between Schwann cells where there’s no myelin sheath.

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14
Q

3 types of neurone

A

Sensory: transmit impulse from receptor to intermediate.
Intermediate: transmit info between neurones, e.g. sensory to motor.
Motor: transmit impulse from intermediate to effector.

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15
Q

How is the resting potential maintained in a neurone? 2 types of protein channel

A

Sodium potassium pump: actively transports 2K+ into the neurone for every 3Na+ out. More Na+ move out than K+ in, so an electrochemical gradient is established across the membrane.
Potassium ion channels - allow for the facilitated diffusion of K+ out of the neurone, down their conc grad.
Sodium ions can’t diffuse back into the neurone as the membrane is impermeable to Na+.

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16
Q

Stages of an action potential

A

STIMULUS: excites the neurone, causing some Na+ channels to open, so Na+ diffuse into the neurone down their EC grad. Inside of neurone becomes less negative.
DEPOLARISATION: if the potential difference reaches a threshold of around -55mv, more Na+ channels open and more Na+ diffuse into the neurone.
REPOLARISATION: at P.D. of around +30mv, sodium channels close and potassium channels open. Potassium ions diffuse out of the neurone down their EC grad and the membrane starts to return to its resting potential.
HYPERPOLARISATION: potassium ion channels are slow to close and more K+ leave the neurone than are needed to reach the resting potential. P.D becomes more negative. (refractory period)
RESTING POTENTIAL: ion channels are reset, the sodium potassium pump returns the membrane to its resting potential.

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17
Q

What is depolarisation in an action potential, and how is it caused?

A

A temporary reversal in the potential difference of the membrane - the inside becomes more positive rather than negative, caused by an influx of Na+.

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18
Q

Passage of an action potential along an unmyelinated neurone

A

the impulse travels as a wave of depolarisation along the whole length of the axon membrane. Sodium ions enter the neurone and diffuse sideways, causing sodium ion channels to open further along.
The wave travels away from parts of the membrane in the refractory period.

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19
Q

Purposes of the refractory period

A

Discrete impulses - a new AP cannot be formed immediately after the first, so APs are separated.
Unidirectionality - action potentials can only move in a forwards direction, as they cannot be generated in a region in the refractory period.
Limit to number of APs - as they are separated from each other, a limited number of APs can pass along an axon in a give time.

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20
Q

What is happening during the refractory period?

A

Ion channels are being reset and can’t be made to open. It is impossible for another AP to be generated.

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21
Q

All-or-nothing nature of action potentials

A

If the threshold is reached, an AP with the same change in voltage is generated, no matter how large the stimulus.
If the threshold isn’t reached, no action potential is generated.
Larger stimulus => more frequent action potentials.

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22
Q

Passage of an AP along a myelinated neurone

A

Depolarisation can only happen at the nodes of ranvier, as ion channels are here only. The neurone’s cytoplasm conducts electrical charge, allowing for depolarisation at the next node. The impulse jumps from node to node.
This is salutatory conduction, and is faster than passage along an unmyelinated neurone.

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23
Q

How does axon diameter affect the speed of conductance?

A

APs are conducted more quickly along axons with larger diameters - there is less resistance to ion flow in the cytoplasm, and depolarisation spreads more quickly.

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24
Q

How does temperature affect the speed of conductance?

A

Speed increases as temperature increases as ions diffuse more quickly. The optimum is around 40oC, as after this proteins denature.

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25
Q

How can drugs interact with synapses?

A

-Mimic neurotransmitter at receptors, so more receptors are activated.
-Block receptors so they can’t be activated by the neurotransmitter.
-Inhibit the enzyme that breaks down the neurotransmitter (more NT remains in the synaptic cleft to bind to and activate receptors)
-Block protein needed for reuptake of neurotransmitter.
-Stimulate the release of more neurotransmitter by the presynaptic neurone.
Inhibit the release of neurotransmitter.

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26
Q

How do skeletal muscles act (not on microscopic scale)

A

in antagonistic pairs against an incompressible skeleton - eg the biceps and triceps.

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27
Q

How is skeletal muscle joined to bones?

A

by tendons

28
Q

What does the sarcoplasm contain?

A

mitochondria and extensive sarcoplasmic reticulum (ER)

29
Q

What do muscle cells that form a fibre share?

A

nuclei and sarcoplasm

30
Q

What is muscle divided into?

A

groups of muscle fibres

31
Q

What is each muscle fibre formed of?

A

protein filaments called myofibrils

32
Q

What else do muscles contain?

A

nerve fibres and blood vessels

33
Q

What is a myofibril?

A

the tiny elongated contractile strands fibres which wrap around each other to form bundles which make up the muscle

34
Q

Structure of actin

A

thinner filament, has binding sites for myosin heads

35
Q

Structure of myosin

A

Has globular heads which bind to actin, ATP binding sites

36
Q

What is a sarcomere?

A

the contractile unit of a myofibril, the distance between 2 Z-lines.

37
Q

What are the light bands of a sarcomere called? Why are they light?

A

I-bands, light as actin and myosin don’t overlap here - there is actin only.

38
Q

What is the Z-line?

A

where actin filaments are connected to each other in a zigzag structure, the boundary between sarcomeres.

39
Q

What are the dark bands of a sarcomere called, and why are they dark?

A

A-bands, where actin and myosin filaments overlap.

40
Q

What is the H-zone?

A

the lighter section in the middle of A bands where only myosin is present.

41
Q

How does the banding pattern of a sarcomere change when the muscle contracts?

A
v) I band – gets shorter
 A band – stays the same
 H-zone – gets shorter
 Z – line – gets closer
 together
42
Q

How does the length of a sarcomere change as the muscle contracts?

A

the sarcomere gets shorter, the Z-lines get closer together.

43
Q

What is a neuromuscular junction?

A

a synapse where a motor neurone meets a skeletal muscle fibre.

44
Q

What is the advantage of there being many neuromuscular junctions throughout the muscle?

A

It allows the entire muscle to receive electrical impulses and contract rapidly and simultaneously. If there was only one neuromuscular junction, it would take time for contraction to travel across the muscle and movement would be slow.

45
Q

What is a motor unit?

A

all the muscle fibres supplied by a single motor neurone, which act together as a single functional unit.

46
Q

Transmission at a neuromuscular junction

A
  1. A nerve impulse reaches a neuromuscular junction.
  2. Synaptic vesicles fuse with the presynaptic membrane and release acetylcholine.
  3. Acetylcholine diffuses to the postsynaptic membrane (membrane of the muscle fibre).
  4. Acetylcholine binds to receptors and causes the permeability of the postsynaptic membrane to sodium ions to increase, so Na+ enter rapidly and cause depolarisation.
  5. This leads to muscle contraction (see later on).
47
Q

What happens to acetylcholine after it has stimulated receptors on the postsynaptic (muscle fibre) membrane and why?

A

The acetylcholine is broken down by acetylcholinesterase into acetyl and choline, which diffuse back into the presynaptic neurone. This means the muscle isn’t overstimulated. Acetylcholine can be remade using energy from mitochondria.

48
Q

Similarities between a neuromuscular junction and cholinergic synapse

A
  • use the neurotransmitter acetylcholine
  • use enzymes to break down the neurotransmitter
  • have receptors on the post-synaptic membrane which cause an influx of sodium ions when the neurotransmitter binds.
49
Q

Differences between a neuromuscular junction and cholinergic synapse (5)

A

N: Only excitatory ( ⇒ contraction)
C: Can be excitatory or inhibitory

N: Link neurones to muscles only
C: Link neurones to neurones or other effector organs

N: Only motor neurones are involved
C: Sensory, motor and intermediate neurones may be involved.

N: The action potential ends here
C: A new action potential may be produced in the postsynaptic neurone.

N: Acetylcholine binds to receptors on the membrane of the muscle fibre
C: Acetylcholine binds to receptors on the postsynaptic neurone.

50
Q

Describe how slow twitch muscle fibres contract

A

They contract more slowly and less powerfully than fast-twitch fibres, but over a longer time period.

51
Q

How are slow twitch fibres adapted? (3)

A

They are adapted for aerobic respiration so they can avoid a build up of lactic acid, which would cause less effective contraction.

  • Large store of myoglobin, which stores oxygen.
  • Rich supply of blood vessels to deliver oxygen and glucose for aerobic respiration.
  • Many mitochondria to produce ATP.
52
Q

Describe the contractions of fast twitch muscle fibres.

A

They contract more rapidly and produce more powerful contractions than STF, but only for a short period. They are adapted for intense exercise, e.g. weight-lifting, sprinting.

53
Q

How are fast twitch muscle fibres adapted? (4)

A
  • Thicker and more myosin filaments
  • High concentration of glycogen
  • High concentration of enzymes involved in anaerobic respiration, which can quickly produce ATP.
  • A store of phosphocreatine, which can rapidly produce ATP from ADP under anaerobic conditions and provide energy for muscle contraction.
54
Q

How are nerve impulses specific to a target cell

A

as the impulse releases a chemical messenger directly onto it, producing a response

55
Q

Describe the role played by calcium ions in muscle contraction.

A

Ca2+ cause tropomyosin to change shape and move, uncovering the binding sites on actin, so allowing action-myosin cross-bridges to form/ myosin to bind.
Ca2+ also activate ATP hydrolase on myosin, allowing ATP hydrolysis to occur.

56
Q

Explain how a muscle cell contracts.

A
  1. Calcium ions diffuse into myofibrils from sarcoplasmic reticulum;
  2. Calcium ions cause movement of tropomyosin on actin;
  3. This movement causes exposure of the binding sites on the actin;
  4. Myosin heads attach to binding sites on actin;
  5. Hydrolysis of ATP on myosin heads causes myosin heads to bend;
  6. Bending pulls actin molecules;
  7. Attachment of a new ATP molecule to each myosin head causes myosin heads to detach from actin sites;
57
Q

Explain the role of ATP in muscle contraction.

A

ATP is the energy source to enable detachment and movement of the myosin head (power-stroke).
active transport of Ca2+ back into SR.

58
Q

What is the role of phosphocreatine in providing energy for muscle contraction?

A

phosphocreatine is a phosphate store which can be used to generate ATP rapidly from ADP in anaerobic conditions. ADP + PCr + H+ ==> ATP+ Cr

59
Q

Explain the advantage of having large amounts of glycogen in fast-twitch muscle fibres.

A

Glycogen can be converted into glucose. Large amounts of glucose are required to produce enough ATP in anaerobic respiration, as glycolysis is inefficient.

60
Q

Explain the advantage of slow-twitch muscle fibres having capillaries in close contact.

A

short diffusion pathway for glucose and oxygen from the blood to muscle fibres, where they are required for aerobic respiration. Also SDP for removal of CO2 and heat.

61
Q

Explain the role of mitochondria in muscle contraction.

A

produce ATP in aerobic respiration, which is needed to release and move myosin head, active transport of Ca2+

62
Q

Explain what happens during the delay between maximum depolarisation in the preSN and postSN.

A

Ca2+enter the preSN, causing vesicles to fuse with the preSM and release neurotransmitter, which diffuses across the synaptic cleft. Neurotransmitter attached to receptors on the postSM, causing Na+ ion channels to open.

63
Q

Acetylcholine is normally hydrolysed by an enzyme at the neuromuscular junction. Some insecticides inhibit this enzyme. Suggest how these insecticides are effective in killing insects.

A

The insecticide binds to the enzyme, preventing it from hydrolysing ACh, which remains attached to receptors. Na+ channels remain open, so muscles are continually stimulated and remain contract. The insect is unable to fly or breathe.

64
Q

Explain the advantage of possessing both slow and fast-twitch muscle fibres.

A

Fast fibres make fast contraction possible in anaerobic conditions, can be used for sprinting/ fast movement.
Slow fibres allow sustained contraction as energy is generated aerobically. Used for maintaining posture and endurance.

65
Q

Why does rigor mortis (muscles become rigid) occur after death?

A

ATP is not being produced, so myosin heads remain bound to actin and cannot unattach for filaments to slide to relaxed positions.

66
Q

Why is ATP a suitable energy source for cells to use?

A
  1. Releases relatively small amount of energy / little energy lost as heat;
  2. Releases energy instantaneously/ energy is readily available;
  3. Phosphorylates other compounds, making them more reactive;
  4. Can be rapidly re-synthesised;
  5. Is not lost from/does not leave cells;