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fundamental neuroscience > Neuronal intracellular signalling > Flashcards

Neuronal intracellular signalling Flashcards

1
Q

What changes are induced by learning in a neuronal aspect?

A
  • Signalling
  • Gene expression
  • Morphology
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2
Q

What is the gill withdrawal reflex in Aplysia Californica?

(4 marks)

A
  • Poke siphon of Ac - perceives a threat and retracts gills
  • Siphon has sensory synapses
  • Sensory neuron project inot abdominal ganglia and synapse w/ motor neuron stimulating to retract gill
  • Modulated by interneurons that synapse onto sensory and motor neurons
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3
Q

What is habituation?

A

Way in which animals learn to respond to non-harmless stimuli

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4
Q

How can you view an example of habituation in Ac?

(4 marks)

A
  • In habituation, repeatedly poke gill and observe action potential in neuron
  • But from measuring motor neuron can see decrease in EPSPs and reduction in gill withdrawal
  • Animal senses no threat
  • Can be short term or long term
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5
Q

What is facilitation?

A
  • Sensory neuron able to adjust how it fires, increased strength at post synaptic potential to a stimulus if closely paired with prior stimulus
  • Can get long and short term facilitation
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6
Q

How can you cause facilitation in Ac?

(4 marks)

A
  • Coupling tactile stimulus with a shock
  • Animal receives noxious stimulus (shock) with light touch of siphon
  • After this coupling you still have same AP in sensory neuron
  • Motor neuron is now elevated - EPSPs - as withdrawal of gill involved
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7
Q

What is dishabituation?

A

Overcoming habituated response

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8
Q

What is forward genetic screening?

(4 marks)

A

Identifying genes that regulate a specific phenotype

Define phenotype⇒Generate mutant animals⇒Screen for modifiers of phenotype⇒identify gene

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9
Q

What types of mutants can forward screening identify?

(3 marks)

A
  1. Mutants that are unable to process stimuli/ perform output response e.g. defective sensory organs
  2. Disrupted developmental of CNS e.g. disrupted neuroanatomy - no MN
  3. Conditioning mutants: disruption of biochemical and physiological mechanisms e.g. unable to process memory
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10
Q

How deos olfactory learning work in drosophila?

(4 marks)

A

Teach flies that one smell is safer than the other

Olfactory learning ⇒ Feeding flies mutagen EMS ⇒ Aversive olfactory learnign paradigm, learn to avoid behaviour ⇒ Complementation of genetic mapping

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11
Q

What is the olfatory learning paradigm experiment?

(6 marks)

A
  • Flies will always climb to rest at top of tube
  • Move tube of flies to odour A that’s coupled with electric shock, then to B with NO electric shock
  • In tube A don’t move up as much because of shock compared to movement in tube B
  • Flies learn to avoid ‘shock smell’
  • Final two tubes - switch shock around
  • Flies ignore A but are fine with B but end up getting shocked
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12
Q

How did they examine what genes were involved in the olfactory learning paradigm experiment?

(3 marks)

A
  • After conditioning, fed flies with mutant
  • Found abundance of genes essential for learning
  • Mutant fles unable of rembering electric shock
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13
Q

What are the memory genes identified by drosophila?

(4 marks)

A
  • Dunce:
    • cAMP phosphodiesterase. Mutation here results in elevated cAMP
  • Rutabaga:
    • Calcium/ calmodulin activated adenyl cyclase mutation
    • Causes slight decrease in cAMP levels

Graph shows how little flies remained in the start tube with dunce mutation - shows important for memory

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14
Q

What processes does the cAMP signalling pathway drive?

A

Habituation and sensitisation

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15
Q

What is heterosynaptic processing?

A

How a synapse can modify activity of neuron

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16
Q

‘Facilitating interneurons release serotonin 5-HT’ - how does this control the first pathway in short term sensitization signalling cascade?

(6 marks)

A
  1. 5-HT released onto synaptic terminal of sensory neuron and activates serotonergic GCPR
  2. This then activates the GCPR that activates Rutabaga which will trigger production of cAMP
  3. Elevation of cAMP activates PKA
  4. PKA then phsohprylates K+ channels at pre-synaptic terminal which leads to influx Ca2+ at pre-synaptic terminal which induces release of neurotransmitters
  5. Facilitating interneurons modify its response by elevating amount of Ca2+ in pre-synaptic terminal
  6. When AP arrives in sensory neuron its ready to fire glutamate into motor neuron - therefore increasing activity at presynaptic terminal
17
Q

How do facilitatin interneurons control the second pathway through the release of PLC?

A
  1. Releasing PLC metabolises PIP2 to produce DAG
  2. Increase in DAG cause activation of PKC - able to locate pre-synaptic terminal
  3. Can target range of proteins which allow reserved neurotransmitter vesicles to mobilise to pre-synaptic terminal
  4. Therefore increasing activity at presynaptic terminal
18
Q

What are the 2 routes used to increase activity at the pre-synaptic terminal?

A
  • Increasing Ca2+ at pre-synaptic terminal
  • Increasing neurotransmitters at presynaptic terminal
19
Q

How does long term sensitisation occur after after 5-HT activtes G coupled 5HT receptors?

(6 marks)

A
  • Increases production of cAMP
  • Elevated activity of PKA causing:
    • PKA translocates to nucleus and targets CREB 1
    • PKA phosphorylates CREB-1 activating its transcription activity
    • In parallel to increasing PKA also targets and activates MAPK in phosphorylation
    • Allows MAPK to phosphorylate CREB-2
20
Q

How is a serotonergic neuron able to activate transcription in another neuron with the help of CREB1?

(8 marks)

A
  1. CREB1 activated and binds to CRE elements
  2. Causes recruitment of CBP acetylase
  3. CBP acetylase able to acetylate histones opens them up and makes them more accesible
  4. Gene more accessible, can then recruit trancription machinery: Pol II and TATA binding protein - turns on genes transcription
  5. Serotonergic neruon able to activate transcription in another neuron
  6. Genes transcribed are ones for formation of synapses and others for acting transcription factors
  7. Gene produced from CREB transcription = ubiquitin hydrolase - degrades ~25% PKA regulatory subunits
  8. Removing these units means increase amount of PKA activity going back to nucleus and regulating process
21
Q

What procedure was carried out to find that newly synthesised proteins were only incorporated in ACTIVE synapses?

(3 marks)

A

Pair of motor neurons and single sensory neurons dissected from Aplysia

Synapse with Motor Neuron A: Five pulse of 5-HT used to initiate long-term facilitation

Synapse with Motor Neuron B: Single pulse of 5-HT used to capture proteins generate by long-term facilitation

  • after A was given 5 shocks after 24hrs, found that if you gave 1 shock to B that BOTH cells had a sensitised response
22
Q

What molecular component is essential to get long term facilitation?

(3 marks)

A
  • Protein kinase - if you put PKA inhbitor and protein synthesis inhibtor will no longer get long term facilitation
  • mRNA found in presynaptic terminal so if block with protein synthesis inhibtor will STOP production of protein
  • Needed: 5-HT, active PKA, active protein synthesis
23
Q

How are genes promoting long term facilitation regulated at both a transciptional and translation level?

(9 marks)

A
  1. Activation of serotonergic receptors causes activation of PKA and MAPK - translocate to SN nucleus and activate CREB1
  2. 5x 5-HT simulation of initiating synapse induces CRE mediated gene expression
  3. mRNA is transported throughout the sensory neuron, to all presynaptic terminal (carrying CRE motif)
  4. Activation of PKA and PI3K by 1x 5-HT
  5. PI3K initiates translation in marked synapses by making CPED undergo conformational change enhancing ability to bind CPE motifs on RNA
  6. Prion-like causes aggregation confirmation CPEB to template monomeric CPRE, causing further accumulation
  7. CPEB bind CPE motifs on mRNA, facilitating poly-adenylation of mRNA transcripts
  8. Poly-adenylated mRNA undergoes local translation in marked synapses
  9. Proteins produced include:
  • CPEB – feedback loop leading to further aggregation of CPEB and increased synapse formation
  • Structural proteins required for synapse formation

fundamental neuroscience (19 decks)

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