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Neuroscience > Lecture 4 - Post synaptic events in synaptic transmission > Flashcards

Lecture 4 - Post synaptic events in synaptic transmission Flashcards

1
Q

What are the two types of receptor that neurotransmitter released by the pre syaptic nerve terminal can interact with?

A
  • ionotropic/ligand gated ion channels

- metabotropic/G-protein coupled receptors

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2
Q

What are the features of ionotropic and metabotropic receptors?

A 
Ionotropic
-fast
-mediate changes in membrane protential
Metabotropic 
-slow
-can influence channel activity via second messengers (e.g. Ca2+, IP1, cAMP)
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3
Q

What did Nigel Unwin elucidate?

A

The first neurotransmitter receptor structure using cryo-EM

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4
Q

What does EPSP and IPSP stand for?

A

EPSP: excitatory post synaptic potential
IPSP: inhibitory “”””””””””””””””””””””””””””””””

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5
Q

What channel mediates depolarisation in the post synaptic nerve? (creates an EPSP)

A

Influx of sodium ions through a sodium channel

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6
Q

What channel mediates hyperpolarisation in the post synaptic nerve? (creates an IPSP)?

A

Influx of chloride ions through a chloride channel

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7
Q

What are the two different types of receptor in the post synaptic nerve terminal?

A

Ligand-gated ion channel (Ionotropic)

G protein coupled receptors (Metabotropic)

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8
Q

How does neurotransmitter release mediate the function of Ionotropic receptors in the post synaptic nerve terminal?

A

Neurotransmitter binds to extra polypeptides on the outside of the cell causing a conformational change in the channel causing it to open
-ions diffuse in along concentration gradient

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9
Q

How does neurotransmitter release mediate the function of Metabotropic receptors in the post synaptic nerve terminal?

A
  • when the neurotransmitter binds to the receptor on the membrane it causes a conformational change leading to the activation of a protein complex coupled to the receptor in the intracellular side of the membrane (G-Protein)
  • G protein unit bound to GTP moves along the intracellular membrane and can activate other intracellular signalling pathways e.g. the indirect opening of other ion channels to regulate the action potential (slow)
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10
Q

Where are Neurotransmitter receptors located and why?

A
  • post synaptic membrane to generate an action potential

- presynaptic membrane to modulate neurotransmitter release

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11
Q

How did Nigel Unwin elucidate the Acetycholine receptor?

A

As membrane protein cannot easily be crystallised (need lipids surrounding)

  • found tissue with a lot of Acetylcholine receptors (torpedo ray) snd imaged the tissue by electron microscopy
  • as there were lots of receptors on the membrane he could average their structure and activity
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12
Q

What is the structure of the acetylcholine receptor?

A 
5 subunits:
-2α (ligand binding site)
-β
-γ
-δ
4 transmembrane spanning domains
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13
Q

What is the function of the acetylcholine receptor at the skeletal muscle neuromuscular junction?

A

mediates muscle contraction

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14
Q

What is the function of the acetylcholine receptor in the CNS?

A

important in the prefrontal cortex in regulating transmission

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15
Q

What is the process of acetylcholine binding to its receptor?

A
  • ACh molecules bind to the α subunits causing the receptor to undergo a conformational change
  • the channel opens to allow cations to pass through (i.e. Na+/K+) due to the large pore size
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16
Q

What are the ionotropic and metabotropic receptors for ACh?

A

Ionotropic
-nicotinic acetycholine receptor (nAChR)
Metabotropic
-muscarinic acetycholine receptor

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17
Q

What are the Ionotropic glutamate receptors divided into?

A
  • non NMDA receptors, AMPA & kainate

- NMDA receptor

18
Q

What are the agonists for the AMPA receptor & the kainate ionotropic glutamate receptor, and what do they gate?

A 
AMPA receptor: 
Alpha-amino-3-hydroxy-5-methyl-4-isoxazole Propionic Acid
(AMPA)
Kainate receptor:
Kianic acid

Gate Na+/K+

19
Q

How do the non-NMDA ionotropic glutamate receptors cause a fast EPSP?

A

via an increase in conductance to monovalent cations (Na+ and K+)1

20
Q

What is the agonist for the NMDA receptor and what does ti gate/dependent on?

A

agonist:
NMDA (N-Methyl-D-Aspartate)

Ca2+ dependent, preference for gating Ca2+ (can act as a second messenger) but can gate other ions

21
Q

When does the NMDA ionotropic glutamate receptor open?

A

in the presence of glutamate

-during depolarisation of the postsynaptic neuron

22
Q

What are the kinetics of the NMDA and AMPA dependent EPSCs, and how have these been observed?

A

When glutamate is added
-EPSC spike and decay very fast up to around 50pA
(due to the very quick opening and closing of the AMPA receptor)
-EPSC increase and decrease (to around 25pA) very slowly
(due to the slow opening and closing of NMDA receptor, slow decay potentially also to do with signalling events e.g. activated by calcium influx)

Observe
Can observe the AMPA mediated ESPC without the NMDA mediated EPSC when in the presence of NMDAR agonists
And the same for NMDA receptors

23
Q

What is the structure of SPINEs and where are they found?

A
  • spine tail (connect to dendrite)

- spine head (containing the presynatpic density)

24
Q

What do SPINEs function as?

A

-post synapses, contain AMPA and NMDA receptors

25
Q

What is the postsynaptic density?

A
  • a region in the postsynaptic membrane of an excitatory synapse
  • forms a disc that consists of a range of proteins with different fucntions
  • some contact the cytoplasmic domains of ion channels in the post synaptic membrane
  • also includes receptors, proteins linked to the actin cytoskeleton, signalling machinery (protein kinases and phosphotases)
26
Q

How do SPINEs appear in an experimental rat’s enriched and un-enriched environmetn?

A

more spines on the dendrites in the Enriched rats environment

27
Q

How do spines appear different on patients suffering with early alzheimers?

A
  • less spines

- consequentially loss of synapses

28
Q

What are features of the GABA receptor?

A
  • found on the cell body
  • regulate excitation from the dendrites due to activation of glutamate receptors (inhibits)
  • GABA A = gates Cl- ions (ion channel part)
  • GABA B = G protein coupled receptor part
29
Q

What occurs without GABA inhibition?

A

neurons fire continuous action potentials under the influence of glutamate

30
Q

What are two examples of pathways that are mediated by Metabotropic glutamate receptor signalling?

A
  • Metbotropic glutamate receptor/phospholipase C pathway

- cAMP signalling

31
Q

What is the Metbotropic glutamate receptor/phospholipase C pathway?

A

-neurotransmitter glutamate binds to the mGluR (metabotropic glutamate receptor) inducing a conformational change that is transmitted to the G protein
-the alpha subunit of the G protein exchanges GDP to GTP and is released
-the G-protein coupled to the receptor activates the effector protein Phospholipase C
-Phospholipase C activates the second messengers Diacylglycerol and IP3
-Diacylglycerol activates protein kinase C
-IP3 acts to release Ca2+
=> leads to an increase in protein phosphorylation and the activation of calcium binding proteins e.g. calmodulin which can affect signalling activity

32
Q

What is the cAMP dependent pathway? (Signalling via the metabotropic receptor of glutatmate)

A
  • neurotransmitter gluatmate binds to the metabotropic glutamate receptor inducing a conformational change that is transmitted to the G protein
  • the alpha subunit of the G protein exchanges GDP to GTP and is released
  • activated alpha subunit binds and activates the enzyme adenyl cyclase which catalyses the conversion of ATP to cAMP
  • this can lead to the activation of protein kinase A enzyme (PKA) which phosphorylates a number of proteins including:
  • kreb which can then regulate gene expression
33
Q

What are three examples of post synaptic second messenger signalling?

A
  • diffusible retrograde signals secreted from the post synapse (NO, cannabinoids)
  • metabotropic receptor dependent activation of cAMP or Ip3 signalling
  • NMDA receptor-dependent activation of Ca2+ signalling
34
Q

What is the downstream endpoint of diffusible retrograde signals secreted from the post synapse (NO, cannabinoids)?

A
  • NO activates guanylate cyclase (cGMP signalling)

- Cannabanoids activate CB1 receptor (metabotropic GPCR) to regulate channel acitivty

35
Q

What is the downstream endpoint of metabotropic receptor dependent activation of cAMP or Ip3 signalling?

A
  • regulation of channel or receptor number or activity by phosphorylation
  • gene expression
36
Q

What is the downstream endpoint of NMDA receptor-dependent activation of Ca2+ signalling

A
  • activation of CaMKII (can bind calmodulin and be activated), regulates gene expression
  • linked to learning and memory
37
Q

What is the function of cannabiniods?

A
  • endogenously released from post synaptic nerve as a regulating mechanism
  • inhibit neurotransmitter release by reducing Ca2+ currents or opening K+ channels, reducing the excitability of the presynaptic membrane
  • acts on receptors for endogenous cannabinoids (anandamine)
38
Q

What experiment was done to show that WIN 55-212 supresses the current through a pre synaptic membrane?

A
  • controlled the current

- added WIN 55-212 and the more was added thr less current passed throuh the membrane

39
Q

What toxin inhibits blocks the effect of cannabinoids and how?

A

pTX toxin

inhibits G protein

40
Q

Through blocking the effects of cannabinoids e.g. WIN 55-212 what was discovered about their function?

A

G protein acts on the Ca2+ channel to block Ca2+ current so there is no influx of Ca2+

41
Q

How was PKA shown to be involved in the function of cannabinoids?

A

using an ATP ortholog that blocks the active site of PKA

Neuroscience (12 decks)

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