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Cellular Neuroscience > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

Chemical signaling consists of…

A

A molecular signal (neurotransmitter)
* A receptor molecule (transduces information
provided by the signal)
* A target molecule (ion channel) that is altered to
cause electrical response in the postsynaptic cell
(can be the same as the receptor)

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2
Q

Criteria that define Neurotransmitters

A
  1. The substance must be present within the presynaptic neuron.
    Problems: Transmitters like glutamate, glycine and aspartate have also other functions in cellular metabolism
    and/or function as precursor for other transmitters (e.g. dopamine for norepinephrine, glutamate for GABA).
  2. The substance should be released in response to presynaptic depolarization
    (but there are exceptions), and the release must be Ca2+
    -dependent.
  3. Specific receptors for the substance must exist on the postsynaptic cell.
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3
Q

Three types of small-molecule neurotransmitters

A
  1. Acetylcholine
  2. Amino Acids
  3. Biogenic Amines
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4
Q

Two types of Metabolism of Neurotransmitters

A
  1. Classical (small molecules)
  2. Neuropeptides
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5
Q

“Classical” transmitter
(small molecules)

A

Local synthesis in the
presynaptic terminal.

Synthesizing enzymes come
from nucleus via slow axonal
transport

small clear core vesicles

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6
Q

Neuropeptides

A

Synthesis in the soma
(nucleus; rough endoplasmic
reticulum [pre-propeptides]
and Golgi apparatus
(propeptides]).

Complete
vesicles reach terminal via
fast axonal transport
through microtubules

large dense core vesicles

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7
Q

Release of neuropeptides requires

A

high frequency stimulation to co-release with small molecule transmitters
→ Importance of calcium levels in the presynaptic terminal

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8
Q

Ionotropic Receptors

A
  • Membrane spanning region forms ion channel.
  • Comprised of 3-5 protein subunits.
  • Mediate rapid postsynaptic effects (millisecond time scale)
  • Glutamate receptors
    (NMDA, non-NMDA) and Cys-loop receptors
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9
Q

Cys-loop receptors

A

nicotinic acetylcholine
receptor (nAChR)
* 5-HT3 receptor
* GABAA receptor
* Glycine receptor
* Purinergic receptors

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10
Q

nicotinic ACh, GABAa, Glycine receptor channels are

A

pentamers

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11
Q

Glutamate receptor channels are

A

tetramers

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12
Q

Acetylcholine Precursors

A

Acetyl coenzyme A and choline

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13
Q

Enzyme that catalyzes precursors into Acetylcholine

A

choline acetyltransferase
(ChAT)

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14
Q

After release,
this breaks up
ACh into acetate and choline

A

Acetylcholinesterase

ACh-esterase is the target of
nerve gases/pesticides

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15
Q

A Na+
/choline transporter
takes

A

choline back up into
the presynaptic terminal

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16
Q

Irreversible Acetylcholinesterase inhibitors

A

Insecticides (so-called organophosphates), and
nerve gases (e.g. Sarin, Soman)

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17
Q

Irreversible AChE-inhibitors completely

A

inhibit ACh breakdown

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18
Q

Irreversible Acetylcholinesterase inhibitors

The lethal effect results from

A

“overstimulation” (persistent depolarization) of the
postsynaptic membrane, particularly muscle cells.

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19
Q

Irreversible Acetylcholinesterase inhibitors

The main effect is

A

neuromuscular paralysis (leading to respiratory failure within 5
min), preceded by cognitive and severe autonomic symptoms.

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20
Q

Irreversible Acetylcholinesterase inhibitors

Treatment involves

A

combined administration of a muscarinic receptor antagonist
(e.g. atropine) and the AChE antagonist pralidoxime, which paradoxically restores
AChE function
(→ Pralidoxime attaches to the site where the cholinesterase inhibitor has attached, then attaches to the
inhibitor, removing the organophosphate from cholinesterase, allowing it to work normally again)

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21
Q

Glutamatergic synapse

A

most prevalent excitatory transmitter (>half of all synapses)

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22
Q

Precursor of glutamate

A

glutamine

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23
Q

Enzyme that catalyzes
glutamate from [precursor]

A

glutaminase

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24
Q

VGluT

A

vesicular
glutamate transporter

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25
Q

Glutamatergic synapse

EAAT

A

excitatory
amino acid transporter
5 different types –
some on presynaptic
terminals, others on
glia cells (→ GLT1,
GLAST)

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26
Q

Neurotransmitter
transporters for
re
-uptake

A

Often use electrochemical
gradients, e.g. co-transport
(symport) of sodium

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27
Q

Ionotropic Glutamate Receptors

A
  • NMDA (GluN)
  • AMPA (GluA)
  • kainate (GluK)

non-selective cation channels
→ Na+, K+, and Ca2+

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28
Q

NMDA-R serves as

A

coincidence detector:

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29
Q

NMDA-R

voltage-dependent block by
Mg2+ ion

A

needs to be
relieved by depolarization,
→ requires simultaneous
activation of AMPA -Rs

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30
Q

NMDA-R

influx of Ca2+ acts as

A

second
messenger at intracellular
signaling pathways
→ relevant for synaptic
plasticity.

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31
Q

NMDA-Rs require __ as
co-agonist

A

glycine

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32
Q

APV

A

NMDA antagonist; blocks NMDA-R
so that only AMPA current remains

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33
Q

AMPA-R (or GluA) consists of

A

four homologous pore-forming subunits (GluA1–4), which mostly
assemble into heteromers.

assemblies

tetrameric
assemblies

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34
Q

“Normally”, AMPARs are
not permeable to

A

Ca++.

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35
Q

some AMPARs
either

A

lack GluA2
subunits (very low permeability to Ca2_), or have an
unedited transcript of
the GluA2 gene (blue)
→ permeable to Ca2+
(CP-AMPA)

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36
Q

mGluRs - metabotropic glutamate receptors

3 groups based on pharmacology and second messenger linkages:

A

Group I (mGluRs 1 and 5)
Group II (mGluRs 2 and 3)
Group III (mGluRs 4, 6, 7, and 8)

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37
Q

Group I (mGluRs 1 and 5)

A

excitatory, Gq-coupled
(→PLC → ion channels; increase NMDA)
- mostly postsynaptic

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38
Q

Group II (mGluRs 2 and 3)

A

inhibitory, Gi/Go- coupled
(→ reduce cAMP),
decrease transmitter release; decrease NMDA
- mostly presynaptic, and on glia cells

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39
Q

Group III (mGluRs 4, 6, 7, and 8)

A
  • inhibitory, Gi/Go- coupled
    (→ reduce cAMP), decrease transmitter release;
    decrease NMDA
  • mostly presynaptic
40
Q

PDZ domains have two main functions:

A

Anchoring receptor proteins to
cytoskeletal components, and regulating cellular pathways

PDZ domains bind to a short region of the
C-terminus of other specific proteins

41
Q

Some important PDZ proteins are

A
  • PSD-95
  • GRIP
  • Homer
  • Shank
42
Q

PDZ domain proteins and their associated receptors:

  • PSD-95
A

NMDAR

function as scaffolds at the
postsynaptic membrane

PSD-95 has three PDZ domains:
The first two PDZ domains interact with the C-terminus of
receptors (mostly NMDA) or with Shaker-type K+ channels.
The third PDZ domain interacts with cytoskeleton-related proteins

43
Q

PDZ domain proteins and their associated receptors:

GRIP

A

AMPAR

44
Q

PDZ domain proteins and their associated receptors:

Homer

A

regulates mGluR signaling.

45
Q

PDZ domain proteins and their associated receptors:

Shank

A

crosslinks NMDARs and mGluRs

46
Q

Glutamate receptors

A

rapidly go in and out of the membrane

move rapidly intracellularly

47
Q

Transmembrane-AMPAR Regulatory Protein (TARP)

A

auxiliary subunits of AMPARs that modulate expression, channel properties and localization of AMPARs.

4 different TARPs which show partly overlapping distributions
in the brain.

48
Q

Stargazin

A

Stargazin is dominant in cerebellum

prototypical TARP that acts as an auxiliary subunit that controls both receptor gating and trafficking.

In the membrane, stargazin interacts with PSD-95 to anchor the AMPARs

49
Q

Stargazin

A

Stargazin is dominant in cerebellum

prototypical TARP that acts as an auxiliary subunit that controls both receptor gating and trafficking.

In the membrane, stargazin interacts with PSD-95 to anchor the AMPARs

50
Q

Homer consists of two major splice variants:

A

The constitutive long-forms (Homer1b-h, Homer2a or b, and Homer3a or b) and
* the short-form (Homer1a)

51
Q

Long-form Homer proteins bind

A

the carboxyl terminus of group I mGluRs and IP3Rs, forming an
efficient signaling complex that generates IP3
and releases Ca2+ from intracellular pools.

Long forms are constitutive

52
Q

Homer1a is

A

nduced by neuronal activity

Homer1a competes with CC
-Homer (long forms) and disassembles the signaling
complex (“uncouples” mGluR signaling

53
Q

the short form of Homer is
considered to be a part of a mechanism of

A

homeostatic plasticity that dampens the neuronal responsiveness when input activity is too high.

54
Q

The long form Homer1c plays a role in

A

synaptic plasticity and the stabilization of synaptic changes during long-term potentiation.

55
Q

Shank is required for

A

proper endocytosis of mGluRs

56
Q

Synaptic inhibition

A

reduces the probability of firing an action potential

57
Q

A synaptic potential can be

A

depolarizing and yet be inhibitory.

58
Q

Depolarizing synaptic
potentials can inhibit neurons as long as

A

ECl- is more hyperpolarized (negative)
than the action potential threshold (C).

59
Q

GABAa or glycine receptors open chloride channels, which

A

results in inward flow of
negatively charged Cl- ions → hyperpolarization (B).

60
Q

In developing neurons the intracellular Cl- concentration is controlled by

A

the Na+/K+/Cl- co-transporter, yielding high intracellular levels of Cl-→ ECl- is often more positive than AP threshold (always depolarizing).

61
Q

In adult neurons the intracellular Cl- concentration is controlled
by

A

a K+/Cl- co-transporter pumps Cl- out of the cell, lowering
the internal Cl-, making ECl- much more negative → hyperpolarization.

62
Q

Ionotropic GABA receptors (GABAa
and GABAc) consists of

A
  • 5 subunits (heterodimeric)
  • Integral chloride (Cl-
    ) channel
63
Q

Ionotropic GABA receptors (GABAa
and GABAc) are found at

A

20%-50% of all
synapses in the brain

64
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
65
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
66
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
67
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
68
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
69
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
70
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
71
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
72
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
73
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
74
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
75
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
76
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
77
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
78
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
79
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
80
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
81
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
81
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
82
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
83
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
84
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
85
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
86
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
87
Q

Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
88
Q

Function of Metabotropic GABA receptors (GABAb)

A
  • stimulate opening of K+ channels.
  • *Opening of K+ channels inhibits/hyperpolarizes
    the cell by bringing the membrane potential closer to EK+
    `
  • inhibit Ca2+ channels (mostly presynaptic) → also leads to hyperpolarization, less NT release
89
Q

Activation of presynaptic GABAB
autoreceptors can

A

inhibit release of
GABA from the terminal.

90
Q

Presynaptic actions of GABAB

receptors

Under some conditions spillover can also occur onto

A

neighboring excitatory
synapses. There, GABAB
activation inhibits release of glutamate (left).

91
Q

presynaptic GABAb
receptors also inhibit

A

release of dopamine,
norepinephrine and serotonin

92
Q

Three types of Catecholamines

A

Dopamine
Noradrenaline
Adrenaline

93
Q

In the CNS, catecholamines act as

A

neuromodulators, influencing
the effects of other, classical neurotransmitters.

do not evoke EPSP or IPSP by themselves,
rather make EPSP / IPSP larger or smaller
→ alter ion channels to modulate cell’s excitability, so that when
synaptic inputs arrive the neuron is either more ready to fire
action potentials or hyperpolarized / less excitable

94
Q

Tyrosine hydroxylase

A

rate-limiting enzyme in synthesis of all
cathecholamines

Can be phosphorylated by at least 9 distinct
protein kinases (including PKA, CaMKII, PKC).

95
Q

Tyrosine hydroxylase is upregulated by

A
  • Stress
  • caffeine
  • nicotine
  • morphine

induce increases
in catecholamine
synthesis

96
Q

Tyrosine hydroxylase is downregulated by

A

antidepressants (chronic!)

Cellular Neuroscience (10 decks)

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