4: Neural Conduction and Synaptic Transmission Flashcards

1
Q

Why isn’t dopamine an effective treatment for Parkinson’s disease?

A

Because it doesn’t penetrate the blood-brain barrier effectively.

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2
Q

What is the membrane potential?

A

The difference in electrical charge between the inside and the outside of the cell.

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3
Q

What do microelectrodes do?

A

They record the membrane potential of neurons.

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4
Q

What is the average resting potential of a neuron?

A

-70mV

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5
Q

What is the term for a neuron that has a resting membrane potential?

A

Polarised.

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6
Q

What is the ionic explanation for the resting potential?

A

There are more negative than positive charges outside the neuron than inside it. Unequal ratio.

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7
Q

What are the 4 ions that contribute to resting potential?

A
  • Sodium/Na+
  • Potassium/K+
  • Chloride/Cl-
  • Protein
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8
Q

What are the passive and active factors that contribute to the unequal distribution of ions in the resting neuron?

A
  • Passive factors continuously drive K+ ions out of the resting neuron and Na+ ions in.
  • ACTIVE pumping required to do OPPOSITE of passive factors.
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9
Q

What is the role of sodium-potassium pumps?

A
  • To take Na+ ions out of the neuron, and to bring K+ ions inside the neuron.
  • It is a type of ‘transporter’.
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10
Q

What does depolarization of the neuron do?

A
  • Decreases resting membrane potential from -70mV to -67mV

- Causes an excitatory postsynaptic potential (EPSP).

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11
Q

What does hyperpolarization of the neuron do?

A
  • Increases the resting membrane potential from -70mV to -72mV.
  • Causes an inhibitory postsynaptic potential (IPSP).
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12
Q

What are graded responses?

A
  • EPSPs and IPSPs

- A weak signal fires weak PSPs, strong signal fires strong PSP.

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13
Q

What is meant by PSPs being decremental?

A

Their signal fades over distance.

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14
Q

Where are action potentials generated?

A

NEXT to the axon hillock on the axon.

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15
Q

What mV is the threshold of excitation?

A

-65mV

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16
Q

What type of response is an action potential?

A

An all-or-none response.

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17
Q

What is integration in an action potential?

A

The adding up of all the EPSPs and IPSPs, then decided whether it exceeds the threshold of excitation or not.

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18
Q

What do voltage-activated ion channels do (2)?

A
  • Responsible for the activation and conduction of action potentials.
  • Open or close in responses to membrane potential level changes.
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19
Q

What is the absolute refractory period?

A

A brief period once an action potential has been fired in which a second one cannot be fired.

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20
Q

What is the relative refractory period?

A

A brief period after the absolute refractory period whereby the firing of a second action potential is possible, providing more-than-normal levels of stimulation are provided.

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21
Q

Why are APs nondecremental, but PSPs are decremental?

A

Because the former is an active conduction, whereas the conduction of the latter is passive.

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22
Q

What is antidromic conduction?

A

Conduction going from the terminal end towards to cell body.

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23
Q

What is orthodromic conduction?

A

Conduction going from the cell body to the terminal buttons.

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24
Q

What are the nodes of Ranvier?

A
  • The gaps between adjacent myelin sections.

- Where the sodium channels are based in myelinated axons.

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25
Q

What is saltatory conduction?

A

The conduction of action potentials in myelinated axons.

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26
Q

What is the average conduction speed of myelinated mammalian neurons?

A

100m per second.

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27
Q

What is the average conduction speed of unmyelinated mammalian neurons?

A

1m per second - HUGE difference from myelinated axons!

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28
Q

Average conduction speed in human motor neurons…

A

60m per second.

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29
Q

Where do many axodendritic synapses terminate?

A

On dendritic spines.

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30
Q

What is the advantage of presynaptic facilitation and inhibition (as opposed to PSPs)?

A

They can selectively influence a particular synapse rather than the whole neuron.

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31
Q

What is the difference between directed and nondirected synapses?

A

The sites of neurotransmitter release and reception are:

  • Close to each other in directed synapses
  • Distant from each other in nondirected synapses.
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32
Q

What are neuropeptides?

A
  • Large neurotransmitters

- Short amino-acid chains comprising between 3-36 amino acids.

33
Q

Where and how are small-molecule neurotransmitters synthesized?

A

In the cytoplasm of the terminal button, where they are packed into the synaptic vesicles by the button’s Golgi complex.

34
Q

Where and how are neuropeptides synthesized?

A

In the cytoplasm of the cell body on ribosomes, and are then packaged by vesicles in the cell body’s Golgi complex and transported by microtubules.

35
Q

What is coexistence?

A

When neurons contain 2, not 1, neurotransmitters.

36
Q

What is exocytosis?

A

The process of neurotransmitter release.

37
Q

Briefly describe the exocytosis of small-molecule neurotransmitters.

A
  • A temporary influx of Ca+ ions from the voltage-activated calcium channels near the presynaptic membrane causes an action potential.
  • In turn, this releases the small-molecule neurotransmitters in a pulse-like manner.
38
Q

How do released neurotransmitters produce signals in postsynaptic neurons?

A

By binding to receptors.in the postsynaptic membrane.

39
Q

What is a ligand?

A

A molecule that binds to another.

A neurotransmitter is a ligand of its receptor.

40
Q

What are receptor subtypes?

A

The different types of receptors to which a particular neurotransmitter can bind.

41
Q

What influences postsynaptic neurons by the binding of a neurotransmitter to a receptor subtype?

A

Whether the receptor is ionotropic or metabotropic.

42
Q

What are ionotropic receptors?

A

Receptors that are associated with ligand-activated ion channels.

43
Q

What are metabotropic receptors?

A

Receptors associated with signal proteins and G proteins.

44
Q

The opening of sodium channels, increasing the flow of Na+ ions into the neuron causes what?

A

An EPSP (depolarization).

45
Q

The opening of potassium or chloride channels, increasing the flow of K+ ions or Cl- ions causes what?

A

An IPSP (hyperpolarization).

46
Q

What does a second messenger do?

A

It diffuses throughout the cytoplasm, potentially influencing neuronal activity.
Can influence genetic expression by binding to DNA.

47
Q

What are autoreceptors?

A
  • A type of metabotropic receptor with unusual features.
48
Q

What are the 2 unusual features of autoreceptors?

A
  • They bind to their own molecules

- Located on the presynaptic, rather than the postsynaptic, membrane.

49
Q

The difference in how neuropeptides and small-molecule neurotransmitters are released is directly reflected by the types of effects they have. What are these?

A
  • Neuropeptides: Slow, diffuse, and long-lasting signals.

- Small-molecule neurotransmitters: Rapid, brief, excitatory or inhibitory signals to nearby cells.

50
Q

How does reuptake work?

A

Transporters immediately bring back the released neurotransmitters into the presynaptic buttons.

51
Q

How does enzymatic degradation work?

A

Enzymes break down the released neurotransmitters in the synapse.

52
Q

What enzyme breaks down acetylcholine?

A

Acetylcholinesterase.

53
Q

How does the the recycling of neurotransmitters and vesicles work?

A

The terminal button draws in the released and broken down vesicles and neurotransmitters and recycles them.

54
Q

What 4 remarkable findings are there for astrocytes?

A
  • Release chemical transmitters
  • Contain receptors for neurotransmitters
  • Conduct signals
  • Involved in neurotransmitter reuptake
55
Q

What are gap junctions?

A
  • A.K.A electrical synapses

- Narrow spaces between neurons bridged by connexins.

56
Q

How are electrical signals and small molecules able to pass through the gap junctions to adjacent neurons?

A

By going through the connecting cytoplasm contained by the connexins.

57
Q

What are the 4 classes of small-molecule neurotransmitters?

A
  • Amino acids
  • Monoamines
  • Acetylcholine
  • Unconventional neurotransmitters
58
Q

What are the 4 most widely studied amino acid neurotransmitters?

A
  • Glutamate
  • Aspartate
  • Glycine
  • Gamma-aminobutyric acid (GABA)
59
Q

What is GABA a synthesis of?

A

Glutamate.

60
Q

Which amino acid is the most prevalent excitatory transmitter in the CNS?

A

Glutamate.

61
Q

Which amino acid is the most prevalent inhibitory transmitter in the CNS?

A

GABA.

62
Q

What are the 4 monoamine neurotransmitters?

A
  • Dopamine
  • Epinephrine
  • Norepinephrine
  • Serotonin
63
Q

What are the two divisions of the monoamine neurotransmitters?

A
  • Catecholamines

- Indolamines

64
Q

Which 3 monoamine neurotransmitters are catecholamines, and what are they synthesized from?

A
  • Dopamine
  • Norepinephrine
  • Epinephrine

They are synthesized from tyrosine:

Tyrosine -> L-dopa -> Dopamine -> Norepinephrine -> Epinephrine

65
Q

Which monoamine neurotransmitter is an idolamine, and what is its synthesis?

A
  • Serotonin (a.k.a 5HT)

- Synthesized from tryptophan.

66
Q

What is one class of unconventional neurotransmitters, and what two chemical compounds does it contain?

A
  • Class: Soluble-gas neurotransmitters.
    Contains:
  • Nitric oxide
  • Carbon monoxide
67
Q

What are the endocannabinoids?

A

A class of unconventional neurotransmitters.

68
Q

What psychoactive constituent of marijuana are endocannabinoids similar to?

A

THC (delta-9-tetrahydrocannabinol).

69
Q

What is the name of the most widely studied endocannabinoid?

A

Anandamide

70
Q

What are the 5 (loose) categories of neuropeptides?

A
  • Pituitary peptides
  • Hypothalamic peptides
  • Brain-gut peptides
  • Opioid peptides
  • Miscellaneous peptides
71
Q

What are agonists?

A

Drugs that facilitate effects of a certain neurotransmitter.

72
Q

What are antagonists?

A

Drugs that inhibit effects of a certain neurotransmitter.

73
Q

How do receptor blockers/antagonists work?

A

They bind to postsynaptic receptors without activating them, thus the access of the neurotransmitter.

74
Q

How does atropine exert its antagonistic effect?

A

It binds to muscarinic receptors, which in turn blocks the effects of Ach (these bind to muscarine).

75
Q

How does curare exert its antagonistic effects?

A

It binds to nicotinic receptors. Serious! It blocks transmissions at neuromuscular junctions, so can cause asphyxiation.

76
Q

How is botox deadly?

A

It is a nicotinic antagonist that blocks the release of Ach at neuromuscular junctions!

77
Q

Which area in the brain contains a high concentration of opioid receptors?

A

The periaqueductal gray.

78
Q

What are the two major families of endogenous opioids?

A
  • Enkephalins

- Endorphins

79
Q

All endogenous opioids are….

A

Neuropeptides with metabotropic receptors.