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A2 Biology > Topic 6B - Nervous Coordination > Flashcards

Topic 6B - Nervous Coordination Flashcards

1
Q

Describe the state of a neurone cell membrane at rest

A

In a neurone’s resting state, the outside of the membrane is + charged compared to inside as there are more + ions outside the cell.
- so the membrane is polarised: there’s a difference in charge (PD/V) across it

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2
Q

Define the ‘resting potential’ (of a neuron cell membrane)

A

The voltage across a neuron cell membrane when it’s at rest - it’s about - 70 mV (millivolts)

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3
Q

How are resting potentials created and maintained?

(EXPLAIN HOW - 3 POINTS)

DIAGRAM

A

By Na-K pumps and K ion channels in a neurons membrane

  1. The Na-K pumps move Na+ out of neurone, but membrane isn’t permeable to Na+, so they can’t diffuse back in. This creates a Na+ electrochemical gradient (conc gradient of ions) as there are more positive Na ions outside cell than inside.
  2. Na-K pumps also move K+ in to neurone, but membrane is permeable to K+ so they diffuse back out through K+ channels
  3. This makes outside of cell + charged compared to inside
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4
Q

Describe and explain the neurone action potential graph.

GRAPH ON PAGE 146

A
  1. Stimulus: excites neurone cell membrane, causing Na+ channels to open. Membrane becomes more permeable to Na, so Na+ diffuse into neurone down Na+ electrochemical gradient, making inside of neurone less negative.
  2. Depolarisation: if potential difference reaches threshold (around - 55 mV), more Na+ channels open. More Na+ diffuse rapidly into neurone
  3. Repolarisation: at PV of approx +30 mV, Na+ channels close and K+ channels open. Membrane is more permeable to K so K+ ions diffuse out of neurone down the K+ conc gradient. This starts to get membrane back to resting potential.
    4) Hyperpolarisation: the K+ channels slow to close so there is a slight ‘overshoot’ where too many K+ diffuse out of neurone. PV becomes more - than resting potential).
    5) resting potential: ion channels are reset. The Na-K pump returns membrane to resting potential and maintains it until membrane is excited by another stimulus.
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5
Q

Define refractory period.

A

The period straight after an action potential, where neuron cell membranes can’t be excited again straight away.
- This is because the ion channels are recovering and can’t be made to open. (Na+ channels are close during repolarisation and K+ channels are closed during hyperpolarisation)

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6
Q

Describe how an action potential leads to a wave of depolarisation

DIAGRAM

A
  1. When an action potential happens, some of the Na+ that enter neurone diffuse sideways
  2. This causes Na+ channels in next region of neurone to open and Na+ diffuse into that part
  3. This causes wave of depolarisation
    - the wave moves away from parts of the membrane in the refractory period as these parts can’t fire an action potential
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7
Q

Draw the direction of the wave of depolarisation

A
  • drawn*

- CGP PAGE 147

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8
Q

How does the refractory period affect action potentials?

A

It creates a time delay between 1 action potential and the next. This means that:

  • action potentials don’t overlap, but pass along as discrete (separate) impulses
  • there’s a limit to the frequency at which nerve impulses can be transmitted
  • action potentials only travel in 1 direction
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9
Q

What type of nature does an action-potential have and what does this mean?

DIAGRAM FOR BULLET POINT 3

A

It has an All-or-Nothing Nature

1) once threshold, is reached, action potential will always fire with same change in voltage, no matter how big the stimulus is.
2) If threshold isn’t reached, an action potential won’t fire.
3) bigger stimulus ≠ bigger action potential,. It’ll only cause them to fire more frequently.

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10
Q

What is a myelin sheath and what is it made out of?

DIAGRAM

A

A myelin sheath is an electrical insulator found on some neurones.

In the PNS, it is made of a type of cell called Schwann cell

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11
Q

What are nodes of Ranvier?

A

Tiny patches of bare membrane between the Schwann cells.

- sodium ions channels are concentrated here

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12
Q

How do impulses travel in myelinated neurones?

A

In myelinated neurones, depolarisation only happens at nodes (where Na+ can get through membrane). The neurones cytoplasm conducts enough electrical charge to depolarise next node, so impulse ‘jumps from node to node’ .
- This is saltatory conduction and it’s really fast.

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13
Q

How do impulses travel in non-myelinated neurones?

A

In non-myelinated, the impulse travels as a wave along the whole length of the axon membrane (so you get depolarisation along the wave length of the membrane).
- This is slower than saltatory (still quite quick)

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14
Q

What three factors affect the speed of conduction of action potentials?

A
  1. Myelination
  2. Axon diameter
  3. Temp
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15
Q

How does the axon diameter affect the speed of conduction of action potentials?

A

Action potentials are conducted quicker along axons with bigger diameters because there’s less resistance ** to the flow of ions than in the cytoplasm of a smaller axon.
- with less resistance, depolarisation reaches other parts of the neurones cell membrane quicker

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16
Q

How does temp affect the speed of conduction of action potentials?

A

The speed of conduction increases with temp, as ions diffuse faster. The speed only increases up to 40 though before enzymes start to denature.

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17
Q

Define Synapse and synaptic cleft?

A

Synapse: Junction between neurone and other neurone, or between neurone and effector cell

Synaptic cleft : tiny gap between the cells

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18
Q

Draw these structures:

  1. Synapse
  2. Synaptic cleft
  3. Synaptic knob
  4. Presynaptic neurone
  5. Postsynaptic neurone
  6. Postreceptor sites
  7. Vesicles

(DIAGRAM)

A

pg 148

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19
Q

What happens when an action potential tial reaches the end of a neuron?

A

neurotransmitters are released from the vesicles, so that they can chemically diffuse across synaptic cleft and be taken up by postreceptor sites on postsynaptic membranes, where message is converted back to electrical.

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20
Q

Why are impulses unidirectional?

A

They are unidirectional as receptors are only found on postsynaptic site.

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21
Q

How does the body make use of neurotransmitters after the impulse has reached the next neurone?

A

They are taken back into the presynaptic neurone or they’re broken down by enzymes and the products are taken into the neurone

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22
Q

What are cholinergic synapses?

A

Synapses that use acetylcholine

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23
Q

Describe how a nerve impulse is transmitted across a cholinergic synapse

DIAGRAM

(STEPS 1-3)

A
  1. Action potential arrives at synaptic knob of presynaptic neurone and stimulates voltage-gated Ca+ channels in presynaptic neurone to open.
  2. Ca+ diffuse into synaptic knob (they’re pumped out afterwards by active transport)
  3. Influx of Ca+ into synaptic knob causes synaptic vesicles to move to presynaptic membrane and fuse with it.
  4. Vesicles release ACh into synaptic cleft (exocytosis)
  5. ACh diffuses across cleft and binds to cholinergic receptors on postsynaptic membrane.
  6. influx of Na+ in postsynaptic membrane causes depolarisation. An action potential on postsynaptic membrane is generated if threshold is reached.
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24
Q

What happens to ACh after it transmits an electrical impulse across a cholinergic synapse?

A

ACh is removed from cleft so response doesn’t keep happening. It’s broken down by acetylcholinesterase (AChE) and products are re-absorbed by presynaptic neurone and used to make more ACh.

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25
Q

What effect do excitatory neurotransmitters have on the postsynaptic membrane?

(GIVE AN EXAMPLE OF AN EXCITATORY NEUROTRANSMITTER)

A

They depolarise the postsynaptic membrane, making it fire an action potential if the threshold is reached.

EXAMPLE: acetylcholine is an excitatory neurotransmitter at cholinergic synapses in the CNS.

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26
Q

What effect do inhibitory neurotransmitters have on the postsynaptic membrane?

(GIVE AN EXAMPLE OF AN INHIBITORY NEUROTRANSMITTER)

A

They hyperpolarise the postsynaptic membrane (making PV more negative) , preventing it from firing an action potential.

EXAMPLE: acetylcholine is an inhibitory neurotransmitter at cholinergic synapses in the heart. When it binds to receptors here, it causes K+ channels to open on postsynaptic membrane, hyperpolarising it.

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27
Q

Define summation

A

Summation: effect of neurotransmitter released from many neurones (or 1 neurone that’s stimulated a lot in a short period if time) is added together

28
Q

Outline the 2 types of summation and they’re main purpose

A
  1. Spatial summation
  2. Temporal summation

PURPOSE: they help synapses accurately process info, finely tuning the response.

29
Q

Describe spatial summation

DIAGRAM

A
  1. Sometimes many neurones connect to 1 neurone

2 small amount of neurotransmitter released from each of these neurones can be enough altogether to reach threshold

  1. If some neurones release inhibitory neurotransmitter, then total effect of all neurotransmitters might be no action potential
30
Q

Describe temporal summation

DIAGRAM

A

When 2 or more nerve impulses arrive in quick succession from the same presynaptic neurone. This makes an action potential more likely because more neurotransmitter is released into synaptic cleft

31
Q

What are neuromuscular junctions?

A

They are synapses between a motor neurone and a muscle cell

32
Q

What neurotransmitters do neuromuscular junctions use and what do these bind to?

A

They use acetylcholine and these bind to nicotinic cholinergic receptors

33
Q

Compare transmission of action potentials in neuromuscular junctions and cholinergic synapses.

DIAGRAM

A

IN NEUROMUSCULAR JUNCTIONS:

  1. postsynaptic membrane has lots of folds that form clefts. These clefts store enzyme that break down ACh (acetylcholinesterase - AChE)
  2. Postsynaptic membrane has more receptors than other synapses
  3. ACh is always excitatory at neuromuscular junction so when motor neurone fires action potential, it normally triggers a response in a muscle cell.
34
Q

Describe 5 ways that show how drugs can affect the action of neurotransmitters at synapses

(DIAGRAM)

A
  1. Drugs, like agonists, are same shape as neurotransmitters so they mimic action at receptors. This activates more receptors. (e.g. Nicotine mimics ACh and binds to nicotinic cholinergic receptors in brain)
  2. Some block receptors so they can’t be activated by neurotransmitters. This means fewer receptors (if any) can be activated. (curare blocks effects of ACh by blocking nicotinic cholinergic receptors at neuromuscular junctions, so muscle cells cant be stimulated. This paralyses the muscle
  3. Some inhibit enzyme that breaks down neurotransmitters so that there are more neurotransmitters in cleft to bind to receptors and they’re there for longer. (e.g. nerve gases stop ACh from being broken down in cleft. This can lead to loss of muscle control).
  4. Some stimulate release of neurotransmitter from presynaptic neurone so more receptors are activated (e.g. Amphetamines)
  5. Some inhibit release of neurotransmitters from presynaptic neurone so fewer receptors are activated e.g. Alcohol.
35
Q

What is skeletal muscle?

give an example of a skeletal muscle

A 
skeletal muscle (or striated/striped or voluntary muscle) is a type of muscle you use to move 
- (e.g. triceps/biceps, which move the lower arm)
36
Q

How are skeletal muscles attached to bones?

A

They are attached to bones by tendons

37
Q

What are ligaments?

A

Ligaments are strong tissue that attach bones to other bones to hold them together.

38
Q

What do skeletal muscles do to move bones at a joint?

A

They contract and relax
- the bones of the skeleton are incompressible (rigid) so they act as levers, giving the muscles something to pull against

39
Q

What are antagonistic pairs?

give an example of antagonistic pairs

A

They are muscles that work together to move a bone
- the contracting muscle is called the agonist and the relaxing muscle is called the antagonist

e.g biceps and triceps

40
Q

Describe the motion of biceps and triceps

A

BICEPS (agonist) /TRICEPS (antagonist)

  • When your biceps contract (agonist), triceps relax (antagonist). This pulls bone so arm bends at elbow.
    OR
  • When your triceps contracts (agonist), your biceps relaxes (antagonist). This pulls bone so arm straightens at elbow.
41
Q

What is skeletal muscle made up of?

A

Skeletal muscle is made up of large bundles of long cells, called muscle fibres

42
Q

How do these structures relate to muscle fibres:

1- Sarcolemma?
2- Sarcoplasmic reticulum?
3. Mitochondria?
4. Nuclei?
5. Myofibrils?

DIAGRAM

A
  1. Sarcolemma (cell membrane of muscle fibre is called sarcolemma) = Bits of sarcolemma fold inwards across muscle fibre and stick into sarcoplasm (muscle cell’s cytoplasm). These folds are called transverse tubules and they help spread electrical impulses throughout sarcoplasm so they reach all parts of muscle fibre.
  2. Sarcoplasmic reticulum = A network of internal membranes that runs through sarcoplasm. This stores and releases Ca+ needed for muscle contraction.
  3. Mitochondria = fibres have lots of mitochondria to provide ATP needed for muscle contraction
  4. Nuclei = muscle fibres are multinucleate
  5. Myofibrils = long, cylindrical organelles in the fibres, that are made up of proteins and are highly specialised for contraction.
43
Q

What do myofibrils contain?

What are these substances made out of

A

They contain thick and thin myofilaments that move past each other to make muscles contract.

thick myofilaments = made of protein myosin
thin myofilaments = made of protein actin

44
Q

What would happen if you looked at a myofibril under an electron microscope?

A

You’d see a pattern of alternating dark and light bands,

  1. Dark bands = contain thick myosin filaments and some overlapping thin actin filaments (these are called A-bands)
  2. Light bands = contain thin actin filaments only (these are called I-bands
45
Q

What are sarcomeres?

DIAGRAM

A

They are the many short units that make up myofibrils

- The ends of each sarcomere are marked with a Z-line

46
Q

What is the M-line and the H-zone?

DIAGRAM

A
  1. M-lines = . The M-line is in Middle of Myosin filaments.

2. H-zone = Around M-line is the H-zone. The H-zone only contains myosin filaments

47
Q

Which theory is muscle contraction explained by?

A

the Sliding Filament Theory

48
Q

Describe the Sliding Filament Theory?

DIAGRAM OF RELAXED AND CONTRACTED SARCOMERE

A
  1. Myosin and actin filaments slide over one another to make sarcomeres contract - myofilaments themselves don’t contract
  2. Simultaneous contraction of lots of sarcomeres means myofibrils and muscle fibres contract.
  3. Sarcomeres return to original length as muscle relaxes
49
Q

What adaptations do myosin filaments have?

A
  1. Globular heads that are hinged, to help filaments move back and forth
    - Each myosin head has a binding site for actin and a binding site for ATP
50
Q

What adaptations do actin filaments have?

A
  1. Binding sites for myosin heads, called actin-myosin binding sites
  2. A protein called tropomyosin is found between actin filaments. It helps myofilaments move past each other
51
Q

What happens to binding sites in a resting muscle?

A

In a resting muscle, the actin-myosin binding site is blocked by tropomyosin.
- This means myofilaments can’t slide past each other as the myosin heads can’t bind to the actin-myosin binding sites on the actin filaments.

52
Q

Describe how muscle contraction occurs?

(steps 1-4)

DIAGRAM

A
  1. When action potential from motor neurone stimulates muscle cell, it depolarises the sarcolemma. Depolarisation spreads down T-tubules to sarcoplasmic reticulum.
  2. This causes sarcoplasmic reticulum to release stored Ca2+ into sarcoplasm.
  3. Ca2+ binds to protein attached to tropomyosin, causing protein to change shape. This pulls attached tropomyosin out of actin-myosin binding site on actin filament.
  4. This exposes binding-site, allowing myosin head to bind (bond formed between myosin head and actin filament is called the actin-myosin cross bridge)
  5. Ca2+ also activates ATP hydrolase which hydrolyses ATP to provide energy needed for muscle contraction.
  6. Energy released from ATP causes myosin head to bend, which pulls actin filament along in a rowing action.
  7. Another ATP molecule provides energy to break actin-myosin cross bridge so myosin head detaches from actin filament after it’s moved.
  8. Myosin head then reattaches to a different binding site further along the actin filament. A new actin-cross bridge is formed and cycle is repeated. (attach, move detach, reattach)
  9. Many cross-bridges form and break very rapidly, pulling actin filament along - which shortens the sarcomere, causing muscle to contract
53
Q

what needs to be present for the muscle contraction cycle to continue?

A

Ca2+

54
Q

What happens to the binding sites and sarcomere when excitation stops?

A
  1. Ca2+ leave the binding sites, and are moved by active transport back into sarcoplasmic reticulum
    - This causes tropomyosin molecules to move back, so they block the actin-myosin binding sites again (so no actin-myosin cross bridges, so no shortening of sarcomere, and therefore, no contraction).
  2. The actin filaments slide back to their relaxed position, which lengthens the sarcomere.
55
Q

Why does the sarcomere get longer again when excitation stops?

A

The actin filaments slide back to their relaxed position, which lengthens the sarcomere

56
Q

How many sodium ions are transported for every 2 potassium ions in the sodium-potassium pump?

A

3 Na2+ are moved for every 2 K+

57
Q

Why does ATP get used up very quickly in muscle cells?

A

They get used up very quickly as a lot of energy is needed when muscles contract

58
Q

Name the 3 main ways that allow ATP to continually be generated?

A
  1. Aerobic respiration
  2. Anaerobic respiration
  3. ATP-Phosphocreatine (PCr) System
59
Q

How does the ATP-Phosphocreatine system make ATP?

A

ATP can be made by adding Pi from PCr to ADP

- PCr is stored in cells

60
Q

What type of activity would aerobic respiration be good for?

A

As it only works when O2 is present, it would be good for long periods of low-intensity exercise.

61
Q

What type of activity would anaerobic respiration be good for?

A

It is good for short periods of hard exercise as lactate can build quickly, which can cause muscle fatigue

62
Q

What are the advantages of the ATP-PCr system?

A

the ATP-PCr system generates ATP very quickly

63
Q

What type of activity would energy generated by the ATP-PCr system be good for?

A

PCr runs out after a few secs, so it’s used during short bursts of vigorous exercise (e.g. a tennis serve)

64
Q

What is creatinine?

A

After PCr releases a Pi, it becomes creatine. creatine gets broken down into creatinine, which is removed from the body via the kidneys
- Creatinine levels are higher in people that exercise regularly or have a higher muscle mass. High creatinine levels can also be an indicator of kidney damage,

65
Q

Name the 2 types of muscle fibres that make up skeletal muscles?

A
  1. Slow twitch muscle fibres

2. Fast twitch muscle fibres

66
Q

Outline the properties of ‘slow twitch muscle fibres’

A

STMF

  1. Muscle fibres contract slowly
  2. Many found in muscles used for posture (e.g. in back)
  3. Good for endurance activities (e.g. long distance run)
  4. Can work for long time without getting tired
  5. Energy released slowly through aerobic respiration. Lots of mitochondria and blood vessels supply muscles with O2.
  6. Reddish in colour as they’re rich in myoglobin - a red-coloured protein that stores O2
67
Q

Outline the properties of ‘fast twitch muscle fibres’

A

FTMF

  1. Muscle fibres contract quickly
  2. Many found in fast movement muscles (e.g. legs/eyes)
  3. Good for short bursts of speed/power (e.g. sprinting)
  4. Gets tired quickly
  5. Energy released quickly through anaerobic respiration using glycogen. Few mitochondria/blood vessels
  6. Whitish in colour as little myoglobin - so can’t store O2

A2 Biology (11 decks)

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