Lecture 6- Synaptic Transmission Flashcards

(61 cards)

1
Q

How are signals sent between neurons

A

Neurotransmitter release

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2
Q

How are signals received within a neuron

A

Postsynaptic signalling machinery

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3
Q

What did Leowi first demonstrate in the 1920s and how

A

-Chemical transmission
-Fluid from a donor heart to recipient slowed down heart rate

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4
Q

Types of synapses

A

-Axodendritic
-Axosomatic
-Axoaxonic

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5
Q

What is the most common type of synapse

A

Axodendritic

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6
Q

Process of classical neurotransmitter synthesis

A

-Dietary precursors cross the BBB
-Enzymes in the axon terminals synthesise classical NTs and pack them into vesicles
-Classical NTs remain in vesicles, don’t readily cross membranes

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7
Q

Neuropeptide transmitters are synthesised where

A

In the cell body (nucleus)

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8
Q

Forms of classical neurotransmitters

A

-Amino acids
-Monoamines
-Acetylcholine

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9
Q

Forms of non classical NTs

A

-Lipids
-Neuropeptides
-Gases

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10
Q

Neuropeptide containing vesicles are transported where

A

Down the axon

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11
Q

NTs are transported into vesicles via

A

Proteins called vesicular transporters

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12
Q

Vesicular transporters are vital for

A

Determining neuronal phenotype

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13
Q

Process of action potential

A

-Voltage gated Ca2+ channels open
-Ca2+ influx
-Activation of CaM Kinase II
-Phosphorylation of proteins
-Proteins move vesicles to release site
-Fusion of vesicles and exocytosis

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14
Q

Vesicles fusion with the cell membrane is mediated by

A

-SNARE
-SNARE complexes form to pull membranes together
-Ca2+ binds to synaptotagmin, catalysing membrane fusion

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15
Q

Opening of a fusion pore is a target for

A

Various toxins

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16
Q

Effects of botulinum toxin

A

-Cleaves and prevents Fusion complex formation at NM junction
-Affects SNARE protein
-Does not release NTs

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17
Q

Do NTs target specific receptors

A

-No
-Significant spill over of NTs at many synapses, reaching receptors at other synapses
-Can activate not targeted synapses

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18
Q

In the cerebellum, spillover of NTs can

A

Give rise to slow rising EPSC

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19
Q

Regulation of NTs release

A

-Rate of AP
-Probability of transmitter release
-Autoreceptors

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20
Q

Somatodendritic does what

A

Regulates firing

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21
Q

LSD is an agonist at

A

5-HT1a AR, which can slow down rate of firing

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22
Q

Autoreceptors vs Postsynaptic receptors

A

-Autoreceptors are receptors on the same neuron that’s releasing NTs
-Autoreceptors modulate activity of cell depending on location

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23
Q

Transporters blockade increases

A

Transmission

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24
Q

Transporters suck up NTs into

A

Presynaptic terminal

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25
Enzymes in synaptic cleft and terminal rapidly
Degrade NTs
26
Are synaptic terminals reliable
-No -Only 10-20% of action potentials trigger release
27
Steps of fast synaptic transmission
-Synthesis, transport and storage -Depolarisation -Open voltage gated Ca2+ channel -Ca2+ influx, activate CaMKII and phosphorylate proteins -Movement and docking of vesicles -Exocytosis-diffusion -Interact with receptors
28
Nomenclature of terminal depends on
Type of transmitter released
29
Most receptors that are acted upon are embedded in
The cell membrane
30
Ionotropic receptors
-Ligand gated ion channels -Fast, allows ions to pass
31
Metabotropic receptors
-G protein coupled receptors -Slow use second messengers
32
Ligand gated channels (ionotropic receptors)
-Made of multiple subunits bound together -Ions flow down electrochemical gradient
33
What is the agonist and antagonists for acetylcholine receptor
-Agonist: nicotine -Antagonist: curare
34
GABA A receptor features
-When activated, opens so chlorine ions pass through -Agonist: GABA, alcohol, BDZ -Antagonists: Picrotoxin
35
G protein coupled receptors (GPCRs) (metabotropic receptors)
-Single proteins with several transmembrane domains -Indirectly influence cell activity -Receptor coupled to an intracellular effector -Over 90% are in the brain
36
Two ways to alter cellular functioning via G proteins
-G protein is coupled to a messenger system -Some are directly coupled to an ion channel
37
Second messengers activate
Protein kinases which in turn activates other second messengers via phosphorylation
38
How does cAMP work
-Gs activates and Gi inhibits adenylate cyclase -Converts ATP into cAMP -This activates proteins or remove phosphate groups
39
Drugs of abuse differentially activate
Kinases compared to non drugs of abuse
40
What is pERK
-ERK that has had a phosphate group added -High levels found in nucleus accumbens after addictive drugs
41
Second messengers can alter gene
Regulation or transcription (DNA to mRNA)
42
Features of glutamate
-Fast chemical signalling -Most important excitatory NT in the brain -All neurons have receptors for glutamate
43
Changes in glutamate signalling appear to be major mechanisms for
Learning and memory
44
vGLUTs package
Glutamate into vesicles
45
EAATs take up
Glutamate from the synaptic cleft
46
Glutamate receptors are both
-Ionotropic and metabotropic -Found pre and post synaptically
47
Receptors located on dendrites
-AMPA -NMDA
48
AMPA receptor features
-Fast excitatory transmission -Only has sodium pass through it -AMPA is the only agonist
49
NMDA receptor features
-Slow excitatory transmission -At rest -70 mV -Has a magnesium blockade -When magnesium is removed, neuron is depolarised at +40 -Calcium and sodium can flow -NMDA is the only agonist for the NMDA receptor
50
Strong stimulation induces waves of
Gene expression
51
Effected IEGs have
-Direct effects on synaptic function or intracellular signalling
52
Arc once induced becomes
-A protein -Stops the signalling of AMPA receptors through internalising them
53
What does MAP kinase phosphate do
Removes phosphate from pERK as a negative feedback function
54
Drugs of abuse can robustly induce
IEG expression
55
IEGs are a marker of what
Activity
56
If you have fos going up
You have arc going up, there is activity
57
True or false, psychomotor sensitisation is likely to occur with closely spaced psychostimulant injections
False
58
Amphetamines are still used legally today to test weight loss and narcolepsy
False
59
Classical neurotransmitters
-GABA -Glutamate -Dopamine
60
What do terminal auto receptors do
Regulate neurotransmitter release
61
Protein kinase activation can elicit
-Activation of transcription factors which results in mRNA expression -Alteration of cytoskeletal proteins and cellular morphology