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Biology Paper 2 Bio notes > Section 6: Nervous co-ordination > Flashcards

Section 6: Nervous co-ordination Flashcards

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1
Q

How is the resting potential established?

A
  • Sodium potassium ion pump actively transports
    • 3 sodium ions out of the axon
    • 2 potassium ions into axon
  • Electrochemical gradient established - higher conc of K+ ions in axon
  • Membrane more permeable to potassium ions (K+ channels open/ Na+ channels closed)
  • K+ ions move out of axon by facilitated diffusion. Therefore inside more negative than outside. Axon is polarised - resting potential
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2
Q

What is the stimulus in membrane permeability leading to depolarisation?

A
  • Membrane more permeable to Na+ ions as the channels open
  • Sodium diffuse into neurone down electrochemical gradient
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3
Q

What is depolarisation part of the graph mean?

A
  • P.d reaches threshold, action potential generated
  • Because more voltage-gated sodium ion channels open and sodium diffuse rapidly
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4
Q

What is repolarisation part of the graph mean?

A
  • Sodium ion channels close (membrane less permeable to sodium ions) whilst voltage gated potassium ion channels open so potassium ion s diffuse out of neurone
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5
Q

What is hyperpolarisation part of the graph mean?

A
  • Potassium ion channels are slow to close so there is a slight overshoot - too many potassium ion diffuse out of neurone
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6
Q

What is the importance of the refractory period

A
  • The refractory period is the time to restore axon to resting potential/ no further action potential can be generated
  • Importance:
  • Produces discrete impulses - action potentials cant overlap
  • Limits frequency of transmission at a certain intensity
  • Unidirectional action potential
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7
Q

What are the factors that affect the speed of conductance?

A
  • Myelination
  • Axon diameter
  • Temperature
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8
Q

How does Myelination affect the speed of conductance?

A
  • Depolarisation occurs at nodes of Ranvier only - saltatory conduction
  • Impulse does not travel whole axon/ no need to depolarise along whole length of axon
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9
Q

How does the axon diameter affect the speed of conductance?

A
  • Bigger diameter means less leakage of ions/ less resistance to the flow of ions
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10
Q

How does temperature affect the speed of conductance?

A
  • Increases rate of movement of ions Na+ and K+ as more kinetic energy
  • Higher rate of respiration so ATP is produced faster - active transport faster
  • But proteins could denature at a certain temperature
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11
Q

What is the passage of an action potential along non-myelinated axons

A
  • Action potential passes as a wave of depolarisation
  • Influx of sodium ions in 1 region increases permeability and causes voltage gated sodium ion channels to open so region depolarises
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12
Q

What is the passage of an action potential along a myelinated axon?

A
  • Depolarisation of an axon at nodes of ranvier only
  • Resulting in saltatory conduction
  • So there is no need for depolarisation along whole length of axon
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13
Q

Exam Question: Damage to the myelin sheaths of neurones can lead to problems controlling the contraction of muscles. Suggest 1 reason why? (2)

A
  • Action potentials travel more slowly/ no saltatory conduction
  • So delay in muscle contraction/ muscles dont contract

OR

  • Action potentials/ depolarisation “leaks” to adjacent neurones
  • So wrong muscle contracts
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14
Q

What is the sequence of steps of the transmission across a cholinergic synapse?

A
  1. Action potential arrives causing calcium ion channels to open - calcium ions diffuses into pre-synaptic neurone
  2. Causing vesicles of neurotransmitters/ acetylcholine to fuse to pre-synaptic membrane - release acetylcholine into synaptic cleft (exocytosis)
  3. Neurotransmitters diffuse across synaptic cleft - bind to neurotransmitter receptors on post synaptic membrane
  4. Sodium ion channels open - sodium ions diffuse into post-synaptic knob - depolarisation initiates action potential
  5. Neurotransmitter removed from cleft so response does not keep happening - broken down by acetylcholinesterase and products reabsorbed by presynaptic neurone.
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15
Q

What is the comparison between the transmission across cholinergic synapses and neuromuscular junctions?

A
  • Cholinergic synapse - neurone to neurone WHEREAS neuromuscular is neurone to muscle
  • Neuromuscular junction: ACh is always exitatory so always triggers action potential
  • Neuromuscular junction - post-synaptic membrane has more receptors than other synapses
  • Neuromuscular junction - lots of folds on post-synaptic membrane which forms clefts to store enzyme AChE to break down ACh
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16
Q

Why synapses result in unidirectional nerve impulses?

A
  • Neurotransmitter only made in presynaptic neurone
  • Receptors only on post-synaptic membrane
17
Q

What is summation?

A
  • Addition of a number of impulses converging on a single post-synaptic neurone
18
Q

What is spatial summation?

A
  • Many pre-synaptic neurones share the same synaptic cleft/ post-synaptic neurone
  • Collectively release sufficient neurotransmitter to reach threshold and trigger an action potential
19
Q

What is temporal summation?

A
  • 1 pre-synaptic neurone releases neurotransmitter many times over a short period of time/ in rapid succession
  • Sufficient neurotransmitter to reach threshold to trigger action potential
20
Q

How does inhibition happen at inhibitory synapses?

A
  • Inhibitory neurotransmitters hyperpolarise the post-synaptic membrane (K+ channels open and diffuse out, Cl- channels open, Cl- diffuse in)
  • Inhibits formation of action potential/ transmission of nerve impulses by post-synaptic membrane - can’t be depolarised
  • Example: Acetylcholine is inhibitory at cholinergic synapses at the heart
21
Q

What are the effects of specific drugs on a synapse?

A
  • Stimulate nervous system - more action potentials e.g minimic neurotransmitter/ stimulate release of more neurotransmitter/ inhibit enzyme that breaks down neurotransmitter
  • Inhibit nervous system - fewer action potentials e.g inhibit release of neurotransmitter/ block receptors
22
Q

What is the effect of this drug on the synapse

Black Mamba’s toxin prevents breathing. Inhibiting acetylcholinesterase at neuromuscular junctions

A
  • ACh not broken down/ stays bound to receptor
  • Na+ continues to enter/ depolarisation continues
  • Intercostal muscles stay contracted/ can’t relax
23
Q

What is the effect of this on the synapse?

Dopamine is a neurotransmitter. Cocaine has a similar shape. Cocaine can bind to dopamine transporter (dopamine transported back to pre-synaptic knob) It is released in parts of brain where pleasure is received.

A
  • Dopamine and cocaine have similar shapes/ so can fit into the transporter
  • Blocks transport of dopamine out of synaptic cleft into pre-synaptic knob
  • Dopamine concentration rises/ remains and continues to bind to receptor
  • Continued firing of impulses in post-synaptic membrane
24
Q

What is the effect of the drug on the synapse/

Cannibinoids prevent muscle contraction. They are hydrophobic and easily pass into neurones. Cannibinoid receptors are found in pre-synaptic membrane of neuromuscular junctions. When a cannabinoid binds to the receptor, it closes calcium ion channels.

A
  • Prevents influx of calcium ions into pre-synaptic membrane
  • Synaptic vesicles do not fuse with membrane - no ACh released
  • No action potential/ depolarisation
25
Q

What is the effect of this drug on the synapse?

Enkephalins are neurotransmitters released to the brain and spinal cord in response to stimuli. Similar shape to acetylcholine. Acts as painkillers by inhibiting synaptic transmission.

A
  • Bind to receptors on post-synaptic membrane as complementary to receptors
  • Acetylcholine can’t bind so reduces/stops depolarisation
26
Q

What is the passage of an action potential along a myelinated axon?

A
  • Depolarisation of an axon at nodes of ranvier only
  • Resulting in saltatory conduction
  • So there is no need for depolarisation along whole length of axon

Biology Paper 2 Bio notes (5 decks)

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