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Year 2 NSB > Synaptic Plasticity > Flashcards

Synaptic Plasticity Flashcards

1
Q

What is synaptic plasticity?

A
  • ability of the brain to re-organise and/or create new neural pathways
  • new neural pathways are adaptations to what the brains needs
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2
Q

The images labelled 1-4 in the image below is a good way to visualise synaptic plasticity, why?

A
  • image 1 - current neuronal pathways
  • image 2 - a potential new neuronal path has developed
  • image 3 and 4 - more and more use of the new path are used and the new pathway becomes embedded
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3
Q

Trauma can lead to adaptive synaptic plasticity and result in changes in synaptic connectivity. What will this then go on to affect?

  1. behaviour
  2. emotions
  3. sensory
  4. co-ordination
A
  1. behaviour
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4
Q

What is Hebbs rule? (think hypertrophy and atrophy)

A
  • if you don’t use it you will lose it
  • synapses not used can be removed as not needed
  • persistence/repetition is required to induce lasting cellular changes and add to its stability
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5
Q

What is Hebbs cell assembly hypothesis?

A
  • cells are reciprocally interconnected
  • activation of the interconnected cell for long enough would provide consolidation
  • these activated reciprocal connections will be more effective and neurons that fire together are wired together
  • future activations requires only a small activation, but still capable of causing the whole cell to become active
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6
Q

What are the 2 key rules of synaptic modification, that also rhyme?

A

1 - neurons that fire together are wired together

2 - neurons that fire out of sync lose their link

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7
Q

When we consider Hebbs rule, do synaptic modifications always get stronger?

A
  • no they can become weaker if not used
  • neurons that fire out of sync lose their link
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8
Q

When we look at rules of synaptic modification, are all individual stimulations sufficient to create an excitatory post synaptic potential?

A
  • sometimes, but sometimes insufficient
  • synaptic integration MUST be positive and larger than threshold
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9
Q

When we look at rules of synaptic modification, if the signal to cell A and cell B fire in isolation or together what could be the possible outcomes, in relation to excitatory post synaptic potential (EPSP)?

A
  • A alone - may or may not provide EPSP
  • B alone - may or may not provide EPSP
  • A+B together - more likely to cause EPSP than A or B alone
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10
Q

When we look at rules of synaptic modification, if the signal to cell A and cell B fire together repeatably these synapse will be strengthened, what can this cause to cells A and B firing in isolation or together, in relation to excitatory post synaptic potential (EPSP)?

A
  • A alone = may cause EPSP in A and B
  • B alone = may cause EPSP in A and B
  • essentially the strength of A+B together has trained A and B so that if either is excited they can activate the other (neurons that fire together are wired together)
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11
Q

What is the connectome?

A
  • complete description of the structural connectivity (the physical wiring, i.e. nerves) of an organism’s nervous system.
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12
Q

Long term potentiation (LTP) (think long term weight training for synapses) is one of the key mechanisms underlying synaptic strengthening. What is LTP?

A
  • a process involving persistent high frequency stimulation that strengthens synapses
  • persistent strengthening leads to a long-lasting increase in signal transmission between neurons
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13
Q

Synaptic plasticity and long term potentiation have been heavily linked with what 2 processes that make us human and allow us to develop that are inherently linked. The 2 key parts of the brain involved are the hippocampus and cerebral cortex. What are these 2 processes?

  1. emotion and learning
  2. memory and pain
  3. memory and addiction
  4. memory and learning
A
  1. memory and learning
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14
Q

Synaptic plasticity and long term potentiation have been heavily linked with learning and memory. How can long term changes be measured in humans that can confirm plasticity?

  1. increased IQ
  2. better memory
  3. modified gene expression and peptide turnover
  4. modified expression of EMG
A
  1. modified gene expression and peptide turnover
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15
Q

What is a tetanic stimulus?

  1. low frequency sequence of individual stimulation of a neuron
  2. low frequency sequence stimulation of multiple neurons
  3. high frequency stimulation of a neuron
  4. high frequency sequence stimulation of multiple neurons
A
  1. high frequency stimulation of a neuron
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16
Q

A tetanic stimulus is a high-frequency stimulation (HFS) of an individual neuron. How long can one and multiple HFS last for?

  1. one = seconds to minutes, multiple = minutes to hours
  2. one = hours, multiple = days
  3. one = days, multiple = days to months
  4. one = weeks, multiple = months to years
A
  1. one = days, multiple = days to months
17
Q

In an inactive cell, what is the activation pathway of the ionotropic ligand gated glutamate receptors AMPA and NMDA?

A

Inactive cell (resting membrane potential)

  • glutamate binds to AMPA receptor, creating an excitatory postsynaptic potential (EPSP)
  • NMDA receptor remains blocked by Mg2+ ion
18
Q

Once the ionotropic ligand gated AMPA receptor has caused depolarisation through binding with glutamate, what is the activation pathway of the glutamate receptor NMDA?

A
  • AMPA receptor activated by glutamate causing depolarisation
  • glutamate and glycine bind to NMDA receptor
  • Mg2+ blockage of NMDA is removed
  • Na+ passes through AMPA and NMDA channels causing depolarisation
  • Ca2+ passes through NMDA receptor causing depolarisation
19
Q

What is a key cation that is involved in the glutamate pathway, that is able to pass through NMDA receptors in the ‘wind up’ phase following continued and strengthening of glutamate binding with AMPA receptors that ultimately will remove the Mg2+ blockage on the NMDA receptor has been suggested to be involved in learning and memory?

  1. Na+
  2. K+
  3. Mg+
  4. Ca2+
A

4 . Ca2+

20
Q

Once Ca2+ enters the cell through the NMDA receptor during ‘wind up’ (neuronal responses to repetitive electrical stimulation), what are the 2 key secondary messengers that become activated in the glutamate pathway? (think Gaq GPCR)

A
  1. protein kinase C
  2. calcium calmodulin-dependent protein kinase II (CaMKII)
21
Q

Once Ca2+ enters the cell through the NMDA receptor during ‘wind up’ (neuronal responses to repetitive electrical stimulation), the Gaq intracellular pathway begins with increased levels of secondary messengers protein kinase C (PKc) and Calcium calmodulin-dependent protein kinase II (CaMKII). These 2 key secondary messengers PKc and CaMKII are then able to perform 2 key functions in relation to AMPA receptors, what are these?

Note:

  • kinases remove phosphate from high energy yielding molecule and add phosphate to another molecule and is called phosphorylation (on/off switch for intracellular proteins)
A

1 - phosphorylates existing AMPA receptors, increasing effectiveness

2 - stimulates insertion of new AMPA receptors into the membrane

INCREASED AMPA RECEPTOR EFFICACY AND NUMBER OF AMPA RECEPTORS CAUSES FURTHER EXCITATORY POST SYNAPTIC POTENTIAL

22
Q

What does autocatalytic activity mean?

A
  • a molecule that once it becomes activated becomes free from Ca2+ and can continue phosphorylation alone
23
Q

Calcium calmodulin-dependent protein kinase II (CaMKII) has autocatalytic activity, which means that once it has been phosphorylated by Ca2+ it becomes constitutively active (no longer needs Ca2+). What 2 things can this do to glutamate AMPA receptors and excitability of neurons?

A

1 - maintain phosphorylation of AMPA receptors even after depolarisation has ended

2 - molecular switch that is able to maintain excitability of neurons for minutes or hours, essentially a form of long term potentiation

24
Q

What does molecular switch mean?

  1. ability of a molecule able to turn other molecules on or off
  2. a molecules that shares similarity to another molecule
  3. molecule that can be reversibly shifted between two or more stable states
  4. molecule that cannot be turned off once activated
A
  1. molecule that can be reversibly shifted between two or more stable states
    • Calcium calmodulin-dependent protein kinase II (CaMKII) is inactive, but once Ca2+ causes CaMKII to become phosphorylated it is switched on regardless of Ca2+
  • demonstration of how CaMKII can switch between 2 stable states
25
Q

Long term potentiation (LTP) can be categorised into 2 categories that are associated with memory, what are they?

  1. acute and chronic LTP
  2. early and late phase LTP
  3. cytotoxic and adaptive LTP
  4. enhanced and dangerous LTP
A
  1. early and late phase LTP
  • early phase LTP = minutes to hours ( short term/working memory)
  • long phase LTP = hours, days or months (long term memory)
26
Q

Long term potentiation (LTP) can be categorised into 2 categories, early or late phase. Early phase LTP can last minutes to hours. What drives this LTP?

  1. Ca2+ binding to AMPA
  2. Na+ binding to AMPA
  3. K+ binding to NMDA
  4. higher concentrations of glutamate
A
  1. Ca2+ binding to AMPA
    - Ca2+ binds AMPA causing subsequent events
    - involved in working memory, but continued potentiation can develop into long term memory
27
Q

Long term potentiation (LTP) can be categorised into 2 categories, early or late phase. Late phase LTP can last hours, days or even months. What 2 secondary messengers that have autocatalytic activity and flip the molecular switch that drives the late phase LTP?

  1. PKa and cAMP
  2. PKa and CaMKII
  3. PKc and CaMKII
  4. PKc and cAMP
  • PKc = protein kinase C
  • PKa = protein kinase A
  • CaMKII = Calcium calmodulin-dependent protein kinase II
A
  1. PKc and CaMKII
28
Q

Long term potentiation (LTP) can be categorised into 2 categories, early or late phase. Late phase LTP can last hours, days or even months and is driven by PKc and CaMKII that once activated by Ca2+ flip the molecular switch that drives the late phase LTP. In order for the neurone to sustain the LTP, what is needed in the neuron?

  1. increased number of AMPA and NMDA receptors
  2. new protein synthesis and morphological changes forming new synapses
  3. increased sensitivity of AMPA and NMDA receptors
  4. new AMPA receptors that are able to bind with more glutamate
  • PKc = protein kinase C
  • CaMKII = Calcium calmodulin-dependent protein kinase II
A
  1. new protein synthesis and morphological changes forming new synapses
29
Q

Once Protein kinase C and Calcium calmodulin-dependent protein kinase II (CaMKII) have been phosphorylated, CaMKII is able to activate a precursor that is involved in the pre-synaptic feedback. What is this precursor?

  1. arganine
  2. glutamine
  3. dopamine
  4. serotonin
A
  1. arganine
    - arganine is turned into nitric oxide (NO) which influences glutamate release at the pre-synapse
30
Q

Once Protein kinase C and Calcium calmodulin-dependent protein kinase II (CaMKII) have been phosphorylated due to the release of Ca2+, CaMKII is able to activate arganine, which is then turned into nitric oxide (NO). What role does NO have on glutamate pathway at the pre-synapse?

  1. binds directly with vesicles containing glutamate, increases pre-synaptic release
  2. NO becomes a second messenger, travels to pre-synapse increasing pre-synaptic release
  3. binds to Ca2+ channels in pre-synapse, increasing glutamate vesicles fusing with membrane
  4. NO inhibits glutamate release
A
  1. NO becomes a second messenger, travels to pre-synapse increasing pre-synaptic release
31
Q

What is excitotoxicity?

A
  • toxic effects of excitatory neurotransmitters
  • can cause neuronal dysfunction or cell death
  • this can happen in chronic stress where cortisol stimulate hippocampus releasing Ca2+ and damaging the hippocampus
32
Q

The activation pathway for NMDA glutamate receptors is activated by increased long term potentiation (LTP) of AMPA and the binding of glutamate and glycine at the NMDA receptors. Ultimately this leads to Na+ passing through AMPA and NMDA channels and then Ca2+ passes through NMDA receptor, which ultimately leads to phosphorylation of protein kinase C and Calcium calmodulin-dependent protein kinase II (CaMKII). In addition to causing synaptic plasticity, this may have detrimental effects?

A
  • can be dangerous
  • overstimulation of neurotransmitters causes excitotoxicity
  • caused by Ca2+ overload
33
Q

Long term depression (LTD) relates to an activity dependent reduction in the efficacy of neuronal synapses that can last hours or longer. This can be beneficial in learning a new skill and form implicit, non-declarative memories. For example when we learn a new skill like riding a bike, the cerebellum constantly modifies the movements until we get the skill correct. Synapses that lead to errors will undergo LTD as they are not useful. How can lLTD affect AMPA receptors?

A
    • pre-synapse receives low frequency stimulation (LFS), meaning low glutamate release
    • LFS leads to decreased glutamate release and reduced excitatory postsynaptic potential through AMPA receptors
    • AMPA receptors undergo de-phosphorylation and reduced efficacy or they can be removed from the membranes as they are not needed
  • NEURONS THAT FIRE OUT OF SYNC WILL LOSE THEIR LINK
34
Q

Which part of the brain has been linked with long term potentiation (LTP) and spatial learning, and which receptor has this been associated with?

  1. glutamate (NMDA receptor) in thalamus
  2. glutamine (AMPA receptor) in hippocampus
  3. glutamate (NMDA receptor) in hippocampus
  4. glutamate (AMPA receptor) in hippocampus
A
  1. glutamate (NMDA receptor) in hippocampus
    - drug AP5 has been shown to inhibit NMDA and impair learning through reduced LTP
    - rat study in image show how important LTP of NMDA receptors in the hippocampus is
35
Q

Glutamate in the hippocampus is important for long term potentiation of NMDA receptors in the hippocampus and contributes to learning and memory. What effect does alcohol have on the NMDA pathway?

  1. acts as a partial antagonist and increases the sensitivity of the pathway
  2. acts as an antagonist, inhibiting NMDA receptors
  3. acts as an antagonist causing long term depression of AMPA receptors
  4. inhibits AMPA receptors
A
  1. acts as an antagonist and inhibition of NMDA receptors
    - linked with blackouts and amnesia
36
Q

What are Benzodiazepines?

A
  • are a type of sedative medication (calm, drowsiness and sleep)
  • facilitating the binding of the inhibitory neurotransmitter GABA at various GABA receptors throughout the CNS
37
Q

Benzodiazepines have been linked with anterograde amnesia (difficulty remembering new information), how could this occur?

A
  • Benzodiazepines facilitate the binding of the inhibitory neurotransmitter GABA at various GABA receptors throughout the CNS
  • GABA increases Cl- and reduces action potentials which slows neuronal activity down
  • short term/working memories may not get stored in long term memories
38
Q

Cholinergic / Anti-cholinergics are drugs that act on the nicotinic and muscarinic receptors in the body or inhibit them, respectively. What effect may these drugs have on learning?

A
  • muscarinic antagonist seems to impair spatial learning
  • acetylcholinesterase inhibitors increase levels of ACh and have been linked with improvements in alzheimers
39
Q

Smoking has been linked with synaptic plasticity, how?

A
  • smokers have been shown to have increased levels of nicotinic receptors in the brain
  • effects of smoking appears to activate nicotinic receptors
  • smoking activates nicotinic receptors causing LTP that can last hours, days or months, which could be good just when you are about to learn something

Year 2 NSB (53 decks)

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