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NPP > Chapter 3: Chemical Signaling by Neurotransmitters and Hormones > Flashcards

Chapter 3: Chemical Signaling by Neurotransmitters and Hormones Flashcards

1
Q

What is the direction of signal transmission in neuron communication?

A

from presynaptic cell to postsynaptic cell

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2
Q

Synaptic cleft:

A

gap between the terminal and dendrites of neighboring cells

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3
Q

Postsynaptic density:

A

dendrites facing the synaptic cleft are filled with neurotransmitter receptors

** this makes them appear darker and somewhat fuzzy

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4
Q

List the three types of synaptic clapses:

A
  1. axodendritic
  2. axosomatic
  3. axoaxonic
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5
Q

What is the most common synapse of the brain?

A

axodendritic

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6
Q

Presynaptic inhibition vs presynaptic facilitation:

A

reduction and enhanced release of transmitter release

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7
Q

Neuromuscular junction:

A

the connection point between a neuron and a muscle

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8
Q

Neurotransmitters:

A

chemical substances released by neurons to communicate with other cells

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9
Q

The major categories of neurotransmitters can be separated into which two groups?

A
  1. classical

2. nonclassical

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10
Q

What are the classical neurotranmitters?

Try to list examples of each!

A
  1. amino acids (GABA/glutamate)
  2. monoamines (Dopamine (DA)/Norepinephrine (NE)/ Serotonin (5-HT)/ Histamine (HA))
  3. acetylcholines (Adenosine triphosphate (ATP))
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11
Q

List the nonclassical neurotransmitters:

A
  1. neuropeptides
  2. lipids
  3. gases
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12
Q

What are some neuropeptides?

A
  1. endorphins and enkephalins
  2. corticotropin-releasing factor (CRF)
  3. Orexin/hypocretin
  4. Brain delivered neurotrophic factor (BDNF)
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13
Q

What are some examples nonclassical gas neurotransmitters?

A
  1. nitric oxide (NO
  2. carbon monoxide (CO)
  3. hydrogen sulfide (H2S)
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14
Q

T/F: A neuron can release more than one type of transmitter.

A

true

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15
Q

T/F: All NT are synthesized in the same manner.

A

false not neuropeptides

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16
Q

Typically NT are synthesized by […] that can occur […] in the cell.

A

enzymatic reactions; anywhere

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17
Q

Neuropeptides have a precursor of […] which can only be made in the […].

A

proteins; cell body (soma)

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18
Q

What else needs to be present in order to fully produce neuropeptides?

A

large vesicles to transport

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19
Q

What is the important site for NT synthesis?

A

axon terminals

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20
Q

Neuromodulators:

A

chemicals that don’t act like typical neurotransmitters

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21
Q

NM could […], enhance, or […] NT effectivness.

A

prolong; reduce

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22
Q

Volume transmission:

A

diffusion away from the site of release to influence cells more distant from the releasing cell than at the standard synapse

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23
Q

Criteria to determine if an endogenous substance is an NT (6)?

A
  1. SYNTHESIZED: presynaptic cell contains the chemical substance and a mechanism to synthesize it
  2. INACTIVATION: a mechanism for inactivating the actions of the chemical should be present
  3. RELEASED: the chemical released from axon terminals during neural stimulation
  4. RECEPTORS: receptors for the substance are present on the postsynaptic cell
  5. IDENTICAL PATHWAY: direct application of the chemical (or the agonist) has the same effect on the post-synaptic cell as if stimulating the presynaptic neuron
  6. AFFECTED BY ANTAGONIST: application of an antagonist that blocks the receptors inhibits both the chemical’s action and the effects of stimulating the presynaptic neuron
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24
Q

What are some of the characteristics of gaseous and lipid transmitters (5)?

A
  1. readily pass through membranes by simple diffusion
  2. cannot be stored in synaptic vesicles
  3. must be made “on demand”
  4. typically released by postsynaptic cells
  5. actions on presynaptic cells or adjacent axons or glial cells
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25
Q

Retrograde NT gas examples:

A

nitric oxide

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26
Q

Nitric oxide has a role as a […] it interacts with […] in both the […] and […] sites.

A

neuromodulator; 2nd messengers; presynaptic; postsynaptic

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27
Q

Retrograde NT lipid examples (2):

A

anandamide and 2-arachidonoylglycerol

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28
Q

Reticulum Theory:

A

Camillo Golgi proposed that the nervous system consisted of a series of vastly interconnected continuous networks

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29
Q

Neuron Doctrine:

A

Santiago Ramon y Cajal proposed the nervous system is composed by individual cells that are not physically connected

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30
Q

Reticulum theory is that information flow is in […]. Neuron doctrine is that information flow is mostly […].

A

any directions among elements; unidirectional from one cell to the other

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31
Q

Neurophysiologists argued that communication between neurons occurred by means of […] crossing the gap between axons and dendrites.

A

electrical currents

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32
Q

Pharmacologists in contrast argued that information between neurons is transmitted by releases of […]

A

neurotranmitters

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33
Q

Anterograde Transmission:

A

the main direction of most transmission in the brain from presynaptic to postsynaptic

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34
Q

Axodendritic synapses:

A

presynaptic axon terminals release NT to postsynaptic dendrites

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35
Q

Axosomatic synapses:

A

axon terminals makes synapses on the cell body (somata) of postsynaptic cells

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36
Q

Axoaxonic synapses:

A

axon terminals make synapses on axon terminals of other neurons

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37
Q

Presynaptic inhibition:

A

a mechanism that reduces transmitter release from the terminal

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38
Q

What is the prime example of presynaptic inhibition?

A

axoaxonic synapses

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39
Q

Presynaptic facilitation:

A

enhanced release of transmitter release

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40
Q

What are the two types of NT?

A
  1. classical

2. nonclassical

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41
Q

List the 3 main classical NT:

A
  1. AA
  2. monoamines
  3. ACh
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42
Q

List the 3 main nonclassical NT:

A
  1. neuropeptides
  2. lipids
  3. gaseous transmitters
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43
Q

T/F: A neuron can release more than one type of transmitter.

A

true

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44
Q

What is the one NT that is synthesized by a unique mechanism?

A

neuropeptides

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45
Q

Typically, NT are synthesized by […] that can occur […] in the cell.

A

enzymatic reactions; anywhere

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46
Q

Required parts for NT synthesis are shipped in large quantities to the…

A

axon terminals

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47
Q

What is the important site for NT synthesis?

A

axon terminals

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48
Q

Neuropeptides have a precursor of […] which can only be made in the […].

A

proteins; cell body

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49
Q

What else has to be present for neuropeptide synthesis (besides proteins)?

A

large vesicles in order for proteins to be transported down to the axon terminals

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50
Q

Neuromodulators (NM):

A

chemicals that don’t act like typical NT

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51
Q

NM could […], enhance, […] a NT […].

A

prolong; reduce; effectiveness

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52
Q

NM could interact through […].

A

volume transmission

53
Q

Volume transmission:

A

diffusion away from the site of release to influence cells more distant from the releasing cell than is the case at a standard synapse

54
Q

Classical transmitter release involves […] and […] of synaptic […].

A

exocytosis; recycling; vesicles

55
Q

Step of NT release from the terminal (5):

A
  1. action potential
  2. depolarization wave
  3. Ca2+ ion voltage channels open
  4. rapid influx of Ca2+ ion in the terminal
  5. NT release
56
Q

Active sites:

A

specialized regions near the postsynaptic cell that are release site for NT

57
Q

Synaptobrevin: […] that plays a key role in helping the vesicle […] with the […] during […].

A

protein; fuse; axon terminal membrane; exocytosis

58
Q

If the synaptobrevin mechanism were to be negatively affected by toxins, what could occur?

A

paralysis: no muscle contraction due to no exocytosis

59
Q

Vesicle recycling: What is it and what does it cause?

A

synaptic vesicle fusion causes it’s membrane to be temporarily part of the terminal membrane

60
Q

What are the 2 benefits of vesicle recycling?

A
  1. prevents depletion of synaptic vesicles (neuron is firing rapidly and many vesicles are releasing their contents into the synaptic cleft
  2. prevents accumulation of vesicle membrane within the membrane of the nerve terminal
61
Q

Clathrin: a […] that forms a coating on the […] that is needed for […] and vesicle […].

A

protein; membrane; invagination; retrieval

62
Q

Ultrafast endocytosis:

A

vesicle retrieval occurs extremely quickly in an area close to the release site

63
Q

Ultrafast endocytosis is completed with the help of…

A

endosomes

64
Q

Endosomes:

A

intracellular organelles that join in vesicle retrieval during ultrafast endocytosis

65
Q

Kiss-and-run:

A

vesicle fuses with the nerve terminal membrane merely to allow the NT molecules to escape the vesicle interor

66
Q

Bulk endocytosis:

A

used to retrieve large amounts of vesicle membrane that have fused with the nerve terminal membrane

67
Q

What are some types of endocytosis?

A
  1. clathrin-mediated endocytosis
  2. ultrafast endocytosis
  3. kiss-and-run
68
Q

GABAergic cells typically release…

A
  1. parvalbumin (PV)
  2. somatosin (SOM, SST)
  3. cholecystokinin (CCK)
  4. vasoactive intestinal peptide (VIP)
69
Q

How can you reduce presynaptic activity?

A

reduce AP

70
Q

Autoreceptors:

A

receptor for the same kind of transmitter that has been released

71
Q

Autoreceptors provide a […] to inhibit/control NT release.

A

NFB

72
Q

What are the two types of autoreceptors?

A
  1. terminal AR

2. somatodendritic AR

73
Q

Terminal AR is located at […] terminals to […] NT release.

A

presynaptic; inhibit

74
Q

Somatodendritic AR is located at […], when activated by […] NT release, it […] the rate of NT release.

A

cell bodies/dendrites; local; slows down

75
Q

Heteroreceptors provide…

A

presynaptic release-modulating effects

76
Q

What are 2 mechanisms for NT inactivation?

A
  1. heteroreceptors

2. autoreceptors

77
Q

At axonal synapses, these receptors can inhibit the release of other NTs.

A

heteroreceptors

78
Q

T/F: Heteroreceptors only inhibit NT release.

A

false; they hold modulating effects, thus, they can enhance as well

79
Q

Mechanisms for NT removal from the synaptic cleft:

A
  1. enzymatic breakdown
  2. reuptake transporters
  3. uptake transporters
80
Q

NT removal: What is the most common mechanism for neuropeptides, lipids, and NO?

A

enzymatic breakdown

81
Q

NT removal: Reuptake transporters move NT molecules […]. An example of this is the […] transporter.

A

back to the axon terminal; serotonin

82
Q

NT removal: Uptake transporters move NT molecules […] into nearby […] cells.

A

away from the synaptic cleft; glial

83
Q

NT removal: What is the most common mechanism for glutamate and GABA?

A

Uptake transporters

84
Q

Receptors:

A

membrane proteins that bind NT

85
Q

Presynaptic Receptors are…

A

autoreceptors or heteroreceptors

86
Q

Postsynaptic receptors main role:

A

pass signal to the postsynaptic cell

87
Q

Postsynaptic receptors are activated by […].

A

NT

88
Q

After activation of postsynaptic receptors, what can result in regards to the environment?

A
  1. inhibition or excitation

2. neuromodulation

89
Q

After activation of postsynaptic receptors, what can result in regards to the NT?

A
  1. disengage and activation of other receptors until inactivated
  2. degraded or reabsorbed
90
Q

Receptor subtypes example…

A

GABA binds on GABAa and GABAb

91
Q

Receptor subtypes can be located in different…

A
  1. compartments of neurons (somata vs. dendrites)
  2. side of the synapse (pre vs. post-synaptic)
  3. neuron types
  4. brain regions
92
Q

Drugs that are designed to affect specific subtypes result in…

A

fewer side effects

93
Q

Ionotropic receptors have a […] but […] response.

A

fast; short

94
Q

Ionotropic consists of […] subunit(s) with an […].

A

4-5; ion channel in the center

95
Q

If an NT binds to an ionotropic receptor, what occurs?

A

channel opening for flow of ions

96
Q

Ionotropic receptors are referred to as […].

A

ligand-gated channel receptors

97
Q 
Na+ = […]
K+ = […]
Cl- = […]
Ca2+ = […]
A

depolarizes; hyperpolarizes; hyperpolarizes; depolarizes

98
Q

Metabotropic receptors have a […] but […] response.

A

slow; prolonged

99
Q

Metabotropic receptors consist of […] subunit(s) that has […].

A

one; 7 transmembrane domains

100
Q

Metabotropic is coupled with…

A

2nd messengers

101
Q

Metabotropic receptors respond to NT binging by work via […], and are typically referred to as […] receptors.

A

G-proteins; G-protein-coupled

102
Q

G-protein stands for…

A

guanine nucleotide-binding proteins

103
Q 
Gs = […]
Gi = […]
Gq = […]
A

stimulation; inhibition; activation

104
Q

In neurons, G-proteins can act via…

A
  1. ion channels

2. effector enzymes

105
Q

Metabotropic receptors: Where are effector enzymes located?

A

on the membrane just like ion channels

106
Q

Gs example = […]
Gi example = […]
Gq example = […]

A

increase cAMP; decrease cAMP; via PLC and IP3

107
Q

Effector enzymes and second messengers.

A

EE can synthesize or break them down

108
Q

Allosteric sites on receptors:

A

additional binding sites on ionotropic or metabotropic receptors

109
Q

Allosteric receptors function ONLY when there’s a presence of…

A

agonist (or NTs) in the main binding site

110
Q

[…] are allosteric modulators and are engineered to bind to alter […].

A

drugs; receptor function

111
Q

If an allosteric modulator is given alone, what is the resulting signal?

A

nothing; there needs to be a presence of an agonist

112
Q

Agonist alone = […]
Agonist + PAM = […]
Agonist + NAM = […]
PAM or NAM alone = […]

A

normal signal; increase in signal; decrease in signal; no signaling

113
Q

First messengers:

A

NTs

114
Q

Second messengers:

A

intracellular molecules or ions that keep carrying out signals from the first messengers

115
Q

Second messengers activate […], which in turn activate other proteins via […].

A

protein kinases; phosphorylation

116
Q

Kinases can trigger many other […] to activate various […].

A

proteins; molecular cascades

117
Q

Activation of nuclear proteins leads to…

A

changes in gene expression

118
Q

Common 2nd messengers (4):

A
  1. cAMP
  2. cGMP
  3. Ca2+
  4. IP3/DAG
119
Q 
cAMP = stimulates […]
cGMP = stimulates […]
Ca2+ = stimulate […]
IP3/DAG = result from […]
A

protein kinase A (PKA); protein kinase G (PKG); protein kinase C (PKC); breakdown of phosphoinositide

120
Q

Calcium/calmodulin kinase (CaMK):

A

mediates Ca2+ activation of protein kinases (phosphoinositide)

121
Q

What is synaptic plasticity?

A

changes in structural/functional features of synapses (leads to synaptic strength)

122
Q

What causes synaptic changes?

A

sensory experience, learning, memory formation, and psychoactive drug use

123
Q

What kind of changes occur to synaptic plasticity?

A
  1. formation of new synapses
  2. adjustments in existing synapses (protein pools, molecular machinery, receptor densities)
  3. growth of spines, dendrites, axon terminals
124
Q

What are examples of molecular cascades (5)?

A
  1. mitogen-activated protein kinase system (MAPK)
  2. Ca2+ dependent molecules (calcium calmodulin)
  3. cAMP, PKA, PKC, etc.
  4. actin and myosin
  5. gene expression and synthesis of new proteins
125
Q

Spines are somewhat pruned during […] but retain […] ([…]).

A

adolescence; plasticity; memory

126
Q

Spines play an important role in […].

A

long-term memory

127
Q

Neurological disorders are associated with […].

A

abnormal levels of spines

128
Q

Key players in synaptic plasticity:

A
  1. molecular cascades

2. spines

NPP (9 decks)

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