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Block 8 Week 1 > CNS Neurotransmission- Craviso > Flashcards

CNS Neurotransmission- Craviso Flashcards

1
Q

(blank) are the individual signaling elements of the brain

A

neurons

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2
Q

An average neuron has (Blank) synaptic connections and receives even more

A

1000

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3
Q

What is activity of the brain dependent on?

A

ratio of excitatory and inhibitory inputs to a neuron

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4
Q

Whar are the small molecules neurotransmitters in the brain?

A 
serotonin
norepinephrine
dopamine
acetylcholine
histamine
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5
Q

What small molecule is this:

affects sleep, arousal, mood, appetite

A

serotonin

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6
Q

What small molecule is this:

affects mood; arousal, appetite

A

norepinephrine (NE)

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7
Q 
What small molecule is this:
affects movement (motor control); behavior, mood, perception
A

Dopamine (DM)

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8
Q

What small molecule is this:

affects arousal, cognition (memory and learning)

A

Acetylcholine (ACh)

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9
Q

What small molecule is this:

affects wakefulness, equilibrium

A

Histamine

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10
Q

What are the amino acids (found primarily in the CNS)- that mediate major excitatory and inhbitiory neutrotransmision?

A

excitatory-glutamic acid (glutamate)

inhibitory- y-amino butyric acid (GABA) glycine

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11
Q

What are the neuropeptide neutrotransmitters and what do they do?

A

methionine and leucine enkephaline -pain transmission

substance p- pain transmission

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12
Q

What are the endocannabinoid neurotransmitters and what do they do?

A

memory, cognition, pain perception

  • anandamide,
  • 2-arachidonylglycerol (2-AG)
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13
Q

Pain is transmitted in a highly sequential and interconnected way called (blank)

A

long-hierarchical

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14
Q

What is this:
neurons from a single anatomical location extend multiple, divergent connections to target cells outside the region in which the neurons originate

A

non-hierarchical projections

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15
Q

Serotonin (5-HT) neurons projected from the (Blank)

A

raphe nucleus

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16
Q

What does this:

functions in sleep, arousal, mood, behavioral changes, hallucinations, feeding behaviors, vomiting

A

serotonin

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17
Q

(blank) projects from the locus coeruleus

A

norepinephrine

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18
Q

How do you treat spasticity in individuals with amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS)?

A

GABA analog called baclofen (Lioresal)

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19
Q

How are the primary sensory and motor pathways transmitted?

A

in a long-hierarchical fashion (relay)

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20
Q

What are the 2 pathways that serotonin (5-HT) is involved in?

A
  • ascending raphe projections

- descending raphe projections

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21
Q

What are the functional aspects of norepinephrine (NE)?

A
  • arousal and mood
  • appetite
  • cardiovascular control
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22
Q

What are the 2 pathways that norepinephrine (NE) participates in?

A
  • locus coeruleus projections

- lateral tegmental projections

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23
Q

(blank) neurons project from the midbrain, striatum and hypothalamus

A

Dopamine (DM)

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24
Q

What are the functional aspects of dopamine?

A
  • mood
  • behavioral changes
  • motor control
  • neuroendocrine function (prolactin secretion)
  • vomiting (area postrema)
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25
Q

What are the three pathways that dopamine participates in?

A

tuberinfudibular pathway
nigrostriatal pathway
mesocortical/mesolimbic pathways

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26
Q

What are the functional aspects of dopamine?

A
  • mood
  • behavioral changes
  • motor control
  • neuroendocrine function (prolactin secretion)
  • vomiting (area postrema)
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27
Q

(blank) neurons project from the forebrain and brainstem

A

CHolinergic (Ach)

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28
Q

What are the functional aspects of cholinergic (Ach)?

A
  • arousal
  • learning and memory
  • motor control (in concert with dopamine)
  • effects via muscarinic (G-protein linked) receptors and via nicotinic (ionotropic) receptors located presynaptically
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29
Q

If Ach is having effects on muscarinic receptors what kind of receptor are they?

A

G-protein linked

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30
Q

If Ach is having effects on nicotinic receptors, what kind of receptors are they? Where are these receptors located?

A

ionotropic

-presynaptically

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31
Q

What are the 2 pathways that acetycholine particpates in?

A
  • basal forebrain pathways

- mesopontine pathways

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32
Q

(blank) neurons project from the hypothalamus

A

Histamine

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33
Q

What are the functional aspects of histamine?

A
  • Arousal and wakefulness

- Equilibrium (cerebellum)

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34
Q

What is the pathway that histamine participates in?

A

-tuberomammillary nucleus of the hypothalamus

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35
Q

Pre-synaptically, how can you modulate the action of a neurotransmitter?

A

-mess with effects of synthesis, storage, release, reuptake and/or degredation of neurotransmitters; agonists or antagonist activity at nerve terminal autoreceptors

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36
Q

Post-synaptically, how can you modulate the action of a neurotransmitter?

A

-mess with receptor agonist, antagonist or modulatory activity; degredation of neurotransmitters

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37
Q

Whar are some other ways you can mess with neurotransmitters?

A

-mess with neurohormones, neuromodulators, effects on voltage-gated ion channels, non-selective effects (anesthetics)

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38
Q

How is acetylcholine primarily removed?

A

via degredation (via acetycholinesterase)

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39
Q

HOw are most neurotransmitters removed?

A

primarily by reuptake

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40
Q

What is another name for metabotropic receptors?

A

G-protein coupled receptors

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41
Q

What is the most common type of receptor OUTSIDE the cns?

A

metabotropic (G-protein coupled receptors)

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42
Q

Which have quicker responses, metabotropic (G-protein) or ionotropic?

A

ionotropic receptors

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43
Q

How long does it take for metabotropic (G-protein receptors) to respond and how long does the response last?

A
  • Several HUNDREDS of milliseconds

- for seconds and even minutes

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44
Q

What receptors are metabotropic receptors?

A

-All known alpha and beta adrenergic, dopamine, muscarinic ACh, histamine, neuropeptide, and endocannabinoid receptors
MOST 5-HT receptors
-metabotropic glutamate and GABA receptors

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45
Q

What is the only small molecule neurotransmitter that does not have a metabotropic receptor?

A

NE (norepinpehrine)

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46
Q

What is another name for ionotropic receptors?

A

Ligand-gated ion channels

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47
Q

Where do you find ionotropic receptors?

A

outside the CNS-predominantly neuromuscular junctions

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48
Q

How long does it take for an ionotropic receptor (ligand-gated ion channel) to respond and how long does the response last?

A

responses occur within a few milliseconds, lasts for only milliseconds

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49
Q

So which is faster and which lasts longer (ionotropic, metabotropic)

A

faster-ionotropic

longer- metabotropic

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50
Q

What are the ionotropic receptors that depolarize cells?

A

Classes of glutamate receptors:

  • AMPA (Na+)
  • Kainate (Na+)
  • NMDA (Ca2+ and Na+)

Nicotinic ACh receptors (Na+ and Ca2+)

5-Ht3 Receptors (Na+)

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51
Q

What are the ionotropic receptors that hyperpolarize cells?

A

GABA (Cl-) receptors

glycine (Cl-) receptors

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52
Q

What is the predominate receptor in the brain?

A

Ionotropic receptors (ligand-gated ion channels)

53
Q

So what kind of receptors do mucarinic acetycholine bind to?

What kind of receptors does nicotinic acetycholine bind to?

A

metabotropic (Ms go together Muscarinic= Metabotropic)

ionotropic (Ns go together Nictoinc =ioNotropic)

54
Q

What is the ion associated with AMPA?

A

Na+

55
Q

What is the ion associated with kainate?

A

Na+

56
Q

What is the ion associated with NMDA?

A

Ca2+ and Na+

57
Q

What is the ion associated with 5-HT3?

A

Na+

58
Q

What is the ion associated with GABA a?

A

Cl-

59
Q

What is the ion associated with nicotinic ACh receptors?

A

Na+ and Ca2+

60
Q

What is the ion associated with glycine?

A

Cl-

61
Q

Amino acid neurotransmitters mediate (blank) by glutamate (pre-synpatically/ post-synaptically).

A

major excitatory inputs

post-synaptically

62
Q

Amino acid neurotransmitters mediate (blank) by GABA (pre-synpatically/ post-synaptically).

A

major inhibitory inputs

post-synaptically

63
Q

How do you balance out excitatory transmission by amino acid neurotransmitters?

A

via feed-forward and recurrent inhibitory actions of GABA released from interneurons

64
Q

Inputs to neurons paired to achieve a coordinated balance between excitatory (ESPS) and inhibitory (IPSP) events but (blank) neuro-transmission predominates

A

Inhibitory

65
Q

What happens if you interfere with the ESPS/IPSP relationship?

A

highly disruptive- results in extremes such as comatose versus seizues

66
Q

How do you make GABA?

A

synthesized from glutamate, by glutamic acid decarboxylase.

67
Q

What does glutamic acid decarboxylase require to make GABA?

A

Pyridoxal phosphate

68
Q

How is GABA metabolized?

A

By glial cells and mitochondria of neurons cuz they have GABA-amino transferase which metabolizes GABA

69
Q

Where is GABA-amino transferase found?

A

in mitochondria of neurons and glial cells

70
Q

A metabotropic receptor (GABA-B) in the nerve terminal can modulate the way GABA is released, does it increase GABA or decrease GABA release?

A

Decrease

71
Q

Which is more important GABA-B or GABA-A?

A

GABA- A

72
Q

Why do metabotropic GABA-B receptors inhibit GABA release?

A
  • decreased Ca2+ conduction
  • coupling to K+ channel which produces inhibitory signal
  • regulating IP3 production and/or inhibit cAMP production
    (i. e make it impossible for the GABA transporter to become stimulated enough to release GABA)
73
Q

Presynatpic receptors (GABA -B) decreases release of (blank) and (blank).

A

GABA

Glutamate

74
Q

GABA b has a role in modulating the effects of GABA at (blank) receptors as well as the effects of other neurotra

A

GABA A

75
Q

Where do you find a high concentration of GABA b receptors?

A

In spinal cord

76
Q

What drug is a GABA B agonist that is used for treating spasticity (involuntary and abnormal muscle contractions) in individuals with Amyotrophic Lateral Sclerosis (ALS) and multiple sclerosis (MS)?

A

baclofen (Lioresal)

77
Q

Majority of GABAs effects are mediated by (blank) receptors.

A

GABA A

78
Q

GABA a receptors are (blank) conducting ion channels.

A

Cl-

79
Q

GABA (blank) postsynaptic cells and generates IPSPs

A

Hyperpolarizes

80
Q

Based on the location of GABA A receptors, there are 2 types of GABA neurotransmission… what are they?

A

Phasic and Tonic

81
Q

How do you get tonic inhibition via GABA?

A

continuous activation of extra-synaptic receptors by ambient GABA

82
Q

How do you get phasic inhibition via GABA?

A

Rapid, synchronous opening of channels in synaptic cleft; resolution in time and space

83
Q

What kind of GABA receptors will cause tonic inhibition?

A

Extrasynaptic GABA A receptors

84
Q

What kind of GABA receptors will cause phasic inhibition?

A

Synaptic GABA A receptor

85
Q

Where do you see the majority of glycine acting?

A

in the spinal cord

minor places-> brain stem, reticular formation

86
Q

What does glycine do?

A

control motor rhythm generation, coordination of reflex responses and processing of sensory signals

87
Q

What are the kinds of receptors that glycine utilizes?

A

Cl- conducting ion channels

NO metabotropic receptors

88
Q

What are the therapeutic agents that work on glycine channels?

A

there aren’t any

89
Q

What is an antagonist of glycine channels that are powerfu convulsants?

A

Strychnine (occurs in nature in certain seeds; an ingredient in rat poison)

90
Q

After being released, glutamine reuptake occurs via tranporters present on (bank) and on (Blank).

A

Nerve terminals

Astrocytes

91
Q

What is responsible for the majority of glutamate reuptake?

A

astrocytes

92
Q

What happens in the astrocyte to glutamate?

A

it is converted to glutamine for the nerve terminal to take it up to replenish the glutamate pool

93
Q

What are the metabotropic receptors for glutamate?

A

there are three:

-Group 1, Group 2, Group 3

94
Q

What are the Group I metrabotropic receptors for glutamate (mGluR)?

A

mGluR receptors (augment responses)

95
Q

What do Group II and Group III mGluR receptors do?

A

decrease response

96
Q

Where do you find metabotropic receptors for glutamate?

A

pre and post synaptically and on astrocytes

97
Q

What are the 2 major types of glutamate ionotropic receptors?

A

Non-NMDA receptors and NMDA receptors (N-methyl-D-aspartate)

98
Q

What are the non-NMDA receptors?

A

AMPA receptors and Kainate receptors

99
Q

What ions conduct through AMPA receptors?

A

primarily Na+

some also permeable to Ca2+

100
Q

What do AMPA receptors do?

A

mediate the majority of excitatory synapses

101
Q

Do AMPA receptors play a major role in neural plasticity?

A

NOOO they play a minor role

102
Q

What kind of ions do Kainate receptors conduct?

A

primarily Na+, some may also be permeable to Ca2+

103
Q

Where do you find Kainate receptors?

A

Pre and Post-synaptically

104
Q

What do Kainate receptors do?

A

play a role in neural plasticity

105
Q

What kind of ions are conducted through a NMDA glutamate receptor?

A

Primarily Ca2+ and also conduct Na+

106
Q

What do NMDA glutamate receptors do?

A

They mediate neural plasticity and change neuronal activity into long-term changes in synapes structure and function (i.e play a role in learning and memory)

107
Q

NMDA glutamate receptors containe (blanK) binding sites for gluatamate and glycine (an essential co-agonist), and an (blank) binding site for Mg2+.

A

External

Internal

108
Q

At membrane potentials more negative than -50mv, what happens in NMDA glutamate receptors?

A

Mg2+ will go inside the channel, bind to the internal receptor and block the channel

109
Q

Normal synaptic release of glutamate activates only (Blank) receptor channels

A

AMPA (or kainate)

110
Q

So glutamate binds to AMPA receptor, then what happens?

A

sodium goes in and depolarizes cell.

111
Q

So glutamate binds to AMPA receptors, sodium enters and you get a strong depolarization… then what happens?

A

glutamate and glucine will bind and kick out the Mg2+ to open the receptor and calcium then will enter which will cause neuroplasticity

112
Q

So how do you activate NMDA receptors?

A

requires strong depolarization and simultaneous binding of 2 different agonists

113
Q

(blank) receptors mediate neural plasticity

A

NMDA

114
Q

What increases sensitivity of post-synaptic neurons to glutamate?

A

Long-term Potentiation (LTP)

115
Q

What does LTP do to AMP receptors?

A

adds them to the post-synaptic terminal in the early phase which will result in changes in synpatic connections

116
Q

What does Long term depression (LDP) do?

A

decreases sensitivity of post-synaptic neurons to glutamate

117
Q

How does LDP affect AMPA receptors?

A

down regulates them -> causes internalization of those receptors

118
Q

HOw does LDP work?

A

NMDA receptors let calcium and sodium in that activates protein phosphatases that dephosphorylate substrates and results in internalization of AMPA receptors

119
Q

How does LTP work?

A

NMDA receptors let calcium and sodium in that activates protein kinase C and Ca, calmodulin kinase II which results in substrate phosphorylation and this insertion of AMPA receptors in post synpatic terminal

120
Q

What receptors afffect your memory?

A

NMDA receptors

121
Q

What is the overall significance of LTP and LDP?

A

maintenance of neuronal networks/circuits

122
Q

What does excessive activation of NMDA glutamate receptors cause?

A

excitotoxicity

123
Q

How can you get excitotoxicity from excessive activation of NMDA glutamate receptors?

A

can result from ischemia, stroke, head injury, hypoglycemia, repeated intense seizures

124
Q

What is the mechanism behind excessive activation of NMDA glutamate receptors causing excitotoxicity?

A

due to large increases in neuronal cytosolic Ca2+ (through both NMDA receptors and Ca voltage gated ion channels) -> that overactivate a variety of cellular processes controlled by calcium

125
Q

How does a large influx of calcium cause excitotoxicity?

A

calcium activates creation of polyamines, makes NO and radicals, makes proteases and endonucleases, and causes mito damage. ALL these things cause neuronal death

126
Q

What besides damaging the neuron do polyamines do?

A

they modulate NMDA receptors to cause swelling of neuron due to increased permeability to sodium and thus neuronal death

127
Q

Why kind of feedback do polyamines exhibit on NMDA receptors?

A

positive feedback

128
Q

Excessive activation of NMDA glutamate receptors causes excitotoxicity and it is thought that this mechanism play a role in (blank) disorders such as (Blank)

A

neurodegenerative disorders

Alzheimers disease

Block 8 Week 1 (13 decks)

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