CNS Neurotransmission - Craviso Flashcards

1
Q

What determines the type of activity that a neuron uses/

A

the ratio of excitatory to inhibitory inputs to that neuron

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2
Q

What small molecule controls sleep, arousal, mood, and appetite?

A

serotonin

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3
Q

What small molecule controls mood, arousal, and appetite

A

NorEpi

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4
Q

What small molecule controls movement (motor control), behavior, mood, and perception?

A

Dopamine

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5
Q

What small molecule controls arousal, and cognition (memory and learning)

A

ACh

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6
Q

What small molecule controls wakefulness and equilibrium?

A

histamine

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7
Q

What is the excitatory amino acid in the CNS?

A

glutamic acid

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8
Q

What is the inhibitory amino acid in the CNS?

A

GABA

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9
Q

methionine, leucine enkephalin, and substance P are all involved in (blank) transmission

A

pain

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10
Q

methionine, leucine enkephalin, and substance P are what class of molecule?

A

neuropeptides

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11
Q

T/F: neuropeptides are also found in the periphery

A

true

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12
Q

What are the function of the endocannabinoids?

A

memory, cognition, and pain perception

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13
Q

Anandamide and 2-AG are what class of molecule?

A

endocannabinoid

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14
Q

Pain transmission uses (hierarchical/non-hierarchical) transmission

A

hierarchical

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15
Q

Primary sensory and motor pathways uses (hierarchical/non-hierarchical) transmission

A

hierarchical

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16
Q

In non-hierarchical projecting, neurons from a single anatomical location extend multiple divergent connectoins to target cells (within/outside) the region in which the neuron originates

A

outside

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17
Q

The raphe nucleus produces what substance?

A

serotonin

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18
Q

Because the raphe nucleus produces serotonin, projections from the raphe nucleus are associated with what activities?

A
sleep, arousal, and mood
behavioral changes
hallucinations
feeding behavior
vomiting (5HT3 ionotropic receptors in area postrema)
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19
Q

NorEpi is produced in what area of the brain/

A

locus ceruleus

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20
Q

Because NorEpi is produced in the locus ceruleus, projections from there would be associated with what types of behavior?

A

Arousal and mood
appetite
cardio control

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21
Q

Dopamine neurons project from what three brain structures?

A

midbrain
striatum
hypothalamus

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22
Q

The mesocortical pathway is involved in what functions?

A

mood and behavior

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23
Q

the nigrostriatal pathways are involved in what functions/

A

motor control

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24
Q

the tuberoinfundibular pathway is involved in what function?

A

endocrine

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25
Q

What pathway is involved in prolactin secretion?

A

tuberoinfundibular pathway

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26
Q

Which ACh pathway is involved in motor control in concert with the dopamine systems?

A

mesopontine

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27
Q

Which ACh pathway is involved in arousal, learning, and memory?

A

basal forebrain pathway

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28
Q

ACh can have effects via muscarinic (GPCR/ionotropic) receptors as well as nicotinic (GPCR/ionotropic) receptors located PREsynaptically

A

muscarinic GPCR

nicotinic ionotropic

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29
Q

Where do histamine projections arise in the brain?

A

tuberomammillary nucleus of the hypothalamus

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30
Q

Histamine works to help regulate equilibrium in what brain structure?

A

cerebellum

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31
Q

T/F: CNS methods of pre and post synaptic transmission are the same as the ones in the periphery

A

true

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32
Q

(Pre/post) synaptic modulation has effects on synthesis, storage, release, reuptake and/or degradation of neurotransmitters; agonist or antagonist activity at nerve terminal autoreceptors

A

presynaptic

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33
Q

(Pre/post) synaptic modulation acts as receptor agonist, antagonist or modulatory activity; degradation of neurotransmitters

A

post synaptic

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34
Q

What are the six major mechanisms of neurotransmitter modulation?

A
  1. presynaptic
  2. post synaptic
  3. neurohormones
  4. neuromodulators
  5. effects on voltage gated ion channels
  6. non-selective effects (anesthetics)
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35
Q

Metabotropic GPCRs are found mostly in the (CNS/periphery)

A

periphery

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36
Q
A and b adrenergic
dopamine receptor
muscarinic ACh
histamine
neuropeptide/endocannabionoid receptors
*most* 5HT receptors
glutamate and GABA receptors 

these are all what class of receptors?

A

metabotropic GPCRs

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37
Q

Describe the process of activating a metabotropic GPCR?

A
  1. neurotransmitter binds
  2. G protein is activated
  3. G protein subunit or second messengers modulate the ion channels
  4. ion channel opens
  5. ions flow across mebrane
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38
Q

What receptor class is found mostly at neuromuscular junctions?

A

ionotropic receptos (aka ligand-gated ion channels)

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39
Q

Describe how a ligand gated ion channel opens?

A
  1. neurotransmitter binds
  2. channel opens
  3. ions flow across membrane
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40
Q

What types of ligand-gated ion channels DEPOLARIZE cells?

A
AMPA (Na)
Kainate (Na)
NMDA (Ca and Na)
certain glutamate receptors
Nicotinic ACh (Na and Ca)
5-HT3 (Na)
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41
Q

What types of ligand-gated ion channels HYPERPOLARIZE cells?

A

GABA-a (Cl-)

Glycine (Cl-)

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42
Q

Excitatory neurotransmission in the CNS is balanced by feed (forward/reverse) and recurrent inhibitory actions of GABA

A

feed forward

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43
Q

Does inhibitory or excitatory neurotransmission dominate

A

inhibitory

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44
Q

T/F: inhibitory and excitatory neurotransmission is paired to a neuron

A

true

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45
Q

Over inhibition leads to….

A

coma

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46
Q

over stimulation leads to….

A

seizures

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47
Q

What mediates major excitatory inputs and inhibitory inputs to postsynaptic neurons in the CNS?

A

amino acid neurotransmitters

48
Q

(blank) is synthesized from glutamate by glutamic acid decarboxylase

A

GABA

49
Q

glutamic acid decarboxylase requires the cofactor (blank)

A

pyridoxal phosphate

50
Q

GABA is metabolized by GABA-amino transferase found where in the cell and in what cell type?

A

in the mito of glial cells

51
Q

What is the precursor to glutamate?

A

glucose

52
Q

Is GABA synthesized in the pre or post synaptic cell?

A

presynaptic

53
Q

what protein allows for GABA to be brought back into the presynaptic cell or into the glial cell?

A

GABA transporter GAT

54
Q

what protein is responsible for the storage of GABA and glycine in neuronal vesicles?

A

VIATT

55
Q

What is the most important type of GABA receptor?

A

GABA-a ionotropi

56
Q

Is GABA a or GABA b metabotropic?

A

GABA-b

57
Q

decrease in Ca conductance via GABA receptors leads to (depol/hyperpol) of the post synaptic cell

A

hyperpolarization

58
Q

GABA uptake may (inc/dec) cAMP production

A

decrease/inhibit

59
Q

GABA receptors that are coupled to activation of K channels produce what type of currents?

A

slow, inhibitory synaptic currents

60
Q

GABA-a and GABA-c channels, when bound to GABA, allow the influx of what ion?

A

Cl-

61
Q

GABA a and GABA c channels mediate (IPSPs/EPSPs)

A

IPSPs

62
Q

T/F: GABA signaling can mediate IP3 production

A

true

63
Q

PRE-synaptic GABA-b receptors (inc/dec) the release of GABA into the cleft, having what effect?

A

decreases GABA, therefore less inhibition

64
Q

In what part of the CNS do we see a high concentration of GABA b receptors?

A

spinal cord

65
Q

Baclofen (Lioresal) is a GABA (a/b) agonist that is used for muscle spasticity in ALS

A

GABAb

66
Q

T/F: GABA uptake by the GABAb receptors on adjacent presynaptic terminals can also inhibit glutamate release

A

true

67
Q

the majority of GABA’s effects are mediated by which GABA receptor?

A

GABA a

68
Q

GABA (hyperpol’s/depol’s) cells and generates IPSPs

A

hyperpolarizes

69
Q

What drugs can act on the GABA a channel?

A

barbiturates

steroids

70
Q

WHat are the two types of GABA transmission?

A

phasic and tonic inhibition

71
Q

Describe tonic GABA inhibition?

A

continuous activation of extra-synaptic receptors (receptors that are on the nerve surface just not in the cleft) by ambient GABA

72
Q

Describe phasic GABA inhibition?

A

GABA a Cl- channels open together and quickly in response to GABA vesicle emptying into the clef, then there is resolution in time and space

73
Q

T/F: glycine channels are both ionotropic and metabotropic

A

FALSE, only ionotropic!!

74
Q

what ion do the ionotropic glycine channels move?

A

Cl-

75
Q

T/F: therapeutic agents against glycine channels have been found to be useful in MS

A

false; no therapeutic agents for glycine channels

76
Q

What is the role of glycine in the spinal cord?

A
  1. motor rhythm generation
  2. coordination of reflex responses
  3. processing of sensory signals
77
Q

What are the two locations besides the spinal cord that glycine is used in the CNS?

A

brain stem and reticular formation

78
Q

What part of rat poison is a glycine antagonist and power convulsant?

A

strychnine

79
Q

T/F: there are Na dependent glycine transporters on both the presynaptic cell and glial cells

A

true

80
Q

What is the precursor to glycine?

A

glucose to serine to glycine

81
Q

What enzyme converts serine into glycine?

A

serine hydroxy methyltransferase

82
Q

What enzyme packages glycine into vesicles?

A

VIATT

83
Q

What cell is responsible for the majority of glutamate reuptake?

A

astrocytes

84
Q

what is glutamate converted into in the astrocytes?

A

glutamine

85
Q

what happens to the glutamine in the astroctyes?

A

it is pumped backed out and taken back up by the presynaptic neuron

86
Q

what transporter allows glutamine back into the presynaptic neuron?

A

EATT

87
Q

What converts glutamine into glutamate?

A

glutaminase

88
Q

What enzyme packages glutamine into vesicles?

A

VGLUT

89
Q

T/F: all three groups of mGluR are found pre and post synaptically and on astrocytes

A

true

90
Q

Which group of mGluR augments the response?

A

group 1

91
Q

which groups of mGluR decreases the response?

A

groups 2 and 3

92
Q

NON-NMDA ionotropic GluR are broken down into what two types of receptors?

A

AMPA receptors

Kainate receptors

93
Q

What are the two major groups of ionotropic GluR?

A

NON-NMDA and NMDA

94
Q

AMPA receptors primarily pump what ion?

A

Na

95
Q

T/F: AMPA receptors can pump Ca as well as Na

A

true

96
Q

What type of receptor mediates the majority of excitatory synapses?

A

AMPA

97
Q

(AMPA/Kainate) receptors play a role in neural plasticity

A

AMPA

98
Q

T/F: Kainate receptors primarily pump Ca

A

false; primarily pump Na but can also pump Ca

99
Q

T/F: Kainate receptors are found pre and post synaptically

A

true

100
Q

T/F: kainate receptors can play a role in neural plasticity

A

true

101
Q

(NON-NMDA/NMDA) GluR primarily conduct Ca

A

NMDA

102
Q

(NON-NMDA/NMDA) GluR are essential for neural plasticity and for long-term potentiation of synapse structure and funtion (aka learning and memory)

A

NMDA

103
Q

NMDA receptors have EXTERNAL binding sites for what two excitatory transmitters?

A

glutamate and glycine

104
Q

what is the role of glycine in NMDA glutamate receptors?

A

an essential co-agonist

105
Q

At what membrane potential does Mg clog the NMDA pore?

A

-50mV

106
Q

Describe the steps in long-term potentiation via the NMDA and AMPA costimulation?

A
  1. Glutamate binds to NMDA, nothing happens
  2. AMPA generally doesn’t let Ca in. BUT if you activate the NMDA receptor, you let Na in through the AMPA receptor
  3. Cell depolarizes, Ca comes in through the NMDA receptor
  4. Now you can do a shit ton with the Ca in the cell
107
Q

after long term potentiation lets Ca into the post synaptic cell, what intracellular enzymes are activated?

A
  1. Calmodulin Kinase II

2. Protein Kinase C

108
Q

What is the result of intracellular enzyme activation in LTP?

A

substrate phosphorylation and increased insertion of AMPA channels into the membrane

109
Q

What intracellular enzymes are activated in LDP?

A

protein phosphatases that dephosphorylate their substrates and cause internalization of AMPA receptors

110
Q

What is the big picture reason for having LTP and LDP?

A

maintenance of neuronal networks and circuits

111
Q

LTP increases the sensitivity to (blank) while LDP decreases the sensitivity to it

A

glutamate

112
Q

Excessive activation of NMDA (blank) receptors causes excitotoxicity

A

glutamate

113
Q

what disease states result in excessive NMDA activity?

A

ischemia, stroke, head injury, hypoglycemia, repeated intense seizures

114
Q

What is the mechanism of toxicity of extra NMDA activation?

A

increased levels of Ca via voltage gated Ca channels that lead to over activation of cellular processes

115
Q

(blank), either alone or with its superoxide free radicals, contributes to the cell death

A

NO

116
Q

In NMDA toxicity, positive feedback of newly maded (blanks) act on the NMDA receptor

A

polyamines

117
Q

Describe the steps in NMDA glutamate receptor excitotoxicity?

A
  1. glutamate is released and activates the AMPA channel
  2. Na flows in via AMPA
  3. Depol from AMPA Na allows Mg to pop out of the NMDA receptor
  4. Ca can flow in via VGCC
  5. Ca in the cell activates a ton of shit including toxic NO production
  6. Polyamines made by intracellular calcium further act on the NMDA receptor and make the problem even worse