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Y13 Biology > Topic 6 B: Nervous Coordination > Flashcards

Topic 6 B: Nervous Coordination Flashcards

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1
Q

Myelinated motor neurone described?

A
  • axon - long fibre insulated by fatty myelin sheath
  • schwann cells - act as electrical insulator, specialised schwann cells make up myelin sheath
  • impulses jumo between gaps in myelin sheath - this speeds up the conduction of the impulse (saltatory conduction)
  • gaps are called nodes of ranvier
  • dendrites - ensure easy communication and also increase sa for axon terminals
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2
Q

Nervous system compared to hormonal system?

A
  1. N = use nerve cells to pass electrical impulses, H = produce chemicals
  2. N = secrete neurotransmitters to stimulate target cells, H = target cells have specific receptors on cell-surface membrane and change in conc of hormones stimulate them
  3. N = transmission by neurones, H = transmission by blood system
  4. N = transmission and response is rapid, H = transmission and response is slow
  5. N = nerve impulses travel to specific parts of body (localised), H = hormones travel to all parts of body (widespread) but only target cells respond
  6. N = response is short lived, H = response is long lasting
  7. N = effect is temporary and reversible, H = effect is permanent and irreversible
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3
Q

Exam question: explain why the speed of transmission of impulses is faster along a myelinated axon than along a non-myelinated axon?

A
  • meylination provides electrical insulation
  • saltatory conduction OR depolarisation at nodes of ranvier
  • in non-myelinated, depolarisation occurs along whole length
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4
Q

Three types of neurones?

A

Sensory
Relay
Motor

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5
Q

Motor neurone structure?

A
  • large cell body at one end, lies within the spinal cord or brain
  • a nucleus that is always in its cell body
  • many highly-branched dendrites extending from cell body
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6
Q

Sensory and relay neurone functions?

A
  • S = carry impulses from receptors to CNS
  • R = found in the CNS - connect sensory and motor neurones
  • R = referred to as intermediate neurones
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7
Q
  1. Role of the sodium-potassium pump in nerve impulses?

(stage one of the nerve impulse)

A
  • maintains resting potential
  • example of a protein
  • example of active transport
  • moves 3 sodium ions out of axon - using ATP (membrane isnt permeable so cant diffuse back in)
  • moves 2 potassium ions in the axon - using ATP
  • creates electrochemical gradient
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8
Q

SOPI?

A

Sodium Out, Potassium In

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9
Q
  1. Selective protein channels role in nerve impulses?

(stage two in the nerve impulse)

A
  • faciliated diffusion
  • allows sodium and potassium to move across the membrane
  • channels are less permeable to sodium ions so cant diffuse back in
  • electrochemical gradient allows FD to occur
  • cell membrane more permeable to potassium ions, allowing them to move from high conc inside axon to low conc outside axon at faster rate
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10
Q

Describe the charges within the axon (sodium and potassium ions)?

A
  • inside of axon is negatively charged in comparison with the outside, difference is about -70mV
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11
Q

Exam question: Explain how a resting potential is maintained in a neurone?

A
  • cell membrane is less permeable to sodium ions
  • 3 sodium ions pumped out
  • 2 potassium ions pumped in
  • done via active transport
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12
Q

Exam question: Sodium and potassium ions can only cross the axon membrane through proteins, explain why?

A
  • cannot cross the phospholipid bilayer because they arent lipid soluble/they are charged.
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13
Q
  1. Action potential within the neurone?

(stage three in the nerve impulse)

A
  • sodium ions pass into the axon down electrochemical gradient, this reduces the potential difference across the membrane as the inside of the axon becomes less negative (depolarisation)
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14
Q

Explain how depolarisation occurs when neurone is stimulated (reference to graph)? Part one

A
  1. (stimulus) sodium channels open, membrane becomes more permeable to sodium. sodium diffuses down electrochemical gradient into neurone at the same time that potassium ions are diffusing out (SOPI)
  2. (depolarisation) if PD reaches threshold, more sodium ion channels (voltage gated channels) open and the voltage continues to increase, this allows more sodium ions to diffuse into neurone
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15
Q

Explain what happens after depolarisation occurs when neurone is stimulated (reference to graph)? Part two

A
  1. (repolarisation) sodium ion channels close but more potassium channels are triggered to open the membrane is now more permeable to potassium ions so potassium ions continue to diffuse out, membrane starts to return to resting potential
  2. (hyperpolarisation) potassium ion channels are slow to close so there is a slight ‘overshoot’ - too many potassium ions diffuse out the neurone so the PD becomes more negative than the resting potential
  3. (refractory period) resting potential reestablished, time between overshoot and resting potential = recovery period-resting state. potassium ions channels close and sodium ion channels become responsive again
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16
Q

Why is refractory period important?

A
  • ensures action potentials are discrete and dont overlap
  • ensures AP are unidirectional
  • ensures a limit to the frequency of nerve impulses transmission (minimum time between APs occuring)
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17
Q

Factors that affect speed of nerve impulse?

A

Myelination
Axon diameter
Temperature

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18
Q

How does myelination affect speed of nerve impulse?

A
  • electrical insulator
  • depolarisation (sodium ions coming in) only occurs at nodes of ranvier
  • sheath stops the diffusion of sodium and potassium ions
  • saltatory conduction - jumps from one node to the next
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19
Q

What happens in non-myelinated neurone?

A

depolarisation occurs along whole length of membrane, much slower.

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20
Q

How does axon diameter affect speed of nerve impulse?

A
  • impulses conducted quicker along thicker axons
  • greater surface area for the diffusion of ions (through channels)
  • increases rate of depolarisation (because there is less resistance to the flow of ions) and action potential generation
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21
Q

How does temperature affect speed of nerve impulse?

A
  • speed of conduction increases with temp
  • enzymes involved in respiration work faster
  • more ATP available for sodium potassium pump (active transport)
  • colder conditions slow conduction due to less kinetic energy
  • less energy available for FD of Na+ and K+
  • too high = enzymes and channel proteins denature
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22
Q

Exam question: Dopamine is a neurotransmitter. Production of too much dopamine is associated with schizophrenia. A drug used to treat schizophrenia binds to dopamine receptors in synapses. This binding doesnt lead to the formation of an AP?

Suggest why the binding of the drug doesnt lead to the production of an AP?

A
  • sodium ion channels dont open (not enough)
  • depolarisation doesnt happen / threshold isnt reached
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23
Q

What is the all-or-nothing principle?

A
  • if a stimulus is below the threshold, no AP generated
  • not enough sodium ion channels are open (less energy)
  • a large stimulus has enough energy to reach threshold (more sodium ion channels open) - AP generated
  • the larger the peak the bigger the increase in the frequency of AP
    - AP will always peak at the same maximum voltage
    - wont cause a bigger AP but will cause them to fire more
    quickly
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24
Q

Why is the all or nothing principle needed?

A
  • ensures animals only respond to large enough stimuli, rather than every slight change in the environment, which would overwhelm them.
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25
Q

What is a synapse?

A

Junction / gap between two neurones.

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26
Q

Can action potential pass across a synapse?

A
  • cannot pass it
  • mechanisms put in place to release neurotransmitter
  • diffuses across the gap
  • neurotransmitters bind to the next neurone to trigger an action potential
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27
Q

What is the synaptic knob?

A

The axon of this neurone ends in a swollen portion known as the synaptic knob - it contains synaptic vesicles filled with neurotransmitters

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28
Q

What is the synaptic cleft?

A

Neurones are separated by a small gap called synaptic cleft
- it has a complementary shape

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29
Q

What is the pre and post synaptic membrane?

A
  • pre = before the synapse
  • post = after the synapse
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30
Q

How synapses work to trigger a action potential?

A
  • electrical impulse / action potential arrives at end of axon on presynaptic neurone
  • neurotransmitters are released from vesicles
  • neurotransmitters diffuse across synaptic cleft and temporarily binds with receptor molecules on the postsynaptic membrane
  • end result = trigger an action potential, a muscle contraction, or cause a hormone to be secreted from a gland
  • only temporary binding - neurotransmitters are removed from the cleft so the response doesnt keep happening, theyre taken back into the presynaptic neurone or they are either broken down by enzymes
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31
Q

Exam question: In the nerve pathway in the diagram, synapses ensure that nerve impulses only travel towards the muscle fibre. Explain how.

A
  • Neurotransmitter only made in / stored in / released from pre-synaptic neurone
  • neuroreceptors only on the post-synaptic membrane
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32
Q

What happens if a stimulus is weak?

A
  • only a small amount of neurotransmitter will be released into the cleft
  • wont be enough to reach the threshold and generate an action potential
33
Q

What is summation and the purpose?

A

The sum total of lots of smaller impulses triggers an action potential.
- needed to add up sufficient concentrations of neurotransmitters
- opens up sufficient numbers of sodium ion channels to trigger impulse

34
Q

What are the two types of summation?

A
  • Spatial and Temporal
35
Q

Benefits of summation?

A
  • allows for the effect of a stimulus to be magnified
  • a combination of different stimuli can trigger a response
  • avoids the nervous system becoming overwhelmed by impulses
36
Q

All about spatial summation?

A

Multiple presynaptic neurones to
one synapse and one postsynaptic neurone.
- multiple impulses arrive at different synaptic knobs at the same cell body
- multiple quantities of neurotransmitters are released from each impulse
- this collectively is enough neurotransmitter to reach threshold potential

37
Q

All about temporal summation?

A

Multiple impulses arrive in quick succession from the same presynaptic neurone.
- one neurone releases neurotransmitters repeatedly over short period of time
- continues until threshold potential is exceeded
- results in a large number of gated sodium ion channels to open

38
Q

Exam question: Dopamine is a neurotransmitter released in some synapses in the brain, the transmission of dopamine is similar to acetylcholine. Dopamine stimulates the production of nerve impulses in postsynaptic neurones.

Describe how. (3)

A
  • Dopamine diffuses across synapse
  • attaches to receptors on postsynaptic membrane
  • stimulates entry of sodium ions and depolarisation / action potential
39
Q

What do excitatory neurotransmitters do?

A
  • depolarise postsynaptic membrane
  • this fires an action potential if threshold reached
40
Q

What do inhibitory neurotransmitters do?

A
  • prevent action potential
  • binds to chloride ion channels, not sodium
  • causes chlorine ion channels to open
  • chlorine ions move into postsynaptic neurone by FD
  • leads to potassium ion channels opening - potassium ions (+) diffuse out of cell body and chlorine ions (-) diffuse in , this cancels out effect that any sodium ions (+) have coming in
  • result = postsynaptic membrane more negative - threshold not met (prevents random impulses from being sent around body)
41
Q

Examples of inhibitory neurotransmitters?

A
  1. Gaba - binds to its receptors and cause potassium ion channels to open on postsynaptic membrane, hyperpolarising the neurone
  2. Acetylcholine - at cholinergic synapses at heart - same process
42
Q

Neuromuscular junction definition?

A

A synapse that occurs between a motor neurone and a muscle.

43
Q

Cholinergic synapse definition?

A

Synapses that use neurotransmitter acetylcholine.

44
Q

Process of information being passed across synapse using calcium ions - part one (calcium ions and depolarisation)

A
  • AP arrives at synaptic knob of the presynaptic neurone
  • calcium ion channels located in plasma membrane
  • these voltage-gated channels open in response to an AP
  • result = calcium ions diffuse into synaptic knob cytoplasm - creating electrochemical gradient
45
Q

Process of information being passed across synapse using calcium ions - part two (vesicle fusion and exocytosis)

A
  • vesicles contain neurotransmitter acetylcholine
  • calcium ions cause vesicles to move towards / fuse with presynaptic membrane
  • result = vesicle releases ACh into synaptic cleft by exocytosis
46
Q

Process of information being passed across synapse using calcium ions - part three (diffusion of ACh)

A
  • high conc of ACh towards presynaptic end of cleft
  • neurotransmitter diffuses towards postsynaptic neurone
  • ACh binds to complementary receptors on postsynaptic membrane
  • result = ACh travels in one direction (unidirectional) as a result of where receptors are
47
Q

Process of information being passed across synapse using calcium ions - part four (sodium ion channels)

A
  • receptors are also attached to sodium ion channels
  • binding of ACh causes sodium ion channels on the membrane to widen
  • sodium ions within cleft able to move into postsynaptic neurone
  • result = enough sodium ions will trigger depolarisation / AP
48
Q

Process of information being passed across synapse using calcium ions - part five (ACh recycling)

A
  • neurotransmitter broken down, recycled and reabsorbed
  • enzymes called acetylcholinesterase break down this neurotransmitter into acetate and choline
  • result = products are reabsorbed by presynaptic neurone
49
Q

Exam question: Why arent neurotransmitters constantly attached to sodium ion channels?

A
  • constantly be triggering an AP
  • cause response even when stimulus isnt there
50
Q

Exam question: Describe the sequence of events involved in transmission across a cholingeric synapse.

Dont include breakdown of ACh.

A
  • depolarisation of presynaptic membrane
  • calcium channels open and calcium ions enter synaptic cleft
  • calcium ions cause synaptic vesicles to move / fuse with presynaptic membrane and release ACh / neurotransmitter
  • ACh diffuses across synaptic cleft
  • ACh attaches to receptors on postsynaptic membrane
  • sodium ions enter postsynaptic neurone leading to depolarisation
51
Q

What are the ways in which drugs effect nerve impulses and transmission?

A
  • mimic actions of neurotransmitters
  • blocking receptors on postsynaptic membrane
  • inhibit breakdown of neurotransmitters
  • stimulating / inhibiting release of
    neurotransmitters
52
Q

How do drugs mimic actions of neurotransmitters?

A
  • same shape as some
  • bind to same specific receptor for neurotransmitter
  • nicotine mimics ACh and binds to its receptors
53
Q

What is the effect of drugs blocking receptors on postsynaptic membranes?

A
  • receptors cannot be activated by neurotransmitters
  • fewer receptors can be activated
  • curare blocks ACh by blocking receptors - muscles cannot be stimulated (paralysis)
54
Q

What is the effect of drugs inhibiting the break down of neurotransmitters?

A
  • more neurotransmitters in synaptic cleft
  • stop working and they’re in cleft for longer
  • nerve gases stop ACh from breaking down, leading to loss of muscle control
55
Q

What is the effect of drugs stimulating / inhibiting release of neurotransmitters?

A
  • opioids block calcium ion channels so fewer vesicles fuse with presynaptic membrane
  • more receptors activated on postsynaptic neurone via stimulation
  • amphetamines force neurotransmitter dopamine into cleft (cause increased alertness)
56
Q

Exam question: The blink reflex involves synapses, channel proteins on presynaptic neurones are involved in reflex responses.

Explain how.

A
  • allows calcium ions in
  • at end of presynaptic neurone
  • causing release of neurotransmitter
57
Q

Three types of muscles?

A
  1. smooth - contracts without conscious control and found in walls of internal organs e.g., stomach
  2. cardiac - contracts without conscious control and found in heart
  3. skeletal - muscles you use to move and often called ‘striated’, also attached to bones by tendons
58
Q

Tendon and ligament function?

A

tendon = bone to muscle
ligament = bone to bone

59
Q

How do muscles work? (pairs)

A
  • antagonistic pairs, as one contracts, other relaxes
60
Q

Isometric contraction definition?

A

Muscle contraction without any movement.

61
Q

Two muscle fibres?

A
  1. slow twitch (slow oxidative type 1)
  2. fast twitch
62
Q

Fast muscle fibres vs Slow muscle fibres?

A
  1. (FM) short / faster contraction (SM) long contraction
  2. (FM) fewer capillaries (SM) denser network of capillaries
  3. (FM) ATP supplied mostly from anaerobic respiration (SM) ATP supplied mostly by aerobic respiration
  4. (FM) fewer, smaller mitochondria (SM) many, larger mitochondria
  5. (FM) large store of calcium ions in sarcoplasmic reticulum (SM) small store of calcium ions in the sarcoplasmic reticulum
  6. (FM) large amounts of glycogen and phosphocreatine present (SM) small amounts of glycogen present
  7. (FM) faster rate of ATP hydrolysis in myosin head (SM) slower rate of ATP hydrolysis in myosin head
  8. (FM) fatigues rapidly due to greater lactate formation (SM) fatigues slower due to reduced lactate formation
  9. (FM) used for short, intense bursts of effort (SM) low intensity e.g., long distance
  10. (FM) contains stores of ATP-phosphocreatine (PCr) to generate energy (SM) rich in myoglobin which is red coloured pigment that stores oxygen
63
Q

Exam question: Both slow and fast muscle fibres contain ATPase

Explain why?

A
  • hydrolysis of ATP
  • contraction requires energy
64
Q

Muscle fibre structure?

A
  • specialised cell-like units
  • surface membrane = sarcolemma
  • cytoplasm = sarcoplasm
  • many nuclei
  • transverse tubules (t tubules) - bits of sarcolemma fold inwards across muscle fibre and stick into sarcoplasm these are t-tubules and spread electrical impulses so that they reach all parts of the muscle fibre that is needed
  • sarcoplasmic reticulum - network of internal membranes that run through sarcoplasm, stores and releases calcium ions needed for muscle contraction
  • within sarcoplasm = contains mitochondria and myofibrils. mitochondria carry out aerobic resp to generate ATP for muscle contraction
  • myofibrils - contains bundles of actin and myosin filaments, which slide past eachother during muscle contraction
65
Q

Myofibril protein structure?

A
  • made up of many short units called sacromeres. the ends of each is marked with z-line - they allow actin filaments to attach. the m-line represents the middle of sacromere
  • h-zone only contains thick myosin
  • dark bands = A bands = contain thick myosin and overlapping thin actin
  • light bands = I bands = contain thin actin only, no overlaps
  • cylindrical so Z line is disc separating one sacromere from another
  • thick filament made from myosin
  • thin filament made from actin (acTHIN)
66
Q

What is a neuromuscular junction?

A
  • point where a motor neurone meets a skeletal muscle fibre
  • specialised cholingeric synapse
67
Q

How are neuromuscular junctions similar to cholingeric synapses?

A
  • both release ACh from vesicles in presynaptic neurone
  • ACh diffuses across synaptic cleft
  • binds to cholinergic receptors on postsynaptic neurone
  • AP triggered if threshold met
    (Neuromuscular junctions causes muscle to contract within muscle fibre rather than triggering AP.)
  • (CS) and (NJ) use ACh as neurotransmitter
  • (CS) and (NJ) stimulated by AP on presynaptic membrane
68
Q

How are neuromuscular junctions different to cholingeric synapses?

A
  • ACh binds to sarcolemma receptor proteins. sodium ion channels are found on the sarcolemma (rather than postsynaptic membrane) and open in response to binding.
  • depolarisation occurs within the sarcolemma (rather than postsynaptic membrane), generating an AP that passes down t-tubules
  • calcium ions bind to troponin and tropomyosin proteins to cause contraction
  • (CS) found between neurones (NJ) found between motor neurone and muscle
  • (CS) can be excitatory or inhibitory (NJ) only excitatory
69
Q

Process of neuromuscular junctions causing muscle contraction?

A
  1. AP
  2. calcium ions diffuse into neurone
  3. ACh containing vesicles fuse with presynaptic membrane
  4. ACh diffuses across neuromuscular junction
  5. ACh binds to sarcolemma receptor proteins
  6. sodium ions diffuse into sarcolemma
  7. AP passes along sarcolemma an down t-tubules
  8. calcium ions diffuse out of Sarcoplasmic reticulum and into sarcoplasm
  9. calcium ions bind with troponin molecules, starting the process of muscle contraction
70
Q

Exam question: role of glycogen granules in skeletal muscle?

A
  • store of glucose
  • for respiration

OR

  • to be hydrolysed to glucose
  • to provide ATP
71
Q

What do muscle contractiosns require? (theory)

A
  • myosin and actin filaments sliding over eachother
  • sliding filament theory
72
Q

Sliding filament theory: part one - binding of troponin and tropomyosin

A
  • AP from motor neurone stimulates muscle cell, sarcolemma depolarised and this spreads down t-tubules and causes SR to release stored calcium ions - triggers muscle contraction
  • At this time, tropomyosin prevents myosin head from attaching to the binding site on actin molecule
  • calcium ions bind to tropomyosin and troponin causing it to change shape, this pulls the proteins out of binding site
  • this exposes the binding site on the actin filament, allowing the myosin head to bind to the site = actin-myosin cross bridge
73
Q

Sliding filament theory: part two - rowing movement of the actin filament?

A
  • calcium ions activate enzyme ATP hydrolase / ATPase - this hydrolyses ATP into ADP + Pi and provides energy for muscle contraction
  • mysoin head then bends which creates tension and pulls actin filament along in rowing action
  • as actin filaments being moved along, I-bands and H-zones getting closer, and Z-lines moving closer together, making sarcomere shorter. A band stays same length
74
Q

Sliding filament theory: part three - breaking the actin-myosin cross bridge?

A
  • hydrolysis of ATP provides energy for myosin head to resume original position. Head would then reattach to another actin binding site
  • cycle repeats
  • another ATP fixes to myosin head, causing it to detach from actin filament and cross bridge is broken
  • at muscle resting state - calcium ions leave their binding sites and are moved back to SR by active transport, binding sites are blocked and sarcomere lengthens
75
Q

Exam question: Describe the roles of calcium ions and ATP in the contraction of a myofibril? (5)

A
  • calcium ions diffuse into myofibrils from SR
  • calcium ions cause movement of tropomyosin on actin
  • this movement causes exposure to the binding site on the actin
  • myosin head attach to binding site on actin
  • hydrolysis of ATP on myosin head causes it to bend
  • bending pulls actin molecules
  • attachment of a new ATP to each myosin head causes myosin heads to detach from actin sites
76
Q

Why is energy needed for muscle contraction? (3)

A
  1. movement of myosin head that cause actin filaments to slide
  2. breaking of actin-myosin cross bridge
  3. reabsorption of calcium ions into the SR
77
Q

Where does the energy for muscle contractions come from?

A
  1. aerobic resp = atp generated in oxidative phsophorylation within mitochondria, when there is enough o2
  2. anaerobic respiration = atp made rapidly by glycolysis, end result is pyruvate which is converted into lactate - this can cause build up and muscle fatigue
  3. ATP-PC system = PCr (phosphocreatine) is stored inside cells, ATP-PC system generates ATP quickly but PCr runs out after few seconds - its anaerobic
78
Q

What is phosphocreatine?

A
  • reserve supply of phosphate
  • molecule absorbed by muscles that can be used for rapid production of ATP.
  • phsophate ion from phosphocreatine transferred to ADP
79
Q

Exam question: Explain the role of calcium ions and ATP in bringing about contraction of muscle fibre?

A
  1. calcium ions = bind to troponin, remove blocking action of tropomyosin, expose myosin binding sites
  2. ATP = allows myosin to detach from actin, break cross bridge, releases energy to swivel / activate myosin head / drive power stroke

Y13 Biology (11 decks)

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