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Neuroscience > Neuronal complexity > Flashcards

Neuronal complexity Flashcards

1
Q

why are complex circuits formed?

A

one neurone can have 1000s of inputs and synapse onto a vast no. of other cells

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2
Q

what are the 5 aspects of synaptic modulation?

A

complex forms of synaptic activity

facilitation, depression + temporary potentiation

Hebbian synapse

long term protection

synaptic plasticity

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3
Q

what is facilitation?

in the long term, what to frequently used pathways become?

A

when 2 or more Abs reach the presynaptic terminals in a short period of time

-> more NT is released per AP

= stronger response in the postsynaptic neurone

more effective pathways

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4
Q

how does the interval between spikes effect facilitation?

A

the smaller the interval between spikes

-> the greater the facilitation

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5
Q

what is a tetanic train?

A

a rapid succession of APs

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6
Q

what is depression?

A
  1. tetanic train causes depletion in NT
  2. decreased NT release
  3. decreased EPSP
    = depression
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7
Q

how can a synapse recover from depression?

A

post-tetanic potentiation

= increase in synaptic vesicles available per incoming AP

-> short term enhancement of synapse’s activity

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8
Q

what are the 2 presynaptic parameters that influence short-term plasticity?

A

local intracellular Ca2+ conc and Ca2+ binding protein conc

readily-resealable pool of vesicles

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9
Q

short term plasticity is specific for?

A

individual synapses
- even if its in the same axon

same activity in same neurone
-> could cause depression in one synapse and facilitation in another

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10
Q

how does post-tetanic potentiation represent an elementary form of memory?

A

a high rate of stimulation in the presynaptic neurone

-> leads to a gradual increase in amplitude of postsynaptic potential

= represent storage of information about a previous activity

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11
Q

what did Hebb hypothesise?

what does this mean?

A

a form of co-ordinated activity for a series of neurones connected together that would strengthen specific pathways

  1. pathways respond better to particular stimuli
  2. pathways would become dedicated to 1 kind of remembered event
  3. a neurone may have several inputs
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12
Q

in a Hebbian synapse, what effects may several inputs have on a neurone?

A

inputs that operate similarly work in harmony
-> strengthens post-synaptic response
= increases efficiency of connections
-> greater post-synaptic response

inputs not working in the same way will be weakened

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13
Q

which receptors have been associated with synapses that can learn?

A

NMDA receptors

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14
Q

what is long term potentiation?

A

neurones responding to a particular kind of stimulation

-> resulting in enhanced synaptic activity

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15
Q

what is involved in LTP formation?

what factors are also involved in this process?

A

activation of NMDA receptors

changes in in the behaviour of calcium/calmodulin-dependent kinases

retrograde acting factors
= those that effect the presynaptic neurone behaviour

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16
Q

what is long term depression?

what can cause it?

A

decreased response to particular inputs

if high activity in the synapse requires high conc of calcium in the presynaptic component

17
Q

what are all forms of memory believed to be due to?

which parts of the brain demonstrate this?

A

LTP

Hippocampus (spatial memory)
Amygdala (fear)
Cortex (motor skill)

18
Q

describe the structure of a rodent hippocampus

A
  1. perforant path carries input to granule cell in Dentate gyrus
  2. granule cell sends out an axon to a pyramidal cell in CA3
  3. this sends out an axon to another pyramidal cell in CA1
19
Q

what are the 3 principle pathways in a rodent hippocampus?

A
  1. Perforant
    - entorhinal cortex to DG
    - granule cells
  2. Mossy fibre
    - DG to CA3
    - pyramidal cells
  3. Schaffer collateral
    - CA3 to CA1
    - pyramidal cells
20
Q

how can activity of LTP of Schaffer collateral- CA1 synapses be measured?

A

apply tetanus to pathway 1 in axon of CA3 pyramidal cells

measure the post-synaptic activity of the different pathways in CA1 pyramidal cell before and after tetanus

look at whether there’s a change between before and after
- if there’s no difference in pathway 2
= no LTP induced

21
Q

what happens after LTP?

A

EPSCs (=currents) are increased

22
Q

what are the pre and post synaptic mechanisms of LTP?

A

pre
= increase in probability of NT release
-> amount of quanta released increases

post
= changes in production of proteins involved in the synapse
-> due to AMPA receptor (glutamate receptor)

23
Q

how does LTP affect kinases?

A

CaMKII

  • normally calcium-calmodulin dependent
  • now autophosphorylated form active without Ca2+

PKC and PKA activity effected too

24
Q

what is AMPA?

what are the changes in AMPA receptors?

A

an agonist for glutamate

activation of NMDA receptors

  • > increase in density of AMPA receptors on PS membrane
  • > increase in sensitivity of PS cell
25
Q

how are silent synapses converted into active synapses via AMPAR insertion?

A
  1. remove blockage that prevents NMDAR activation
  2. Ca2+ enters via NMDARs
  3. alters activity of Ca-CaM II
  4. alters protein synthesis
    - > inclusion of AMPA receptors into PS membrane
26
Q

why are NMDAR the most important aspect of considering how LTP occurs?

A

they lead to a change in protein synthesis

= long term change

27
Q

describe how NMDAR is activated

A
  1. glutamate or NDMA binds to agonist binding site
  2. glycine (co-agonist) binds to allosteric site
  3. independent depolarisation of membrane
    - > removes Mg2+ block
  4. Ca2+ and Na+ ions flow through
28
Q

what are the other regulatory regions of NMDAR?

A

endogenous polyamines

  • low microM potentiates
  • high microM inhibits

phosphorylation site

redox site

  • reducing agents potentiate
  • oxidation reduces NMDAR activation
29
Q

describe NDMAR structure

how is NMDAR effected by its subunits?

A

(at least)
2 x NR1
2 x NR2

variability in the types of NR subunits
-> impacts variability in NMDAR

30
Q

what are retrograde messengers?

give 3 examples

A

messengers released by the post-synaptic cell that modify the response of the pre-synaptic cell

  • > modified quantal release
  • > impacts how NMDAR respond + how AMPAR are incorporated in the synapse

nitric oxide
carbon monoxide
arachidonic acid

Neuroscience (17 decks)

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