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Neuroscience > Neuronal Cell Signalling > Flashcards

Neuronal Cell Signalling Flashcards

1
Q

what happens when the voltage gated calcium channels are activated?

A
  • couples the action potential to the neurotransmitter
  • NT binds and opens ligand gated ion channels
  • mediate direct excitation or inhibition of postsynaptic cell
  • NT interacts with G protein coupled receptors
  • initiates intracellular signalling effects
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2
Q

what are GPCRs?

A
  • not ion channels

- regulates voltage gated and ligand gated ion channels

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3
Q

what are the functions of GPCRs?

A
  • Binds NTs, neuropeptides and hormones
  • they bind and activate heterotrimeric G proteins that they’re associated with
  • subunits initiate different events that lead to a change in the gating of ion channels
  • trigger excitation/inhibition
  • modulate excitability
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4
Q

what are GPCRs on the presynaptic membrane?

A
  • VGCCs - couple AP to NT release
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5
Q

what are GPCRs on the postsynaptic membrane?

A

ligand gated and voltage gated ion channels

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6
Q

how are signalling events triggered?

A

by GPCR coupled receptors and Ca2+

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7
Q

how does receptor activation cause a conformational change in GPCR regulated ion channels?

A
  • alpha unit exchanges GDP for GTP
  • alpha subunits interact with and influence activity of an effector protein
  • terminated by GTPase activity of alpha subunits
  • alpha subunit reunites with beta gamma subunits
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8
Q

what are G alpha effectors?

A

enzymes that generate second messengers

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9
Q

what is PkA/camK?

A

voltage and ligand gated channels, vesicle proteins, transcription factors

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10
Q

what do G beta gamma interact with?

A
  • directly interact with ion channels in the membane to alter the activity
  • G alpha and G beta gamma have different effectors/targets
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11
Q

how do we test for second messenger v G beta gamme mediated effects?

A
  • electrical isolation (in the patch pipette)
  • physical separation
  • can put compounds in the patch and won’t have access to the bathing medium
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12
Q

how is a NT in the bathing medium affecting an ion channel thats in a patch pipette?

A
  • NT interacting with a receptor (GPCR)
  • to initiate a signalling cascade
  • allows generation of a diffusible messenger
  • allowing Ca2+ channel to open for longer
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13
Q

how is PkA involved?

A
  • phosphorylates voltage gated calcium channels

- alters their opening

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14
Q

how can a cell attached patch test for second messenger vs G beta gamma mediated effects?

A

giga-ohm seal prevents movement of NT between extracellular medium and solution in pipette

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15
Q

what have cell attached patch recordings been used to show?

A
  1. intracellular inject of cAMP (elicits the same effects as NT)
  2. PkA phosphorylates the channel to increase open probability and open time
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16
Q

how to examine G beta gamma?

A
  • Detached membrane patch ‘inside out’
  • Patch pipette  pull pipette away and rupture the membrane
  • Inside of cell is facing the bathing medium
  • Have to use GTP to see any activity
  • Depolarising pulse  can see activity of K+ channels
  • Put acetylcholine in the pipette  interacts with a GPCR (Mescarinic Ach)
  • As you pull the membrane away from the cell you lose channel activity
     α subunit is using up the GTP  hydrolyses
     becomes GDP reassociates with β γ subunits
     can restore reactivity with GTP in the solution
  • Proves there is a membrane delimited regulation
  • Prove the importance of β γ by just using those subunits
17
Q

what are beta gamma subunits?

A
  • potassium channels (GIRKs)

- beta gamma can activate K+ channels and can inhibit Ca2+ channels

18
Q

what can cannabinoids activate?

A
  • activates K+ channel and inhibits
19
Q

what happens when K+ channels are activated?

A

less excitable, modulation

20
Q

how is there presynaptic inhibition?

A

decrease in NT release due to inhibition of VGCC and activation of K+ channels via Gi/o coupled receptors

21
Q

how is there presynaptic facilitation?

A
  • increase NT release due to activation of VGCC
22
Q

how can you modulate postsynaptic receptors?

A
  • changing the number of PS receptors
  • trafficking and gating
  • Ca2+ downstream of NMDA can activate CAM kinase II
  • CAM kinase II and PkC mediation phosphorylation of postsynaptic AMPA receptors
  • intracellular Ca2+ can increase in many ways
23
Q

what are the features of Ca2+ signalling??

A
  • regulated tightly
  • glutamate binds to a receptor causing depolarisation and an influx of Ca2+
  • IP3 interacts with receptors on ER and causes a release of Ca2+
24
Q

how can ER release Ca2+ in a controlled and effective manner?

A
  • also has a RyK receptor
  • activated by Ca2+
  • causes more Ca2+ release
25
Q

what happens when the intrallelar store is emptied?

A
  • calcium levels in the cell needs to go back down
  • pumped out using plasma membrane ATPase
  • exchanges Ca2+ for Na+ exchanger
  • refills calcium stores, pumps back into stores through another ATPase (SERCA)
26
Q

what happens when the neuron has a depletion of Ca2+?

A
  • calcium stores can send a depletion signal to the plasma membrane allows calcium back in
27
Q

what are some extracellular Ca2+ sources?

A
  • SOC (store operated channels)
  • LGC (NMDA receptor
  • VGCC (postsynaptic L type voltage gated Ca2+ channels)
28
Q

what are the intracellular Ca2+ release channels on the ER?

A
  • IP3 receptors

- Ryanodine receptors

29
Q

how do IP3 receptors work?

A
  • activated by increased IP3 levels via Gq-cuopled metabotropic glutamate receptors
30
Q

how do ryanodine receptors work?

A

activated by Ca2+ coming through NMDA receptor/VGCC causing Ca2+ increase –> induced Ca2+ release

31
Q

what is Ca2+ removed?

A
  • SERCA (sarcoplasmic endoplasmic reticulum Ca2+ ATPase, pumps Ca2+ back into the ER)
  • PMCA (pumps Ca2+ out of the cell)
  • NCX (Na+/Ca2+ exchanger)
32
Q

what is the cyclic nucleotide gated channels?

A

direct opening of ion channels by second messengers

33
Q

what do cGMP gated Na+ channels mediate?

A

changes in the activity of photoreceptor cells ‘ receptor potentials’

34
Q

what is cGMP?

A
  • gated by cyclic nucleotides eg cyclic AMP or cyclic GMP
  • a photoreceptor
  • change in membrane potential which causes a receptor potential
35
Q

what are the basics of a cGMP photoreceptor?

A
  • activation of GPCR (rodopsin)
  • activates a G protein (transducin)
  • activates effector molecule which decrease cGMP levels through a phosphodiesterase
36
Q

what are transient receptor potential cation channels?

A
  • TRP channels

- some TRP channels in sensory neurons are store operated channels, modulated by second messengers

37
Q

what are the functions of TRPs?

A 
olfaction
vision
touch
pain
- sense that the ER is empty
38
Q

how does an odorant interact with a TRP?

A
  • increase in IP3, intracellular Ca2+ increase
  • sends a signal (STM1 mediated) to plasma membrane
  • activates TRP channel to cause primary excitation of a sensory neuron

Neuroscience (11 decks)

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