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Neuro > Consequences of neurotransmitter exocytosis > Flashcards

Consequences of neurotransmitter exocytosis Flashcards

1
Q

What dictates what effect a release neurotransmitter will have?

A

The type of receptor and the signalling pathway activated

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2
Q

What are the main types of receptors?

A

Fast acting inotropic (IR)

Slow acting metabotropic (MR)

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3
Q

Which inotropic receptors are structurally similar, describe their structure?

A

ACh, GABA and glycine

Pentamer of 4 different proteins (alpha, beta, gama, omega) each with 4 transmembrane domains, the C and N termini are extracellular

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4
Q

Describe the structure of glutamate inotropic receptors

A

Tetramers of 2 different proteins with 3 transmembrane domains (N terminus outside and C terminus inside cell)

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5
Q

Describe the structure of the ATP ionotropic receptor

A

Trimer, of one protein with 2 transmembrane domains

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6
Q

TRUE or FALSE?

Each NT will have a single receptor for itself

A

FALSE

It will have a family of receptors.

There are different forms of the component proteins of these receptors which can influence their properties

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7
Q

What properties can be affected by the differences in the structure of component proteins of receptors?

A

Regulation, sensitivity to drugs or toxins, etc.

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8
Q

How many subunits do metabotropic receptors have?

A

1

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9
Q

What is the structure of a metabotropic receptor?

A

1 subunit with 7 transmembrane domains

N terminus out C terminus in

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10
Q

Name NTs and their corresponding MRs

A

Glutamate - mGlut 1-7
Ach - Muscarinic M1-M5
GABA - GABAb
Dopamine - D1, D2

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11
Q

What is the inotropic receptor for GABA called?

A

GABAa

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12
Q

How do metabotropic receptors generally work?

A 
NT binds receptor
• Conformational change exposes Gs protein binding site
• Receptor and Gs protein complex bind
• GDP is displaced by GTP
• αs subunit dissociates from the βγ subunits
• αs subunit binds and activates adenylyl cyclase --> cAMP from ATP
• αs subunit hydrolyses GTP
• Returns to its original conformation
• Dissociates from cyclase – inactive
• Binds to the βγ subunits
• Gs protein complex binds to receptor
• Process cycles until the transmitter
is inactivated
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13
Q

What are certain effectors (enzymes) which help make second messangers with MRs?

A

Adenylate cyclase

Phospholipase C

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14
Q

Name some secondary messangers involved in MR signal transduction

A

cAMP

IP3/DAG

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15
Q

TRUE or FALSE?

All MRs are found all over the body and can do a broad range of things

A

FALSE

Receptors can be very specific as to where they can be found and what they do

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16
Q

What are the types of receptors for Ach and where are they found/what do they do?

A

Nicotinic: fast excitatory synaptic transmission especially in NMJ (activates ion channel)

Muscarinic: Both excitatory and inhibitory depending on tissue (slows heart, contraction of visceral smooth muscle) - uses G protein

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17
Q

What are the receptors for glutamate and what are their physiological roles?

A

AMPA: Fast excitatory synaptic transmission in CNS (inotropic)

Kainate: Inotropic receptor

NMDA: Slow excitatory transmission in the CNS (inotropic)

Metabotropic: Neuromodulation

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18
Q

What ions pass through nicotinic receptors?

A

Na+ and Ca2+ to enter the post synaptic neurone and some K+ goes out

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19
Q

Nicotinic receptors produce a ___ by ___.

A

Excitatory post synaptic potential, increasing the chances of depolarisation leading to the firing of an AP

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20
Q

What is the main inhibitory NT in higher brain regions?

A

GABA-A

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21
Q

Name another (not GABA) inhibitory NT

A

Glycine

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22
Q

Where is glycine found?

A

The brain stem and spinal cord

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23
Q

How are GABA-A and glycine receptors similar to nicotinic receptors?

A

Fast acting

Inotropic

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24
Q

How are GABA-A and glycine different from nicotinic receptors?

A

Allow Cl- into the cell
Induce inhibitory post synaptic potentials
Make the post synaptic terminal less likely to reach the threshold for AP to fire

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25
Q

How do inotropic receptors create specificity?

A

If too large they won’t go through

If they are the wrong charge the ions won’t go through

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26
Q

Which receptor is important for status epilepticus and HD?

A

NMDA

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27
Q

What are the inotropic receptors of glutamate?

A

Kainate, AMPA, NMDA

28
Q

How do the AMPA and Kainate IRs work?

A

When glutamate binds to them, they allow Na+ into the cell and K+ out

29
Q

Why is NMDA interesting?

A
  1. Permeable to Ca2+,K+ and NA+
  2. They need glycine cofactor to open
  3. Unique: Opening depends on membrane voltage as well as transmitter
30
Q

What is the role of Mg2+ in NMDA?

A

Mg2+ usually is bound tightly to the site in the pore of the channel, blocking the ionic current

31
Q

How does NMDA work?

A

Slight depolarisation (due maybe to AMPA opening) –> Mg2+ is expelled by electrostatic repulsion.

At the same time glycine binds to NMDA –> opens and allows Ca+,Na+ out and K+ in.

32
Q

What effect do the glutamate inotropic receptors have?

A

They make depolarisation more likely

Fast acting

Cause EPSPs

33
Q

TRUE or FALSE?

There is little variation in glutamate IRs

A

FALSE there are many different subunits which are alternatively spliced to give further variations

AMPA subuntis encoded by 4 genes - Glu A1-A4

KA receptor subunits encoded by 5 genes
GluK1-K5

NMDA encoded by 5 genes GluN1 and 4GluN2(A-D), [each NMDA has 2 GluN1 and 2 GluN2 subunits]

34
Q

What do most NMDA expressing neurones have and why?

A

AMPA receptors so that upon release of glutamine they will lead to depolarisation

35
Q

What happens if glutamine degradation is impaired?

A

Too much calcium enters the cell –> activating proteases, NOS, kinases , and free radicals –> damage mitochondria and cell –> decrease ATP –> cytotoxicity

36
Q

How do some people propose preventing excitotoxicity and in which diseases

A

NMDA-R antagonists:

HD
Ischaemia (stroke)
Status epilepticus

37
Q

Which amino acid residues can be phosphorylated?

A

Tyrosine and Lysine

38
Q

What is the effect of Ca2+ inside the cell?

A

It activates calmodulin dependent kinase II (CaMKII) which phosphorylates other proteins to activate them

39
Q

Why do synapses further from the soma have more receptors?

A

To give greater depolarisation to account for decrease in depolarisation as moves through the soma

40
Q

What are the differences between type 1 and 2 synapses?

A

Type 1 v. 2:

Excitatory v. inhibitory
Glutaminergic v. GABAnergic
SSV-round v.SSV-flattened
Cleft wider v cleft narrow
Active zone larger v. Smaller
Densities more prominent v less prominent
41
Q

Name 3 NTs that make a fast EPSP

A

Glutamate
Aspartate
Acethylcholine

42
Q

What does an increased number of excitatory synapses do to the post synaptic potential?

A

Even though presynaptic outputs are standard (although they can increase frequency), this can have an additive effect on the post synaptic potential and make it more likely for that neurone to fire an action potential

The reverse happens with IPSPs

43
Q

TRUE or FALSE

Summation can occur in any part of the NS not just the CNS

A

TRUE

44
Q

Is a single input sufficient to depolarise a neuron below its threshold?

A

No

45
Q

How is the axon hillock specialised to its role of deciding whether the AP should fire or not?

A

Has more VG Na+ channels

So more sensitive to milder depolarisation

46
Q

What 2 properties of a neuron influence summation?

A

Temporal summation - over what time inputs have an influence

Length constant - how much depolatisation lost in transfer to axon hillock due to e.g. leakage of ions across the plasma membrane

47
Q

What makes a neuron more likely to fire?

A

Longer temporal summation have longer length constants

Dendrites also have VG Na+, K+ , and Ca2+ VG channels so can influence depolarisation

48
Q

Describe feed forward inhibition

A

Where you want to stimulate the extensor muscle and relax the flexor:

Afferent neurons innervate both extensor and flexor motor neurons but the one that innervates the extensor synapses with an inhibitory interneuron which synapses with the flexor motor neuron, cancelling out the other afferent neuron

49
Q

Describe feedback inhibition

A

Stimulation of the extensor muscle will be self limiting:

Afferent neuron synapses with motor extensor neuron, but this motor neuron also synapses with an inhibitory interneuron which inhibits itself

50
Q

Why are metabotropic receptors described as modulatory?

A

They modulate the influence of any de/repolarisation in the neuron

There is no direct effect on ion movement, just changes in shape in response to a ligand which can cause changes (e.g. opening channels) in other parts of the cell

51
Q

What does activated PLC do?

A

IT makes IP3 and DAG from PIP2 which cause CA2+ release and protein kinase activation respectively –> Ca2+ regulates ion channels and enzymes (NOS, proteases), while PKC phosphorylated proteins do the same plus affect transcription

52
Q

What do cAMP do after being made by adenylyl cyclase?

A

Bind to PKA binding site–> release the catalytic subunit (no more inhibitory binding) –>Affect protein phosphorylation –> affects K+, Ca2+, inotropic receptor channels –> influences when AP fires

53
Q

What does the G protein gated K+ channel activated by the muscarinic acid receptor for Ach do?

A

Affects membrane potential

54
Q

Do different NTs have different G proteins?

A

Yes

55
Q

What is the role of Gs?

A

Activation of adenylyl cyclase

Activation of Ca2+ channels

56
Q

What do G0 and G1 do?

A

Inhibit Adenylyl cyclase
Inhibit Ca2+ channels
Activate K+ channels

57
Q

hat do G11 and Gq do?

A

Activate PLC

58
Q

What provides the huge amount of heterogeneity in MRs?

A

Different receptors

Different typesof G protein

Different G protein subunits

Different down stream differences

59
Q

Explain the convergent and divergent effects of NTs

A

Convergent: Each NT has many diff MRs with diff G protein specificities. So, one NT can activate many diff receptors

Divergent: An NT may activate a different receptor but lead to the same result down stream if (e.g. they share the same G protein)

60
Q

What are 3 ways (examples) of modulating PSPs with MR activation?

A
  1. Post synaptic - prolonged opening of inotropic receptor –> increase depolarisation
  2. Cell body-prolonged depolarisation (K channel is closed to stop repolarisation)
  3. Pre-synaptically - increase in the size and duration –> more NT release –> more depolarisation post synaptically
61
Q

What is the effect if a metabotropic receptor causes a K+ channel to stay open longer?

A

Hyperpolarisation –> Ca2+ channel decreases Ca2+ entry (decreased depolarisation) –> decreased NT release –> less likely to get an AP post synaptically

Reverse is true if it causes the K channel to close

62
Q

Explain the gill withdrawl mechanism of aplysia

A

Touching the siphon leads to gill withdrawl. This can be sensitised by the role of interneurons, increasing the effect on the motor neurons.

5HT –> activates MR1 –> Gs–> Ad cyclase activation, cAMP activaties PKA –> phosphorylates K+ channel which closes–> enhancing
depolarisation and NT release

5HT also activates MR2 linked to PLC activation–>DAG –> PKC activation
enhances the exocytosis machinery increasing NT release. (Process lasts several mins)

Now sensitised to touch of the siphon which generates AP in main terminal –> Increased depolarisation in post synaptic neuron –> firing –> stimulate movement away

63
Q

What happens if you keep poking at aplysia’s siphon?

A

Repetitive touching leads to the adaptive response of habituation

Influence on transcription factors–>
sensitisation: increases synapses/receptors

Habituation:

  • decreases SSV, NT repease
  • decreases nr. of synapses

All this leads to a slower response

64
Q

What are 3 drugs which directly activate the post-synaptic Dopamine receptors (for PD)?

A

Bromocriptine
Pramiexole
Ropinirole

65
Q

What treamtent mimicks PD?

A

Haloperidol (DA antagonist-antipsychotic)

Neuro (23 decks)

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