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Neuro > Neurotransmission > Flashcards

Neurotransmission Flashcards

1
Q

What are most CNS synapses?

A

Chemical

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2
Q

Describe the main features of direct synapses

A

Direct continuity between the cytoplasm of the interconnected neurones

Gap junctions form the connections between cells

Upon depolarisation –> very rapid response

Can conduct a variety of ions between cells

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3
Q

Name the proteins that make up gap junctions and their subunits

A

Connexon channels are made of connexin proteins

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4
Q

What are electrical synapses useful for?

A

Fast actions

Orchestrating and synchronising actions of many neurones (small cells coordinate like a large one) - triggered explosively

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5
Q

What cells other than neurons use electrical synapses and how?

A

Astrocytes are connected to each other via gap junctions (intercellular)

Stimulate intracellular Ca2+ release –> wave of Ca2+ travels from astrocyte to astrocyte by diffusion

Successive layers made by wrapping schwann cell are connected by gap junctions (intracellular)

May help to hold the layers of myelin together and promote the passage of small metabolites and ions across the many layers of myelin

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6
Q

Name a disease relating to electrical synapses (and describe how it happens)

A

Charcot Marie Tooth disease is caused by a connexin 32 mutation which blocks gap junctions

Leading to a demyelination disorder of the peripheral nerves

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7
Q

Where on the neuron can chemical synapses occur and how does this affect the neuron?

A

The body, dendrites, axon, etc.

Where it is can influence different things: eg

Axon: Upregulate/inhibit neurotransmission

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8
Q

What are the 4 criteria for something to be a neurotransmitter?

A

It is stored and synthesized in an identifiable pathway in the neuron.

It is present in the presynaptic terminal and is released in amounts sufficient to exert a defined action on the postsynaptic neuron or effector organ when presynaptical stimulation occurs.

When administered exogenously in reasonable concentrations it mimics the action of the endogenous transmitter (for example, it activates the same ion channels or second-messenger pathway in the postsynaptic cell).

A specific mechanism usually exists for removing the substance from the synaptic cleft (reuptake/degradation).

Additional: Identify antagonist to prevent its actions - may be mimics

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9
Q

What is the post synaptic thickening?

A

Where all the molecules needed for the post synaptic cleft to receive the signal are

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10
Q

What are active zones?

A

Specialized areas that are thought to be docking and release sites for synaptic vesicles (NT release)

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11
Q

If APs arrive very frequently at the presynaptic membrane, what does the post-synaptic neuron need to do?

A

It needs to be able to receive the APs and recover in time for the arrival of more APs

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12
Q

What happens if neurotransmitter levels are not maintained fast enough?

A

Synaptic depression:

There is a fall off in communication with the post-synaptic neuron

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13
Q

Describe the general process that links the arrival of AP to neurotransmission

A
  1. AP arrives – depolarises terminal
  2. VG calcium channels at synapse active zone open
  3. Calcium enters the active zone
  4. Small synaptic vesicles (SSV) fuse with plasma membrane and releases NT into synaptic cleft
  5. Calcium removed from cytoplasm
  6. NT has an effect on adjacent cells
  7. NT removed from synaptic cleft (broken down or taken back up)
  8. SSV are recycled
  9. NT is packaged into SSV which dock in active zone
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14
Q

How are electrical and chemical synapses different?

A

Chemical:
Bigger distance between synaptic membranes

No cytoplasmic continuity

Has presynaptic vesicles, active zone, and post synaptic receptor, not gap-junction channels

Transmitted by chemical transmitter not ion current

Has synaptic delay (min 0.3 ms)

Has unidirectional transmition, unlike electrical

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15
Q

Name amino acid NT and their substrate

A

Glutamate - glutamine
Aspartate - oxaloacetate
GABA - glutamine
glycine - serine

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16
Q

Name some amine NT and their substrate

A

Dopamine, Adrenaline, Noradrenaline - tyrosine

Serotonin (5HT) - Tryptophan

Histamine - Histidine

ATP - ADP

Adenosine - ATP

Acetylcholine - Choline

Nitric oxide - Arginine

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17
Q

Name neuropeptide NTs

A

Substance P
Enkephalin
Vasopressin
Somatostatin

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18
Q

Describe glutamate synthesis all the way through neurotransmission and back into the neuron as glutamate

A

Synthesis:

a) 2 oxoglutarate +NAD –> glutamate (via glutamate dehydrogenase in mitochondria)
b) 80% made by glutamine –> glutamate +NH3 (via glutaminase in mitochondria)

Neurotransmission:

  1. Glutamate is packed into SSV via VGLUT (H+/glut antiporter)
  2. SSV is exocytosed and glutamate is release into synaptic cleft
  3. Glial cells take up glutamate via Na+/Glut symporter
  4. Glutamate +NH3 –> glutamine
  5. Glutamine is returned to the neuron (start cycle over)
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19
Q

What kind of NT is glutamate?

A

Excitatory

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20
Q

What can happen if glutamate releases is not tightly regulated?

A

Cell loss due to cytotoxicity:

Huntington’s disease
Motor neuron disease
Status epilepticus

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21
Q

Describe GABA synthesis all the way through neurotransmission and back into the neuron

A

Synthesis:
Glutamate –> GABA +CO2 (via GAD)

Neurotransmission:

  1. VGAT (GABA/H+ antiporter) into SSV
  2. Release into synapse
  3. Bind to GABAa receptor (opens Cl- channel
  4. GABA is taken up by the neuron directly or by a glial cell via GAT1/3
  5. In glial cell GABA is broken down to succinic semialdehyde (via GABA-T)
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22
Q

What disorders can be related to GABA

A

Increasing GABA concentration can be used to treat epilepsy

In HD, medium spiny neurones transplatation to make GABA in the striatum die

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23
Q

What kind of neurotransmitter is GABA?

A

Inhibitory

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24
Q

Where can GABA making inhibitory interneurons be found?

A

Spinal cord

Striatum

Cerebellum

Hippocampus

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25
Q

What methods of treating epilepsy?

A

GABA:

  1. Stop reuptake by blocking GAT1/3 - tiagabine
  2. Stimulate GABAa receptor - benzodiazepines, barbiturates
  3. Decrease GABA degradation by inhibiting GABA-T - vigabatrin
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26
Q

Describe Ach synthesis all the way through neurotransmission and back into the neuron

A

Synthesis:
1.Citrate from the TCA cycle –> oxaloacetate + acetyl coA (via citrate lyase)

2.Acetyl CoA + choline (either from diet or recycled) –> Ach (via choline acetyl transferase)

Neurotransmission:

  1. Ach enters SSV via VAChT (Ach/H+ antiporter)
  2. Released into synapse
  3. Ach –> choline +Acetate (via acetylcholinetransferase)
  4. Choline reenters neuron via CHT (choline/Na+ symporter)
27
Q

Where is Ach found?

A

CNS
NMJ
Autonomic nervous system

28
Q

What is Ach important for?

A

Arousal

Wakefulness

Sleep

Consciousness

29
Q

Describe Catecholamine synthesis

A
  1. L-tyrosine +O2 +NADPH + pteridine –> L-DOPA +NADP (via tyrosine hydroxylase)
  2. L-DOPA–>Dopamine +CO2 (via dopamine decarboxylase)
  3. Dopamine enters SSV via VMAT (H+/Dopamine) antiporter
  4. Dopamine +H2O –> Noradrenaline (via Dopamine B-Hydroxylase)
  5. Noradrenaline pumped put of SSV via H+ antiporter
  6. Noradrenaline –> Adrenaline (via Phenylethanolamine N-methyl trasnferase)
  7. Adrenaline pumped back into SSV via H+ antiporter
30
Q

How is tyrosine hydroxylase activated?

A

Increased transcription and phosphorylation

31
Q

Where is Dopamine B Hydroxylase found?

A

In the SSV membrane

32
Q

What are the methods of treating Parkinson’s?

A
  1. L-DOPA (Increases dopamine)
  2. Inhibit MAO and COMT (decrease dopamine degradation) - Selegiline and Entacapone respectively
  3. Agonist of most-synaptic dopamine receptors
33
Q

How is dopamine broken down?

A

a) Dopamine –> DOPAC (by MAO)–> homovanilic acid (by COMT)

b) Dopamine–> 3-MT (by COMT)–> homovanilic acid (by MAO)

34
Q

How and why is L-DOPA used to treat Parkinson’s?

A

L-DOPA allows us to bypass the rate limiting step in dopamine production and is actively taken up through the BBB

It is taken with Carbidopa since DOPA decarboxylase exists on both sides of the BBB

35
Q

What does Carbidopa do?

A

Inhibit DOPA decarboxylase and thus increases L-DOPA bioavailability

36
Q

Which of the following can pass through the BBB easily? Carbidopa, L-DOPA, Dopamine

A

L-DOPA only

37
Q

Describe neuropeptide synthesis and neurotransmission

A
  1. Neuropeptides are translated and packaged by trans-golgi complex into LDCV
  2. LDCV transpoted via anterograde axonal transport
  3. Rapid firing globally increases Ca2+ in cell
  4. Ca2+ binds to high affinity Ca2+ receptor on LDCV
  5. Exocytosis
  6. Neuropeptide–> AA (via protease in synaptic cleft)
38
Q

How are neuropeptides special?

A

Made in cell body

> 50 neuractive peptides

Packed into LDCVs:

  • Not localised in synaptic active zone
  • Exocytosis needs global [Ca2+] increase
  • LDCVs aren’t recycled
  • Slower than SSV
39
Q

What do neuropeptides do?

A

Cause inhibition, activation or both

40
Q

Describe NO synthesis and its downstream effects

A
  1. Depolarisation causes Ca2+ to enter the cell via NMDA-R
  2. Ca2+ binds to calmodulin
  3. NOS is activated (Arginine –> citrulline +NO)
  4. NO diffuses out through membrane
  5. Some binds to Hb, some binds to guanylyl cyclase in the post-synaptic neuron
  6. GTP–>cGMP
  7. Downstream effect
41
Q

What part of guanylyl cyclase does NO bind?

A

Haem

42
Q

Describe the properties of NO as a neurotransmitter

A

Free radical (half-life of seconds, reacts with O2 to make NO2)

Found throughout CNS but only in select neurones

43
Q

What does NO regulate?

A

Protein kinases, channels, etc.

44
Q

What is the first evidence that a particular neuron may use a certain NT?

A

Presence of the biosynthetic machinery

45
Q

Why is the presence of biosynthetic machinery not enough to tell us a neurone uses a specific NT?

A

Glutamate found in both excitatory and inhibitory neurones even though it’s only made by excitatory ones

46
Q

How do you definitively show that a neurone uses a NT?

A

Show that the NT is localised to vesicles and released upon depolarisation

47
Q

What do MDMA and amphetamines do?

A

They interfere with catechopamine and VMAT2 SSV packaging

48
Q

What does VMAT2 package?

A

Dopamine

49
Q

Explain how exocytosis works with SSV upon arrival of action potentials

A
  1. Upon the depolarisation as the AP arrives at the synapse the VG Ca2+ channels open
  2. Calcium enters the terminal creating a very high local increase in [Ca2+]
  3. Within hundreds of msec NT has been released into the synaptic cleft
  4. The terminal has already begun to repolarise, Calcium is quickly buffered by:
    - Mitochondria
    - Calcium binding proteins
50
Q

What is very abundant in the active zone membrane?

A

VG Ca2+ channels

51
Q

How to LDCV release their contents?

A
  1. Cytosolic [Ca2+] to increase following prolonged neuronal activity
    where [Ca2+] increases slightly throughout the terminal due to saturation of Ca2+ buffering
  2. High affinity receptor initiates fusion of LDCV
52
Q

Where are many SSV found in the neuron?

A

In the active zone where they are ‘docked’

53
Q

There are reserve vesicles in addition to those which are ‘docked’ at the membrane. TRUE or FALSE?

A

TRUE

54
Q

What are the 3 mechanisms to retrieve vesicles after fusion?

A
  1. Reversible fusion pore: vesicle does not collapse and NT is released through a fusion pore
    a) ‘Kiss and stay’: vesicle fuses with the PM, releases its contents, but reseals and awaits the next release event
    b) ‘Kiss and run’, where after fusion the vesicle reseals and leaves the active zone to be ready to dock again
  2. Clathrin mediated: after fusion clathrin is used to retrieve the vesicle membrane and is
    recycled through the endosome
  3. Bulk retrieval after prolonged sustained stimulation vesicle membranes re recovered
55
Q

Are there many proteins associated with the SSV?

A

Yes

56
Q

Name some proteins on the SSV and their actions

A

Synapsins: bind the SSV to actin

v- SNARES: snares on the vesicle membrane
-e.g. synaptobrevin (VAMP)

t-SNARES: snares on the target membrane (plasma membrane here)
-e.g.SNAP-25, syntaxin

Munc18: needed for v and t SNARE fusion

Synaptotagmin: calcium sensor that allows the phospholipids of the 2 membranes to fuse

57
Q

Describe how fusion of the SSV and plasma membrane occurs

A
  1. Ca2+ increases synapsins are phosphorylated
  2. Release the SSV
  3. Allows the reserve SSV pool to be mobilised
  4. Upon activation the v and t SNARES form a tight complex and zip together via Munc18
  5. Ca2+ also activates synaptotagmin
  6. Makes PM fuse w SSV
58
Q

Why are SNARE proteins required?

A

Because fusion of the membranes is not energetically favourable

59
Q

Where are the majority of the NT in the synaptic cleft taken to?

A

Adjacent glial cells or the presynaptic terminal

60
Q

What do NT use to re enter cells after being in the synaptic cleft

A

Specific symporters that utilise Na+ moving down its gradient

Eg.
Dopamine-DAT  	
Noradrenaline-NET 	
Serotonin (5HT)-SERT 	
Glutamate-GLT 
GABA-GAT1/3
61
Q

What does MDMA do?

A

Inhibits SERT and DAT

62
Q

What disease were Ach-esterase inhibitors used for?

A

Alzheimers but it had a limited effect

63
Q

Why did MPTP cause so much damage to dopaminergic neuones?

A

Because it is so similar to dopamine that is is actively taken up by the dopamine transporter in dopaminergic neurons

64
Q

Which part of the synapse develops first?

A

The presynaptic part

Neuro (23 decks)

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