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Block 5 week 1 Dani > Neurotransmission 2 - Kenyon > Flashcards

Neurotransmission 2 - Kenyon Flashcards

1
Q

How many families of neurotransmitter receptors are there? What are they called?

A

4 families

  1. Ionotropic ligand gated ion channels
  2. Tyrosine kinase enzyme-linked receptors
  3. G-protein coupled receptors (GPCRs)
  4. Intracellular receptors for unconvential neurotransmitters.
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2
Q

What is the difference between ionotropic and inotropic?

A

Ionotropic: single transmembrane protein binding a neurotransmitter that acts as the channel for cation movement.

Inotropic: ability of muscle to generate force at a given length.

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3
Q

Are ionotropic receptors made from a specific set of subunits or a combination?

A

A combination of many!

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4
Q

What the ionotropic receptors for glutamate? (3)

A
  1. AMPA
  2. NMDA
  3. Kainate
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5
Q

Do GPCRs directly or indirectly influence opening/closing of ion channels?

A

Both!

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6
Q

Are GPCRs 1TM or 7TM?

A

1TM

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7
Q

Can GPCRs elicit multiple intracellular effects?

A

yes!

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8
Q

What is an orphan receptor?

A

A 7TM receptor that looks like a metabotropic receptor but the neurotranmisster is unknown.

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9
Q

Describe the function of a metabotropic (GPCR) receptor?

A
  1. Nuerotransmitter binds.
  2. g-protein activated
  3. G protein subunits or intracellular messengers modulate ion channels
  4. Ions flow across membrane
  5. Ion channel opens.
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10
Q

Describe the function of an ionotropic receptor?

A
  1. neurotransmitter binds
  2. Channel opens
  3. Ions flow across the membrane.
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11
Q

Can you form an ionotropic receptor by mixing and matching subunits?

A

Yes! Can make hundreds of receptors from subunit pool.

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12
Q

Are there many or few metabotropic receptors?

A

Few, <10

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13
Q

Do ionotropic receptors have a limited or extensive set of intracellular responses?
What is the primary effect?

A

Limited response, mostly changes membrane potential.

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14
Q

Allowing (blank) ions through an ionotropic receptor will increase the number of intracellular effects?

A

Calcium!

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15
Q

Do metabotropic receptors have limited or extensive intracellular effects?

A

“UNLIMITED” biochemical responses!

GPCR->signaling cascade systems

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16
Q

Activation of a (blank) receptor will change a neuron’s likelihood of firing an action potential

A

Metabotropic

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17
Q

Why does Ca influx alter the function of ionotropic receptors?

A

Calcium is central in all vitally controlled cell processess–death, growth, continuation of life, etc.

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18
Q

Do tyrosine kinase enzyme linked receptors directly or indirectly open and close ion channels?

A

Indirectly!

Enzyme-LINKED

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19
Q

The (blank) enzyme involved in nitric oxide synthesis dependent on (blank) ions.

A

NO synthase

Calcium

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20
Q

What are the four general groups of small molecule neurotransmitters?

A
  1. ACh
  2. Amino acids
  3. Biogenic amines
  4. Purines
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21
Q

What are the amino acid NT’s? (4)

A
  1. Glutamate
  2. Aspartate
  3. GABA
  4. Glycine
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22
Q

What are the biogenic amines (3)?

A
  1. Catecholemines (NEpi, Epi)
  2. Serotonin (5-HT)
  3. Histamine
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23
Q

What are the purines (4)?

A

ATP, ADP, AMP, Adenosine

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24
Q

Gastrin releasing peptide is involved in remembering (blank).

A

Fearful situations

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25
Q

What is the general postsynaptic effect of ACh?

A

Excitatory

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26
Q

What is the general postsynaptic effect of glutamate?

A

Excitatory

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27
Q

What is the general postsynaptic effect of GABA?

A

Inhibitory

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28
Q

What is the general postsynaptic effect of glycine?

A

Inhibitory

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29
Q

What is the general postsynaptic effect of catecholemines?

A

Excitatoryo

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30
Q

What are the precursors to ACh?

A

Choline, acetyl CoA

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31
Q

what is the rate limiting step in ACh synth?

A

CAT

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32
Q

How is AcH removed?

A

AChEase

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33
Q

How are glutamate, GABA, glycine removed?

A

Transporters

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34
Q

How are catecholemines removed?

A

Transporters and MAO

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35
Q

What is the general postsynaptic effect of 5-Ht?

A

Excitatory

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36
Q

What is the general postsynaptic effect of Histamine?

A

Excitatory

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37
Q

What is the general postsynaptic effect of ATP?

A

Excitatory

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38
Q

What is the general postsynaptic effect of neuropeptides?

A

Excitatory and inhibitory

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39
Q

What is the precursor to 5-Ht?

A

Tryptophan

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40
Q

What is the rate limiting step in 5-HT synth?

A

tryptophan hydroxylase

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41
Q

How is 5-Ht removed?

A

Transporters and MAO

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42
Q

How is histamine removed?

A

Transporters

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43
Q

What is the precursor to ATP?

A

ADP

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44
Q

How is ATP removed?

A

Hydrolysis to ADP and adenosine

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45
Q

What are the precursors to neuropeptides?

A

amino acids

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46
Q

How are neuropeptides removed?

A

proteases

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47
Q

What are the precursors to endocannabinoids?

A

Membrane lipids

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48
Q

what is the rate limiting step for endocannibinoids?

A

enzymatic mod of lipids

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49
Q

what is the precursor for NO?

A

ARRRRginine!

50
Q

What is the rate limiting step for NO? What ion does it require?

A

NO synthase, requires Ca

51
Q

How is NO removed?

A

Spontaneous oxidation

52
Q

At what types of synapes do you find ACh? (3)

A
  1. Neuromuscular junction
  2. Preganglionic autonomic ganglia
  3. Post-ganglionic parasympathetic neurons
53
Q

How is choline recovered from the broken down ACH in the synaptic cleft?

A

via Na/choline transporter

54
Q

What are the two general classes of ionotropic nicotinic ACH receptor (nAChR)?

A
  1. Muscle nAChR

2. Neuronal nAChR

55
Q

How many types of muscle nAChR are there?

A

2: one adult and one fetal

56
Q

Are there multiple or few neuronal nAChR?

A

ZILLIONS

57
Q

How many subunits are required to form an nAChR?

A

4-5

58
Q

ACh, nicotine, curare, and bungaratoxin, d-tubocurarine, and succinylcholine bind at which subunit on muscle nAChR?

A

alpha 1

59
Q

Does hexamethonium bind at muscle or neuronal nAChR?

A

Nueronal

60
Q

Are muscarinic AChR metabotropic or ionotropic?

A

Metabotropic

61
Q

In what types of tissue do you find muscarinic AChR? (3)

A
  1. Neurons
  2. Smooth muscle
  3. Cardiac muscle
62
Q

Do muscarinic AChR’s mediate normal neuromuscular transmission?

A

NO

63
Q

What is the priniciple fast excitatory neurotransmitter?

A

Glutamate

64
Q

What transporter collects glutamate?

A

EAAT’s.

65
Q

What cell type actively collects glutamate?

A

Glial cells

66
Q

What are the three artificial agonists?

A
  1. AMPA
  2. NMDA
  3. Kainate
67
Q

Do all artificial agonists pass cations?

A

YES

68
Q

Do all artificial agonists pass Ca?

A

only some

69
Q

Do all artificial agonists mediate EPSPs?

A

YES

70
Q

Different receptors show different kinetics?

A

Most certainly

71
Q

What ions does the NMDA pore allow to pass? (3)

A

(Na, K, and Ca)

72
Q

What change to cell polarization will NDMA receptors have

A

they can depolarize the cell and and activate Ca processes.

73
Q

What ion blocks the NMDA channel?

A

MG

74
Q

Is activation of the NMDA receptor sufficient for alteration of resting potential?

A

NO, that Mg messes everything up

75
Q

Describe the process of NMDA receptor activation and subsequent cellular responses?

A
  1. Glutamate binds NMDA, but nothing happens yet.
  2. AMPA generally doesn’t let calcium in. However, binding glutamate to NMDA lets AMPA let Na in
  3. Cell depolarizes from NA influx
  4. Ca comes in through NMDA
  5. Ca in the cell can now go do its thang
76
Q

AMPA depolarization leads to (blank) potentiation

A

Long-term

77
Q

What effect does AMPA have on EPSP?

A

it makes them larger

78
Q

where is there vesicle fusion during AMPA activation?

A

both pre and post synaptically

79
Q

Is the power of a glutamate synapse adjustable?

A

Yes!

80
Q

What changes does a tetanic stimultion have on EPSPs?

A

it makes them LARGER

81
Q

The combo of (blank and blank) receptors is necessary for Ca entry.

A

NMDA

AMPA

82
Q

Ca in the cell can cause long term (blank) or (blank)

A

potentiation

depression

83
Q

What is the effect of high extracellular glutamate on nerve cells?

A

IT KILLS THEM

84
Q

What ion precedes cell death via glutatmate/

A

Ca, blocks glutamate receptors

85
Q

Are glutamate receptors metabotropic or ionotropic?

A

Metabotropic

86
Q

What special neural cell type has glutamate receptors?

A

Astrocytes!

87
Q

Which two GABA receptors are ionotropic? what ion do they mediate?

A

GABA A
GABA C
Chloride ions

88
Q

what class of drug is a common ionotropic GABA agonist?

A

Benzo’s

89
Q

What GABA receptor is metabotropic?

A

GABA B

90
Q

do ionotropic GABA receptors effect EPSP or IPSP?

A

IPSP, they’re inhibitory!

91
Q

What is the enzyme that pumps GABA into vesicles presynaptically?

A

VIATT: Vesicular inhibitory Amino Acid Transporter

92
Q

The effects of alcohol are mediated by what neurotransmitter? The ionotropic or metabotropic variety?

A

GABA, ionotropic

93
Q

Activation of the inhibitory neuron (that released GABA) stops the action potentials in the (blank)-synaptic neuron but does not (blank)-polarize the postsynaptic neuron. The action potentials stop because the depolarization to threshold is (blanked).

A
  1. post-synaptic
  2. hyperpolarize
  3. slowed
94
Q

Glycine activates ionotropic (blank) ion channels

A

Cl

95
Q

What blocks glycine receptors in the spinal cord?

A

Strychnine

96
Q

What are the 5 biogenic amines?

A
  1. Dopamine
  2. NEpi
  3. Epi
  4. histamine
  5. serotonin
97
Q

What does the presence of tyrosine hydroxylase indicate about a neuron?

A

THEY RELEASE THE CATECHOLEMINES

98
Q

How is dopamine inactivated?

A

Na-dependent uptake (DAT)

99
Q

What drug inhibits dopamine uptake?

A

COCAINE

100
Q

What class of receptor are dopamine receptors?

A

Metabotropic

101
Q

Dopaminergic neurons stem from what region of the brain?

A

originate in substantia nigra, continue to the corpus striatum (caudate and putamen)

102
Q

What processes are dopamine involved in?

A
  1. Coordination of movement (PARKINSON)
  2. Motivation
  3. Reward
  4. Reinforcement
  5. Addiction
103
Q

Where is NEpi released?

A

sympathetic post-ganglionic neurons

104
Q

What inactivates Nepi?

A

NET; also transports dopamine

105
Q

what inhibits NET?

A

Amphetamines, man!

106
Q

What class of receptor are alpha and beta adrenergic receptors?

A

metabotropic

107
Q

Noradrenergic neurons in locus coeruleus project to forebrain and cause (blank)

A

sleep wakefulness, attention, feeding.

108
Q

Adrenergic neurons containing Epi are located in lower brainstem (medulla). They project to (blank) and (blank). The function is not clear.

A

hypothalamus and thalamus

109
Q

what class of receptor is histamine?

A

metabotropic

110
Q

Histamine is involved in what three processes?

A
  1. Allergic response
  2. Pain
  3. itch
111
Q

Serotonin is important in:

A
  1. psych disorders
  2. pain (centrally and peripherally)
  3. GI tract
112
Q

Prozac does what?

A

Selective serotonin reuptake inhibitor

113
Q

5-HT3 class of receptors are metabo or ionotropic?

A

Ionotropic, nonselective cation channels

114
Q

Purine transmission is important where?

A 
Periphery (smooth muscle)
Nervous system (mechanosensation and pain)
115
Q

What enzyme creates a “soup” of purines?

A

extracellular ecto-5’ nucleotidases

116
Q

Nueropeptide pre-propeptides are are targeted with a signal plexus that sends them where in the cell?

A

ER and Golgi

117
Q

can neuropeptides travel to affect distant neurons?

A

YES

118
Q

Are neuropeptides slow or fast? Short or long lasting?

A

SLOOOOOOWW AND LOOOOONG

119
Q

Do endocannibinoids have brain pain control?

A

NO NO NO NO

120
Q

What is considered a retrograde messenger?

A

NO

Block 5 week 1 Dani (10 decks)

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