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Yr 1 - Nerves & Muscle > Neural Signalling and Communication > Flashcards

Neural Signalling and Communication Flashcards

1
Q

When do neural impulses occur?

A

When a stimulus depolarises a cell membrane, prompting an action potential

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2
Q

How do electrical impulses travel along the axon?

A

Via depolarised voltage-gated ion channels in the membrane

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3
Q

How do electrical impulses travel along myelinated axon?

A

‘Jump’ (salutatory) due to Nodes of Ranvier

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4
Q

How do electrical impulses travel along non-myelinated axon?

A

Travel continuously

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5
Q

When does an action potential occur?

A

When an electrical signal disrupts the original balance of Na+ and K+ within a cell membrane (briefly depolarises the concentrations of each)

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6
Q

What is depolarisation?

A

Change within a cell, when cell undergoes a shift in electric charge distribution, resulting in a less negative charge inside the cell

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7
Q

How does one neurone affect another?

A

A neurone affects other neurones by releasing a neurotransmitter that binds to chemical receptors

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8
Q

What is the effect on the postsynaptic neurone determined by?

A

The effect upon the postsynaptic (receiving) neurone is determined by the receptor that is activated (not the presynaptic neurone or the neurotransmitter itself

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9
Q

What must occur for a presynaptic neurone to release a neurotransmitter?

A

A series of changes in electric potential

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10
Q

How can the potential difference (voltage difference) between inside and outside of cell be measured?

When both are in the bath solution, what is the potential difference?

A

Stick electrodes inside a neurone and measure the potential difference between the inside and outside of the cell

The record is of the potential difference between the 2 electrodes

Zero

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11
Q

What does insertion of electrode into cell reveal?

A

The resting potential –> negative (approx -65mV)

i.e. inside of cell is -65mV lower than outside

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12
Q

What does the magnitude of resting membrane potential depend on?

A

Type of cell involved

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13
Q

What is the resting potential?

A

Name for the electrical state when a neurone is not actively being signalled (the nearly latent membrane potential of inactive cells)

A neurone at resting potential has a membrane with established amounts of Na+ and K+ ions on either side –> inside of neurone is negatively charged relative to outside

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14
Q

What 4 factors contribute to resting membrane potential?

A
  1. Charged intracellular proteins
  2. Na+/K+ pump
  3. Potassium ions
  4. Sodium ions
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15
Q

How do intracellular proteins contribute to membrane potential?

A

Large negatively charged intracellular proteins cannot cross cell membrane to leave as to big (lack of membrane permeability). Contributes to its negativity.

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16
Q

How does Na+/K+ pump contribute to membrane potential?

A

Na+/K+ pump moves 3 Na+ ions out for every 2 K+ ions in (cell gets more negative)

N+/K+ ATPase pump is to maintain resting potential so that the cells will be keeping in a low concentration of sodium ions and high levels of potassium ions within cell

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17
Q

What form of transport is Na+/K+ pump?

A

Active transport (uses hydrolysis of ATP)

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18
Q

What are the gradients acting on potassium ions?

A
  1. Concentration gradient (K+ tends to leak out of cell down concentration gradient)
  2. Electrical gradient (K+ also wants to move back into cell down electrical gradient due to large -vely charged protein molecules trapped in cell)

Eventually becomes balanced –> equilibrium

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19
Q

What is the equilibrium potential for any ion determined by?

A

Nernst Equation

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20
Q

Does the cell resting membrane potential equal the potassium equilibrium potential?

A

No - cell resting membrane potential is close to but not equal to the potassium equilibrium potential as there is also a small leak for Na+ ions

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21
Q

What are the gradients acting on sodium ions?

A

Net inward diffusion of Na+ slightly adds to positivity of cell

Both concentration and electrical gradients operate in same direction (inward flow of ions)

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22
Q

Why is the effect of Na+ on the cell’s resting potential only small?

A

Membrane is only slightly permeable to Na+

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23
Q

At the resting potential, what gradients are acting on ions?

A

Electrical and chemical gradients

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24
Q

What is an action potential?

A

The means by which a neurone sends information down its axon, away from the cell body. The action potential (aka ‘spike’ or ‘impulse’) is an explosion of electrical activity

A short-term change in electrical potential (polarity) that travels along a cell (such as a nerve or muscle fibre) which enables nerves to communicate

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25
Q

When does an action potential occur?

A

Created by a depolarising current, when an electrical signal disrupts the original balance of Na+ and K+ within a cell membrane, briefly depolarising the concentrations of each

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26
Q

While one action potential is being generated by a cell, can another be generated at the same time?

A

No, no other action potential may be generated until the cell’s channels return to their resting state

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27
Q

What is the threshold of excitement?

A

Level of stimulation that a neurone must receive to reach action potential

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28
Q

Why are Ads described as ‘all or none’ signals?

A

The signal reaches the threshold for communication or it doesn’t
o Amplitude of action potential is independent of the amount of current that produced it  larger currents don’t produce larger action potentials
o No signal is stronger or weaker than another

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29
Q

What is reuptake?

A

The absorption of a neurotransmitter by a presynaptic neurone after it has performed its function of transmitting a neural impulse

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30
Q

Why is reuptake important?

A

Necessary for normal function  allows for recycling of neurotransmitters and regulates neurotransmitter level in synapse

Controls how long a signal resulting from neurotransmitter release lasts

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31
Q

What is phase 1 of the AP?

A

Resting membrane potential (-70mV)

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32
Q

What is phase 2 of AP?

A

Depolarisation

Stimulus. Na+ channels open and Na+ enters cell. Membrane potential becomes less. negative. Threshold potential reached and AP spikes.

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33
Q

What is phase 3 of AP?

A

Repolarisation

AP reaches peak at reverse potential. Na+ channels close when Na+ equilibrium is reached. Voltage-gated K+ channels open and K+ ions flow out of cell. Membrane potential reverses and becomes -ve again.

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34
Q

What is phase 4 of AP?

A

Hyperpolarisation

K+ ions continue to flow out of cell while Na+ channels are closed (brief period where membrane potential overshoots past normal resting level before normal resting potential is restored)

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35
Q

Describe voltage-gated Na+ and K+ channels during resting state

A

Both closed

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36
Q

Describe Na+ channel during depolarising phase

A

Na+ channel opens (when membrane potential reaches threshold (about -40mV))

Na+ ions entering cell cause it to becomes more positive which opens more activation gates, accelerates flow of ions

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37
Q

Describe Na+ and K+ channels during repolarising phase

A

K+ channels open and K+ can now leave cell

Na+ ions can no longer enter the cell as the inactivation gate is now fully closed.

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38
Q

Describe K+ channels during undershoot phase (after potential)

A

K+ continue to leave cell, so inside becomes more negative than the resting potential, it hyperpolarises

Even though cell has reached resting potential, K+ channels remain open

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39
Q

What is the change in membrane potential proportional to?

A

The stimulus strength, but once the stimulus (and change in potential) is great enough to reach threshold, a greater stimulus does not result in a greater amplitude of action potential

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40
Q

What does a greater stimulus result in?

A

A greater number of action potentials

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41
Q

What is ensured during the absolute refractory period?

A

No further Paps can be elicited –> ensures AP propagation is unidirectional

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42
Q

What is purpose of AP being unidirectional?

A

Can only travel along the axon from cell body to axon terminal, not in the opposite direction. It cannot reverberate (i.e. go backwards towards its point of origin

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43
Q

How is an AP propagated along a non-myelinated axon?

A
  • Na+ influx depolarises area in front of it and triggers voltage gated Na+ channels to open
  • Causes AP in next membrane section
  • Membrane behind impulse is refractory (APs only induce in next section and propagated in one direction)
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44
Q

How is an AP propagated along a myelinated axon?

A

The excess of positive charge in the red depolarised area inside the axon causes current flow along the axon to the next Node and from there out into the extracellular space, causing depolarisation and an AP at the next Node

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45
Q

Where are voltage-gated channels found in myelinated axons?

A

At Nodes of Ranvier –> only area where membrane can depolarise

46
Q

Why can current only pass through membrane at Nodes of Ranvier?

A

Due to high electrical resistance of myelin sheath, nodes of Ranvier are low resistance

47
Q

Is salutatory or continuous conduction faster?

A

Salutatory

48
Q

Where are voltage-gated channels found in non-myelinated axons?

A

Throughout the membrane

49
Q

What is resting potential largely due to?

A

Passive influx of K+ ions across membrane

50
Q

Where are APs propagated away from?

A

Away from cell body towards axon terminal

51
Q

What are sensory neurone endings often modified to form?

A

Specialised sensory receptors which are ‘tuned’ to specific signals or sensory modalities (different forms of energy)

52
Q

What does a detection of a stimulus by a receptor cause?

A

A receptor potential

53
Q

What is a receptor potential and what does it cause?

A

A graded electrotonic response (not AP)

Causes AP

54
Q

What are the sensory receptors in muscles?

A

Proprioceptors and mechanoreceptors

55
Q

What is a muscle spindle?

A

Bundle of modified skeletal muscle fibres (intramural fibres) enclosed in connective tissue capsule

56
Q

What is the muscle spindle activated by? Where is it located?

A

Located in muscle

Stimulated when muscle is passively stretched

57
Q

What is the function of intramural fibres?

A

Detect stretch initiate reflex which causes muscle to contract –> prevents over stretching

58
Q

How does muscle spindle prevent muscle being overstretched?

A

Muscle stretched passively –> spindle activated –> initiates reflex

Muscle contracts and shortens –> spindle switches off

59
Q

What is the Golgi Tendon Organ?

A

Small bundles of tendon (collagen) fibres enclosed in a layered capsule with the terminal branches of a large diameter (mechanoreceptive) afferent fibre intertwined with collagen bundles

60
Q

When is GTO stimulated? What is the effect?

A

When associated muscle contracts or its stretched. Sets up reflex causing muscle to relax and removing stimulation. Senses changes in tension/force.

61
Q

When is GTO active?

A

Active during both passive stretch and active contraction

62
Q

Where is GTO located?

A

In tendon and responds to tension

63
Q

What is function of GTO?

A

It is a tension detector that protects muscle against excess load

64
Q

Describe knee-jerk reflex pathway

A
  1. Stretching of muscle stretches spindle
  2. Increased discharge of sensory nerves (stimulus produced impulses in the sensory afferent fibres )
  3. Increased firing of motor neurones
  4. Muscle contracts
65
Q

What is a monosynaptic reflex?

A

When a reflex arc consists of only two neurons, one sensory neurone, and one motor neurone (no spinal interneurone involved)

66
Q

What is function of GTO?

A

Protects muscle & connective tissue from injury. Helps prevent excessive muscle contraction or passive muscle stretch by causing reflex inhibition of muscle

67
Q

What are receptors?

A

Pores that admit chemical or electrical signals into the postsynaptic cell

68
Q

What are the 2 main types of receptors?

A
  1. Ligand-gated ion channels

2. G-protein coupled receptors

69
Q

Which receptors receive neurotransmitters?

A

Ligand-gated ion channels receive neurotransmitters (G-protein receptors don’t)

70
Q

What are the 2 different types of synapses?

A
  1. Electrical synapses

2. Chemical synapses

71
Q

What occurs at electrical synapses?

A

Direct passage of current via ions flowing through gap junctions

72
Q

What occurs at chemical synapses?

A

Release of vesicles containing chemical transmitter which has an effect on receptors on a target cell

73
Q

What is a neurotransmitter?

A

A substance that is released at a synapse by one neurone and has physiological action on specific receptors on target cell (e.g. acetylcholine)

74
Q

What is the presynaptic cell?

A

Specialised area within the axon of the giving cell that transmits information to the dendrite of the receiving cell

75
Q

What is the synaptic cleft?

A

The small space at the synapse that receives neurotransmitters

76
Q

What are G-protein coupled receptors?

A

Receptors that sense molecules outside the cell and activate signals within it

77
Q

What are ligand-gated ion channels?

A

Receptors that are opened or closed in response to the binding of a chemical messenger

78
Q

What is a postsynaptic cell?

A

A specialised area within the dendrite of the receiving cell that contains receptors designed to process neurotransmitters

79
Q

How are electrical synapses formed?

A

Formed by interlocking connexon channels of adjacent neurones (gap junctions present)

80
Q

How does current flow between electrical synapses?

A

Can flow and pass directly from one cell to the next (direct, very fast electrical transmission)

81
Q

What are gap junctions?

A

Formed by channels called connexions that comprise connexion proteins

82
Q

Difference between chemical and electrical transmission?

A
  • Chemical are slower than electrical synapses but result in stronger, more complex changes to postsynaptic cell
  • Chemical require neurotransmitters
83
Q

What does the release of neurotransmitters trigger?

A

The opening of ligand-gated ion channels on the membrane of the postsynaptic cell

84
Q

What causes the release of a transmitter from synaptic vesicles?

A

Arrived of an AP

85
Q

Describe stages of chemical reaction at synapse

A
  1. AP travels along membrane of presynaptic cell until it reaches synapse
  2. Depolarisation of membrane at synapse causes Na+ channel to open
  3. Na+ influx activates a set of ion-sensitive proteins attached to vesicles
  4. These proteins change shape, causing membranes of some ‘docked’ vesicles to fuse with the membrane of the presynaptic cell
  5. This opens the vesicles and neurotransmitter is released into synaptic cleft
  6. Neurotransmitter diffuses within the cleft. Some of it escapes, but the rest of it binds to chemical receptor molecules located on the membrane of the postsynaptic cell
  7. The binding of neurotransmitter causes the receptor molecule to be activated in some way
86
Q

What causes neurotransmitters to eventually break loose from receptors?

A

Thermal shaking

87
Q

What happens to the neurotransmitter after it is released from receptor?

A

Either reabsorbed by presynaptic cell and repackaged, or broken down metabolically

88
Q

When are voltage-gated calcium channels opened?

A

When AP reaches synapse

89
Q

What does influx of Ca2+ into cell lead to?

A

Vesicles move to active zone, fusion of vesicle with membrane, release contents

90
Q

Where does Ca2+ enter the axon terminal?

A

Directly at the active zone

91
Q

What is the active zone?

A

Specialised area on presynaptic membrane, where vesicles are primed and ready for exocytosis, ensuring rapid release of neurotransmitter

Guide the viscose toward the membrane in a Ca2+ dependent fashion

92
Q

How is the fused vesicle membrane taken back into the cell?

A

By endocytosis

93
Q

What is the probability of release?

A

Either vesicle will or won’t be released

94
Q

How can the probability of release be increased?

A

By increasing calcium conc

95
Q

How can the probability of release be decreased?

A

By blocking depolarisation of membrane and preventing calcium influx

96
Q

How does binding of neurotransmitter to receptor affect receptor proteins?

A

Causes conformational change

97
Q

What is an ionotropic receptor?

A

Cluster of similar subunits forming ion channels that open or close in response to the binding of a chemical ligand (neurotransmitter)

98
Q

How do ionotropic receptors work?

A
  • Depolarise or hyperpolarise postsynaptic cell (fast response)
  • When transmitter (ligand) binds  conformational change that briefly opens pore and ions pass through to cause rapid change in resting potential of underlying cytoplasm
99
Q

What is a metabotropic receptor?

A
  • 7-transmembrane molecule coupled to intracellular proteins
  • Do not form an ion channel pore but transduce a signal to cell interior (slow response)
100
Q

How do metabotropic receptors work?

A

Ligand binds, conformational change in molecule that causes intracellular part to interact with a G-protein that sets of chain of intracellular events (may include opening of ion channels)

101
Q

What is necessary for a neurotransmitter to be released?

A

An AP

102
Q

What can too much of a neurotransmitter do?

A

Block receptors –> schizophrenia

103
Q

What can too little of a neurotransmitter do?

A

May cause overaccumulation of protein –> Alzheimer’s

104
Q

What does binding of a released transmitter to ligand-gated channel receptor cause?

A

Opening of channel so ions can flow along concentration gradient

105
Q

What does binding of glutamate or acetylcholine cause?

A

Influx of Na+ ions gives rise to excitatory post-synaptic potential (EPSP) in postsynaptic cell

106
Q

What is effect of ESPSs?

A

Depolarise cell towards threshold potential and may initiate AP

107
Q

What does binding of GABA or glycine cause?

A

Influx of Cl- ions gives rise to inhibitory post-synaptic (IPSP) in postsynaptic cell

108
Q

What is effect of ISPSs?

A

Tend to hyperpolarise cell and make initiation of an action potential less likely

Brings postsynaptic cell further away from threshold for firing action potentials (hyperpolarises)

109
Q

What are examples of excitatory transmitter receptors?

A

Glutamate, acetylcholine

110
Q

What are examples of inhibitory transmitter receptors?

A

Glycine, GABA

111
Q

Do ISPSs/ESPSs have a threshold? A refractory period?

A

No

Yr 1 - Nerves & Muscle (11 decks)

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