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BIOL 367 > Neural Communication > Flashcards

Neural Communication Flashcards

1
Q

How does the presence or absence of channels with differing properties affect neurons?

A

1) how they fire to brief or continuous stimulation

2) how excitable or non-excitable in general

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2
Q

How can the properties of channels within a neuron be changed and what is the consequence?

A

post-translational modifications (like phosphorylation) which change how the neurons respond to stimuli or how well they signal to other neurons

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3
Q

How does the diversity of electrical properties arise?

A

1) from a diversity of ion channel types

2) post-translational modifications

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4
Q

What are some ion-specific and ligand-gated channels formed from?

A

different combinations of channel forming subunits

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5
Q

What associates with channel forming subunits?

A

diversity of modifying subunits

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6
Q

What is the basis of many types of neuromodulation?

A

post-translational modifications (primarily phophorylation)

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7
Q

What are K channels composed of?

A

4 separate subunits clustered together (diversity of subunits and sub-types of subunits)

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8
Q

What is a selectivity filter?

A

makes each channel specific to one type of ion

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9
Q

What is “water of hydration”?

A

water that is combined with other molecules to form a hydrate mineral

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10
Q

What must a potassium do to pass through a potassium channel?

A

remove all of its surrounding water molecules except two (one on front and one on back)

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11
Q

What must a sodium do to pass through a sodium channel?

A

sodium ion can pass through with up to three water molecules

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12
Q

What is the “delayed rectifier” family of K channels?

A

V2.1

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13
Q

What is the transient family of K channels?

A

V4.1 (also called “A” or IA channels)

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14
Q

What do the ligand-gated K channels respond to?

A

1) Ca
2) combined Ca and V-dep
3) chemical changes (pH)

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15
Q

What are the calcium activated K channels?

A

1) BK channel (Big g)
2) SK channel (Small g)
3) IK channel (intermediate g)

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16
Q

What is the notation of the BK channels and what is there defining characteristic?

A
  • KCa1.x

- also voltage sensitive over a physiologically relevant range

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17
Q

What is the notation of the SK channels and what is there defining characteristic?

A
  • KCa2.x

- blocked by apamin (component of bee venom)

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18
Q

What is the notation of IK channels and what do some consider them to be?

A
  • KCa3.1
  • some consider these a sub-type of SK
  • not blocked by apamin
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19
Q

Which ligand-gated ion channels have an external ligand?

A

1) neurotransmitter receptor

2) acid sensing ion channel

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20
Q

Which ligand-gated ion channels have an internal ligand?

A

1) Calcium activated K+ channels

2) Cyclic nucleotide gated channels

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21
Q

What are statocyst hair cells an example of?

A

how channel properties can create complex electrical properties

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22
Q

Is the affinity for Ca high or low for CaK channels in statocyst hair cells?

A

low affinity for Ca

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23
Q

Are Ca channels and K channels tightly or loosely co-localized in statocyst hair cells?

A

tightly co-localized

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24
Q

Why is there a low affinity for Ca?

A

allows Ca to diffuse and potassium channels to close

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25
Q

Why is there tight co-localization between Ca and K channels?

A

creates a calcium domain so that CaK channels may open (since diffusion takes time)

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26
Q

What are the voltage-gated calcium channel families?

A

1) Cav 1.x: “L-type”
2) Cav 2.1: “P-type”
3) Cav 2.2: “N-type”
4) Cav 2.3: “R-type”
5) Cav 3.x: “T-type”

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27
Q

What are the characteristics of Cav1.x (L-type)?

A

1) blocked by dihrdropyridines

2) medium speed, moderate inactivation

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28
Q

What are the characteristics of Cav 2.1 (P-type)?

A

1) blocked by agatoxin from funnel web spider

2) fast open, little to no inactivation

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29
Q

What are the characteristics of Cav 2.2 (N-type)?

A

1) blocked by conotoxin GVII from cone snail

2) fast open, little to no inactivation

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30
Q

What are the characteristics of Cav 2.3 (R-type)?

A

1) resistant to blockers of P and N

2) fast, little to no inactivation

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31
Q

What are the characteristics of Cav 3.x (T-type)?

A

1) blocked by Ni2+ ions, synthetic blockers
2) slowest opening, very inactivating
3) low voltage activated

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32
Q

Which voltage gated calcium channel family is commonly used for fast neurotransmission?

A

Cav 2.1, Cav 2.2, Cav 2.3

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33
Q

What can many beta subunits do?

A

act to modify gating properties (e.g. inactivation)

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34
Q

What can change the opening probability?

A

phosphorylation

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35
Q

What is the “simplest bursting neuron”?

A

a central pattern generator with all inhibitory neurons that are driven by excitatory outside neurons

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36
Q

What 3 currents does a simplest bursting neuron need?

A

1) persistent Na current
2) voltage gated Ca
3) Ca dependent K

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37
Q

What would happen if you add Ca buffer to a simplest bursting neuron?

A

the cell would keep firing

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38
Q

What are some Na channel toxins?

A

1) tetrodotoxin (puffer fish)

2) saxitoxin (marine dinoflagellates)

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39
Q

What are some K channel toxins?

A

1) dendrotoxin (snake)
2) charybdotoxin (scorpion)
3) batrachotoxin (frog)

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40
Q

What does alpha-toxin from Leiurus scorpion do?

A

delays Na+ channel inactivation

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41
Q

What can toxins from venoms do?

A

block channels, lock them open, a or alter their activation or inactivation kinetics

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42
Q

What does the toxin apamin from bees do?

A

1) blocks SK Ca activated K channels
2) affects the afterhyperpolarization (reduces it) which in turn can affect firing rate/excitability of neuron to sustained input

43
Q

What are “chnnelopathies”?

A

diseases caused by mutation in voltage gated channels (Na K, Ca channels)

44
Q

What occurs during “generalized epilepsy with febrile seizures”?

A

slowing of Na+ channel inactivation leads to neuronal hyperexcitability

45
Q

What happens during “benign familial neonatal convulsions”?

A

1) frequent seizures within the first week of life disappearing spontaneously within a few months
2) affects K+ channels

46
Q

What is myotonia and what channel does it affect?

A

1) muscle weakness

2) Cl- channel

47
Q

What are the main two categories of neurotransmitters?

A

1) small molecule

2) peptide

48
Q

What are the classes of neurotransmitter molecules under “small molecule”?

A

1) Acetylcholine
2) Amino acids
3) Purines
4) Biogenic amines

49
Q

What are the neurotransmitters classified as amino acids?

A

1) glutamate
2) aspartate
3) GABA
4) Glycine

50
Q

What is the neurotransmitter classified under purines?

A

ATP

51
Q

What are the subclasses of neurotransmitters under biogenic amines?

A

1) Catecholamines
a) dopamine
b) norepinephrine
c) epinephrine
2) Indoleamine
a) serotonin (5-HT)
3) Imidazoleamine
a) histamine

52
Q

Which small molecule transmitters are not contained in vesicles and why?

A

1) endocannabinoids (lipid soluble)
2) nitric oxide (gas)
3) carbon monoside (gas)
4) adenosine (made from ATP in extracellular space)

53
Q

What are peptide neurotransmitters composed of?

A

more than 100 peptides, usually 3-30 amino acids long

54
Q

Where are peptide neurotransmitters produced?

A

made in cell body because they need ER and golgi for production

55
Q

What are the steps in acetylocholine production?

A

1) glucose -> pyruvate
2) pyruvate -> acetyl CoA (in mitochondria)
3) Acetyl CoA + Choline -> acetylocholine (using chline acetyl-transferase)

56
Q

How is choline brought into the cell?

A

Na+/choline transporter

57
Q

How is acetylcholine degraded after use?

A

1) turned into acetate and choline by acetylcholinesterase

2) choline taken up by transporter for reuse

58
Q

Where does acetylcholine production take place?

A

In the presynaptic terminal

59
Q

What is the transport system to load vesicles?

A

1) proton-pumping ATPase

2) exchange of nt and H+

60
Q

What are examples of toxins that bind postsynaptic receptors?

A

1) bungarotoxin
2) epibatidine
3) conotoxins
4) betel nut

61
Q

What is bungarotoxin from and what does it do?

A

1) cobra alpha neurotoxin

2) nACh antagonists

62
Q

What is epibaidine from and what does it do?

A

1) ecuadoran frog

2) nicotinic and muscarinic AChR

63
Q

What is conotoxin from and what does it do?

A

1) several peptides from cone snail

2) some block presynaptic Ca channels but many also block postsynaptic Gky- and ACh receptors

64
Q

What is the betel nut toxin and what does it do?

A

1) arecoline

2) muscarinic AChR agonist

65
Q

What is the general architecture of ligand-gated receptors?

A

1) 5 subunits
2) need alpha
3) pore

66
Q

What specifications in structure do acetylcholine (nACh) receptors need?

A

need 2 alpha subunits, need two nt to bind to open

67
Q

What is the effect of needing two binding alpha subunits?

A

more sensitive to higher concentration because of increase in probability not affinity

68
Q

What does myasthenia gravis do?

A

1) attacks nicotinic receptors
a) reduces # of receptors
b) disorganizes receptors
2) leads to muscle weakness

69
Q

What is the treatment for myasthenia gravis?

A

neostigmine

70
Q

What is the structure of metabotropic receptors?

A

1) g-protein coupled
2) no pore
3) neurotransmitter binding site and g-protein binding site

71
Q

What receptor classes are metabotropic receptors?

A

1) glutamate
2) GABA
3) Dopamine
4) NE, Epi
5) Histamine
6) serotonin
7) purines
8) muscarinic

72
Q

What receptor classes are ligand-gated receptors?

A

1) AMPA
2) NMDA
3) Kainate
4) GABA
5) Glycine
6) nACh
7) Serotonin
8) Purines

73
Q

What are the steps in glutamate synthesis?

A

1) glutamine -> glutamate (using glutaminase)

74
Q

How is glutamate taken up after being released?

A

1) Taken directly back into presynaptic terminal
2) taken up by glial cell
a) enters cell by excitatory amino acid transporter (EAAT)
b) glutamate -> glutamine (by glutamine synthetase)
c) released by SN1 channel
d) taken into presynaptic terminal by SAT2 channel

75
Q

What is the voltage dependent “blocker” in NMDA receptors and how is it removed?

A

Mg2+

needs to bind two glutamates and be depolarized

76
Q

What are NMDA receptors dependent on?

A

voltage and ligand dependent

77
Q

What are the cofactors for NMDA receptors?

A

glycine or serine

78
Q

Compare NMDA and AMPA.

A

1) AMPA is quick to turn on and off, whereas NMDA is longer lasting
2) NMDA has Ca permeability (all but one AMPA do not pass Ca)

79
Q

What are the three classes of iono GluR?

A

1) NMDA
2) AMPA
3) kainate receptors

80
Q

What is the Ca-permeant AMPA sub-type also involved in?

A

synaptic plasticity

81
Q

What is the structure of AMPA receptors?

A

dimer of dimers: glurR2-glu-R2 + dimer of gluR1, 3 or 4

82
Q

What does the AMPA receptor lack if it is Ca permeable?

A

lack gluR2

83
Q

What is the general process of GABA synthesis?

A

1) glucose -> glutamate

2) glutamate -> GABA (by glutamic acid decarboxylase and pyridoxal phosphate)

84
Q

What is GAD?

A

glutamic acid decarboxylase (a marker of GABA synthesizing terminals)

85
Q

How is GABA taken up after release?

A

1) directly into presynaptic terminal (GAT) and into vesicle (VIATT)
1) directly into presynaptic terminal (GAT) and to mitochondria for breakdown
3) into glial cell (GAT)

86
Q

What is GAT?

A

a GABA and Na co-transporter

87
Q

What is the process of glycine synthesis?

A

1) glucose -> serine

2) serine -> glycine (by serine hydroxymethyltransferase)

88
Q

How is glycine taken up after being released?

A

1) directly into presynaptic terminal by glycine-Na transporter
2) into glial cell by glycine-Na transporter

89
Q

What do many of the sites where ligands can bind cause?

A

modulation of receptor function (potentiate or block)

90
Q

What binding sites modulate efficacy of GABA binding?

A

1) barbiturates
2) steroids
3) picrotoxin

91
Q

What ions flow through GABA receptors?

A

chloride ions

92
Q

What happens when GABA is increased?

A

shut off neurons (inhibitory except in early development because of different chloride transporters)

93
Q

Which site is very addictive?

A

barbiturate site

94
Q

What are some clues in the “Mother’s Little Helper” song?

A

1) little yellow pill
2) tranquilize
3) help through the night
4) overdose

95
Q

What pill might they be talking about in “Mother’s Little Helper”?

A

1) Valium
2) Meprobamate
3) Carodosoprodol

96
Q

Why is GABA excitatory in immature neurons and inhibitory in mature neurons?

A

1) high concentration of Cl inside the cell (immature) so Cl leaves and causes depolarization
2) low concentration of Cl inside causes Cl to enter and hyperpolarize (mature)

97
Q

What are the steps in the biosynthetic pathway for catecholamine nts?

A

1) Tyrosine -> Dihydroxyphenylalanine (DOPA) (by O2 + tyrosine hydroxylase)
2) DOPA -> dopamine (by -CO2, DOPA decarboxylase)
3) dopamine -> norepineprine (by O2 + dopamine-beta hydroxylase)
4) norepinephrine -> epinephrine (by RCH3+ phenylethanol-amine N-methyl-transferase)

98
Q

What is the rate limiting step in the biosynthetic pathway for catecholamine nts?

A

tyrosine hydroxylase (if increased the amount of synthesis increases)

99
Q

What is the drug L-DOPA used for?

A

help increase the amount of dopamine synthesized by neurons as a therapy for Parkinson’s

100
Q

Where are catecholamines released from?

A

relatively small groups of neurons in hindbrain/brainstem and project

101
Q

What is the process of the synthesis of histamine?

A

histidine -> histamine (by -CO2, histidine decarboxlyase)

102
Q

What is the process of the synthesis of serotonin?

A

1) Tryptophan -> 5-Hydroxytryptophan (by O2 + tryptophan-5-hydroxylase)
2) 5-hydroxytryptophan -> serotonin (5-hydroxytryptamine) (by -CO2, aromatic L-amino acod decarboxylase)

103
Q

What are the effects of tetrahydrocannabinol (THC)?

A

motor learning, synaptic plasticity, memory/learning, appetite, pain sensation, mood

BIOL 367 (4 decks)

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