6 Responding to Change- Nervous Coordination Flashcards

1
Q

What are neurones and the 3 main types? (+ description)

A

Neurones= cells that transmit information from receptors to effectors

Sensory neurones- carry nervous impulses from receptors into CNS

Motor neurones- carry impulses from CNS to effector organs (eg muscle/glands)

Relay neurones- intermediate neurones, receive impulses from sensory neurone & relay them to motor neurones

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2
Q

What is the basic structure of neurones?

A

-Can be myelinated/non-myelinated
-Dendrites; carry nervous impulse towards cell body
-Axons; carry nervous impulse away from cell body
-Cell body; where nucleus is normally located

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3
Q

What is the structure of myelinated motor neurones?

A

-Motor neurones in vertebrates= usually myelinated
-Schwann cells= wrapped around axon of neurone, form myelin sheath
-Nodes of Ranvier= gaps between adjacent Schwann cells

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4
Q

What is resting potential?

A

When a neurone hasn’t been stimulated

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5
Q

Why is there a potential difference at resting state?

A

-At resting potential—> diff in charge across neurone membrane: inside neurone more negatively charged than outside, as there are more positive ins outside cell than inside
-Diff in charge= potential difference

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6
Q

What is the resting potential maintained by and how?

A

-Resting potential maintained by sodium-potassium pumps in neurone membrane
-3 Na+ ions are actively transported out of neurone by pumps for every 2 K+ ions transported in
-This leads to build-up of positive ions outside of cell

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7
Q

How do potassium ion channels in the neurone membrane affect the sodium ions?

A

-Potassium ion channels are in neurone membrane—> it’s permeable to K+ ions
-When K+ ions are transported into neurones, can diffuse back
-Neurone membrane—> also impermeable to Na+ ions so ions can’t diffuse back into cell after they’ve been transported out

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8
Q

What actions establish the resting potential?

A

-Together, action of sodium-potassium pumps & potassium ion channels lead to potential diff across neurone membrane—> called resting potential (about -70mV)
-Neurone is said to be polarised

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9
Q

When does repolarisation happen?

A

When a resting neurone is stimulated, its membrane experiences a change in potential difference

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10
Q

What happens when a neurone is stimulated?

A

-Na+ ions channels in cell membrane open when neurone is stimulated
-Na+ ions flood into neurone
-Potential difference across membrane changes, becomes more positive inside neurone

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11
Q

How does depolarisation occur and what happens as a result?

A

-If potential diff increases above threshold value (about -55mV) then membrane becomes depolarised
-More sodium channels open and there’s a sharp increase in potential difference to about +30mV

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12
Q

Why is depolarisation called an all-or-nothing response?

A

-If potential diff reaches threshold, depolarisation always takes place & charge in potential diff will always be the same
-If stimulus= stronger, action potentials will be made frequently but size won’t increase

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13
Q

What is the process of repolarisation?

A

-After neurone has been depolarised to +30mV, sodium ions channels close & potassium ion channels open
-K+ ions transported back out of neurone, potential diff becomes more negative—> repolarisation

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14
Q

How does hyperpolarisation happen and what is the refractory period?

A

-Short period after repolarisation of neurone where potential diff becomes slightly more negative than resting potential—> hyperpolarisation
-Hyperpolarisation Prevents neurone from being restimulated instantly—> refractory period

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15
Q

What occurs after the refractory period?

A

-Potassium ion channels close, membrane returns to resting potential
The process where neurone= depolarised, returns to resting potential—> action potential

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16
Q

What is an action potential?

A

Stages involved in depolarisation of neurone membrane
Move along neurone in a wave

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17
Q

What happens when an action potential is generated?

A

-When action potential is generated, there’s more Na+ ions inside neurone than outside.
-Some of the Na+ ions diffuse sideways along neurone axon.

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18
Q

Action potential: How does the part of the neurone become depolarised?

A

-Presence of Na+ ions creates change in potential difference further along neurone membrane.
-If this reaches threshold value, sodium ion channels at this membrane part open.
-Na+ ions diffuse into neurone.
-This part of the neurone becomes depolarised.

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19
Q

Action potential: How does a wave of depolarisation and refractory period occur?

A

-Na+ diffuse all along neurone in this way.
-Depolarisation takes place along neurone membrane; creates a wave of depolarisation.
-The period of hyperpolarisation in action potential= refractory period, ion channels recovering here
-This means an action potential cannot be stimulated again instantly.
-Ensures wave of depolarisation travels in 1 direction.

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20
Q

How does myelination speed up transmission of nerve impulses?

A
  • Schwann cells wrap around axon of neurones to create a myelin sheath, which acts as an electrical insulator as it’s impermeable to ions (Na+ & Ka+).
  • Depolarisation & action potentials can’t occur at myelinated parts of axon, only in gaps between (nodes of ranvier)
  • The nervous impulse jumps from one node to next → saltatory conduction
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21
Q

How does temperature speed up the transmission of nerve impulses?

A
  • Increase in temperature → increase in kinetic energy
  • Ions move across membrane more rapidly with more kinetic energy
22
Q

How does axon diameter speed up transmission of nerve impulses?

A
  • Giant axons → found in giant squid, allow it to have rapid escape respond
  • Greater axon diameter = greater surface area for movement of ions across cell membrane
23
Q

What is a synapse?

A

A junction between 2 neurones (eg relay) or between a neurone & effector (eg motor neurone & muscle cell)

24
Q

What is a synaptic cleft and its use?

A

-A gap between the cells in a synapse
-When an action potential reaches a synapse,it must be transmitted across it

25
Q

What is the presynaptic neurone & its use?

A

-Neurone before synapse
-When action potential reaches end of neurone, its transmitted across presynaptic membrane to postsynaptic membrane or to effector cell

26
Q

What is the synaptic knob and its uses?

A

-End of axon of the presynaptic neurone
-Swelling, contains synaptic vesicles
-Location where nerve impulse is transmitted across synaptic cleft
-Lots of mitochondria here; lots of energy needed to synthesise neurotransmitters

27
Q

What are synaptic vesicles and their uses?

A

-Located in synaptic knob
-Contains neurotransmitters
-Fuse w/ presynaptic membrane, release neurotransmitters into synaptic cleft

28
Q

What are neurotransmitters and their uses?

A

-Chemicals allowing action potential to be transferred across synapse
-When are released from synaptic vesicles into synaptic cleft, bind to specific receptors on postsynaptic membrane

29
Q

What is the postsynaptic membrane and its use?

A

-Membrane of postsynaptic neurone/effector cell
-Its receptors have complementary shape to neurotransmitters released from synaptic knob
-When neurotransmitters bind to their receptors, action potential continues
-Only receptors on here; ensures nerve impulses only moves in 1 direction

30
Q

What is the function of excitatory neurotransmitters? + eg

A

-Generate action potential in postsynaptic cell
-When they bind to receptors on postsynaptic membrane, membrane is depolarised
Eg- when acetylcholine binds to receptors on postsynaptic membrane in CNS; action potential is established

31
Q

What is the function of inhibitory neurotransmitters? +eg

A

-Prevent action potential from being generated in postsynaptic cell.
-When neurotransmitters bind to receptors on postsynaptic membrane, membrane= hyperpolarised.
E.g. when acetylcholine binds to receptors on postsynaptic membrane in heart, potassium ion channels are open in membrane; prevents action potential from being established.

32
Q

What is summation and its 2 types?

A

-Process where neurotransmitters from multiple neurones are summed together to produce a response.
-Spatial & temporal summation

33
Q

When does spatial summation occur and how?

A

-Takes place when multiple presynaptic neurones form junction w/ single neurone
-Each presynaptic neurone releases neurotransmitters. Overall= many neurotransmitters binding to receptors on 1 postsynaptic membrane.
-Together, neurotransmitters can establish generator potential that reaches threshold value, action potential is generated.

34
Q

When does temporal summation occur and how?

A

-Takes place when multiple nerve impulses arrive at same synaptic knob within short period of time.
-More neurotransmitter released into synaptic cleft—> more neurotransmitter available to bind to receptors on postsynaptic membrane.
-Together, neurotransmitters can establish generator potential that reaches threshold value, action potential is generated.

35
Q

What is a neuromuscular junction and its use?

A

-A synapse between a motor neurone & muscle cell
-An action potential is transmitted across the synapse using the neurotransmitter acetylcholine

36
Q

Action potential being transmitted across synapse using acetylcholine 1; What does the arrival of an action potential at the synaptic knob cause?

A

-Action potential arrives at synaptic knob at end of motor neurone
-Action potential depolarises membrane of synaptic knob. Causes voltage-gated calcium (Ca²+) ion channels to open
-Ca²+ ions diffuse → synaptic knob

37
Q

Action potential being transmitted across synapse using acetylcholine 2; What causes acetylcholine to be released and what is this process called?

A
  • Ca²+ ion concentration inside synaptic knob start to increase
  • causes synaptic vesicles to more & fuse w/ presynaptic membrane
  • acetylcholine (neurotransmitter inside vesicles) released → synaptic cleft
  • this = exocytosis
38
Q

Action potential being transmitted across synapse using acetylcholine 3; what happens as a result of acetylcholine binding to receptors, how can an action potential be generated?

A

-Acetylcholine binds to specific receptors (nicotinic cholinergic receptors) on postsynaptic membrane
- binding of neurotransmitters opens sodium ion channels in postsynaptic muscle cell
- as Na+ ions diffuse → cell, membrane= depolarised
- if potential difference reaches threshold value, action potential generated + flows along motor cell

39
Q

Action potential being transmitted across synapse using acetylcholine 4; How is acetylcholine removed and why is this important?

A
  • acetylcholinesterase (AChE) enzyme breaks down acetylcholine in synaptic cleft
  • products of break down reabsorbed by presynaptic neurone & reused to synthesise more acetylcholine
    -It’s important that acetylcholine = removed from receptors as this stops action potentials from being continuously generated in postsynaptic cell
40
Q

What are cholinergic synapses?

A

Synapses that use acetylcholine as a neurotransmitter

41
Q

How do cholinergic synapses and neuromuscular junctions differ in terms of type of postsynaptic cell?

A

Cholinergic synapses = between 2 neurones
Neuromuscular junctions = between motor neurone & muscle cell

42
Q

How do cholinergic synapses and neuromuscular junctions differ in terms of number of receptors?

A

Less receptors in postsynaptic membrane at cholinergic synapse than at neuromuscular junction

43
Q

How do cholinergic synapses and neuromuscular junctions differ in terms of type of response?

A
  • Cholinergic synapse can trigger inhibitory/ excitatory response in postsynaptic membrane
  • action potential at neuromuscular junction always triggers excitatory response in muscle cell
44
Q

How do cholinergic synapses and neuromuscular junctions differ in terms of result of depolarisation?

A

Cholinergic synapse = depolarisation of post synaptic membrane results in action potential

Neuromuscular junction = depolarisation of postsynaptic membrane results in muscle contraction

45
Q

Where is acetylcholinesterase stored in the cholinergic synapses vs the neuromuscular junctions?

A

Cholinergic synapses - enzyme located in synaptic cleft
Neuromuscular junction - enzyme stored in clefts in postsynaptic membrane

46
Q

What do excitatory drugs do?

A

Stimulate nervous system, producing more action potentials on post-synaptic membrane

47
Q

How can excitatory drugs mimic neurotransmitters? + example

A

Drugs w/similar shape to neurotransmitters can mimic their function;
-They bind to receptors on postsynaptic membrane → produce action potential
-The drugs are called agonists
-Eg nicotine can bind to nicotinic choinergic receptors in brain to mimic acetylchoire

48
Q

How can excitatory drugs inhibit enzymes? + example

A

-Drugs can bind → enzymes = prevents breakdown of neurotransmitter, which would continue to generate action potential in postsynaptic membrane
- eg. nerve gas inhibits acetylcholinesterase, stops breakdown of acetylcholine → loss of muscle control

49
Q

How can excitatory drugs cause the release of neurotransmitters?

A

-Drugs can cause presynaptic neurones to release neurotransmitters
-More neurotransmitters → more receptors activated → action potential more likely to be created

50
Q

What do inhibitory drugs do?

A

Inhibit nervous system to fewer action potentials produced

51
Q

How can inhibitory drugs block calcium ion channels & what does this result in?

A

Drugs can block calcium ion channels in presynaptic membrane → prevent release of neurotransmitters from presynaptic membrane

52
Q

How can inhibitory drugs block receptors and what does this result in?

A

Drugs (called antagonists) can block receptors on postsynaptic membrane → neurotransmitters can’t bind & action potential not generated postsynaptic neurone