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Biological Foundations of Mental Health > The effects of activity, experience and deprivation on the nervous system > Flashcards

The effects of activity, experience and deprivation on the nervous system Flashcards

1
Q

What is Hebbian synaptic plasticity?

A

Activity-dependent strengthening of synapses between co-active neurons,
or weakening of synapses between neurons with uncorrelated activity
-> allows experience to shape connections that already exist by increasing or decreasing their efficacy
-> does not involve creation of synapses

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2
Q

Why does ‘Fire together, wire together’ doesn’t describe Hebbian plasticity?

A

This implies plasticity occurs between cells that are not already connected

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3
Q

What do synapses represent in the context of Hebbian plasticity?

A
  • Major unit of information storage in the brain

- Reflects the history of activity at that synapse

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4
Q

What makes Hebbian plasticity input specific?

A

Synaptic plasticity occurs only at synapses that have undergone activity, and does not occur at neighbouring inactive synapses on the same neuron
- its also long-lasting

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5
Q

What is a ‘tetanus’ stimulation?

A

High frequency electrical stimulation that allows experimenters to guarantee electrical activation of both pre-synaptic and post-synaptic terminals at the same time
-> Hebb’s conditions necessary for the strengthening of synapses

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6
Q

What is the most commonly studied form of Hebbian plasticity?
Does it rely on?

A

LTP

- relies upon electrophysiological stimulation and recording techniques

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7
Q

Who discovered LTP and in which brain region?

A

British neuroscientist Tim Bliss and his Norwegian colleague Terje Lømo
- discovered in granule cells of dentate gyrus - hippocampus

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8
Q

How can neurons of a resected human hippocampus be kept alive?

A

By maintaining the hippocampus at the correct temperature, in carefully oxygenated solutions that contain all required ionic concentrations and metabolites

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9
Q

What does it mean that synapses are bidirectionally modifiable?

A

Both LTP and LTD can be observed longitudinally at the same synapses

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10
Q

What is the modification threshold for LTD/LTP?

A

The frequency at which no change in synaptic strength will occur

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11
Q

How do frequencies result in LTP or LTD?

A

> Low frequency stimuli induce LTD by ensuring uncorrelated activity between pre- and post-synaptic cells
Higher frequencies induce LTP by strongly correlated pre- and post-synaptic activity

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12
Q

What is bidirectional plasticity? What does its direction reflect?

A

A perfect system to shape the functional response of neurons in the brain to activity and sensory input
- its direction reflects the recent history of activity at the synapse

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13
Q

Are the principles of bidirectional plasticity generalisable?

A

Its principles generalise from rodent hippocampus to neocortex and to other species
- all show similar degrees of LTP and LTD when assessed with electrophysiology

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14
Q

What are AMPA receptors? What are their characteristics?

A

> Ion channel opened by Glu which allows flow of cations into a neuron

> Carries major synaptic current

> Responsible for excitatory fast synaptic transmission

> LTP and LTD are expressed through changes in AMPA conductance

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15
Q

What are NMDA receptors? What are their characteristics?

What makes it a ‘coincidence detector’?

A

> Ion channel allowing flow of cations

> Glu-binding and voltage-dependent
- channel opens only when Glu is bound and is depolarised

> Ideal coincidence detector to fulfill the Hebbian criterion of simultaneous pre- and post-synaptic activity

> Ca2+ conductance through NMDAR is the critical factor for plasticity to occur

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16
Q

What is the consequence of NMDA receptor antagonist AP5 (APV) on LTP and LTD?
What does it demonstrate?

A

AP5 (APV) blocks the induction of both LTP and LTD

  • > NMDAR are the biological solution to Hebb’s theory
  • > LTP can still be induced after washout
  • > The ex-vivo slice is advantageous as it allow drugs to both be washed on and off at appropriate times -> synapses are not irreparably altered by drug delivery
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17
Q

How can the same receptor serve both LTP and LTD (opposite directions of synaptic change)?

A

> The concentration of post-synaptic Ca2+ is very different between LTP and LTD:

  • summates to high concentrations for high frequency stimulation while remaining elevated
  • considerably lower in concentration as a result of pulsatile, non-summating in Ca2+ ion concentration

> Different Ca2+-sensing enzymes are activated by high and low concentrations of Ca2+ ions:

  • protein kinases (e.g. AMPAR) change their properties -> phosphorylated synaptic protein -> LTP
  • protein phosphatases -> unphosphorylated synaptic protein -> LTD
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18
Q

Why are primary sensory areas best studied and understood?

A
  1. They receive relatively unprocessed sensory information relayed from the relevant sensory apparatus via few intermediaries
  2. They provide a general model of neocortical function
  3. Their structure and function are well understood and they often exhibit visible specialisations that reflect spatial recapitulations of the sensory world
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19
Q

What are ‘whisker barrels’?

A

Columnar anatomical specialisations in primary somatosensory cortex of rodents that are dedicated to input from a single whisker

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20
Q

What do whisker barrels allow?

A

To constrain sensory stimulation to a very specific region of interest and study the resulting plasticity

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21
Q

Where do ocular dominance columns reside?

A

In the primary visual cortex of most highly binocular mammals

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22
Q

What is in the lateral geniculate nucleus?

A

Layers dedicated to contralateral and ipsilateral eye

23
Q

What is in the primary visual cortex?

A

White matter projections

-> zones restricted to layer 4

24
Q

What happens with the early visual system through Hebbian plasticity?

A

Early visual system integrates ocular inputs to form binocular representation

  • segregation turns into ocular dominance columns in layer 4 of V1 (primary visual cortex)
  • integration into binocular representations occurs in layer 2/3 of V1
25
Q

Where is the segregation of ocular input maintained?

A

In the optic nerve and lateral geniculate nucleus (LGN)

26
Q

Where are ocular dominance columns maintained?

A

In layer 4 of V1

27
Q

What is the spontaneous activity recorded prior to eye opening?

A

Ca2+ imaging reveals that:

  • retinal neurons produce spontaneous activity
  • waves of this activity pass across the retina

-> retinal waves occur prior to eye opening

28
Q

What are the enzymes used to inactivate the retina in experiments?

A
  1. Epibatine: Ach receptor antagonist
    - derived from the poison dart frog
  2. Tetrodotoxin (TTX): antagonist of voltage-gated Na+ channels
    - derived from the puffer fish (numbs the lip of those who eat it)

=> Block neural activity
- commonly used as experimental tools to assess the importance of activity in specific neural populations

29
Q

What are the consequences of inactivating the retina (binocular inactivation) prior to eye opening?

A

> Prevents normal LGN segregation of ipsilateral and contralateral zones
-> spontaneous activity (retinal waves) must play a major role

> Prevents segregation of ocular dominance columns in V1

30
Q

Is the spontaneous activity between the two eyes correlated?
Why?
What is the consequence of that?

A

Spontaneous activity is not correlated between the 2 eyes, since the retinae are not receiving shared sensory input
-> forces Hebbian plasticity to segregate ocular dominance zones

31
Q

How does Hebbian plasticity result in ocular dominance zones?

A

Activity-dependent plasticity prior to eye opening segregates inputs with uncorrelated spontaneous activity (lack of correlation between pre- and post-synaptic neurons -> LTD)

> Post-synaptic neuron has a monocular receptive field, more or less dedicated to processing information from one of the 2 eyes only

> Post-synaptic neurons have their activity driven by 1 eye slightly more powerfully than the other, because the 2 inputs are not in synchrony
-> Hebbian plasticity, modelled by LTP, strengthens inputs from the favoured eye

32
Q

How could genetic programming result in ocular dominance columns (highly segregated zones)?

A

Highly segregated zones - ocular dominance columns - could arise from a population of neurons that initially had a largely binocular response

  • > prior existence of a very slight bias in one direction or another
  • may arise through chance or some genetic mechanism not activity-dependent, which create some very rough bias before this is hugely refined by activity-dependent plasticity (Hebbian)
33
Q

Does functional segregation require the NMDA receptor in cortical neurons?
What is the evidence?

A

Yes - NMDAR require in cortical neurons for functional segregation based on spontaneous activity
- knockout approach: mice that do not express NMDAR in the neocortex have severally ill-defined whisker barrels in V1

=> Hebbian plasticity plays a key role

34
Q

Who discovered ‘imprinting’ and what is it?

A

Conrad Lorenz
- persistent attachment formed if carer role is taken on by a human throughout a defined period of early post-natal development

35
Q

What is the critical period?

A

A relatively brief time window during which the effects of sensory experience or deprivation on the nervous system are most pronounced
-> defining plasticity is permitted

  • usually occurring quite early in post-natal development
36
Q

How is the ocular dominance shifting after monocular deprivation in five-weeks old kittens, in 14-weeks old cats, and adult 14+ weeks old cats?

A

Ocular dominance shift after monocular deprivation:

  • reversible in kittens through reversing the eye sutured
  • not reversible in the 14-week old cats that had monocular deprivation as kittens, using reverse lid suturing (critical period)
  • capacity of the cortex for plasticity is lost after the critical period (adult 14+ weeks old cats)
37
Q

What characterises the restoration of binocular vision regarding the critical period?

A

No functional recovery can occur if the visual experience does not return to normal prior to closure of the critical period

Deficits occurring in kittens persist even when binocular vision is fully restored in adulthood:

  • monocularly deprived kittens show normal binocular vision a week approx. after the eye is open post-critical period
  • BUT, vision limited to the deprived eye never recovers
  • > animals remain functionally blind in this eye, even though the eye is fully operational
38
Q

How does the visual critical period vary between species?

A

> Varies in time and longevity

> Closure of the critical period for vision:

  • cats: 8-9 weeks
  • monkeys: 8-9 months
  • humans: 8-9 years
39
Q

What is the role of cortical inhibition in the critical period?

A

Cortical inhibition is a central factor in the onset and offset of the critical period

  • inhibition develops late in the cortex relative to excitatory circuits
  • critical period = ‘sweet spot’ between too little inhibition and too much inhibition
40
Q

How can inhibition be a key determinant in wether or not Hebbian plasticity occurs?

A
  1. Too little inhibition -> noise in the overall activity
    - > Hebbian plasticity cannot operate to integrate signals
  2. After maturation of inhibition during critical period, only the strongest visual inputs can drive enough cortical activation to initiate plasticity (differentiation of correlated and uncorrelated activity)

=> GABAergic inhibition is required to open the critical period, and increased inhibition closes it (prevents sufficient post-synaptic activity to allow Hebbian plasticity)

41
Q

How can the capacity for change still exist in cortical circuits after the critical period?

A

If inhibition in the cortex can be modified:
- Opening of critical period can be advanced (precocious) by positively modulating GABA receptors with benzodiazepines
- Critical period can be reopened with treatments that reduce inhibition
e.g. genetic knockdown of key enzyme for synthesising GABA (Glutamic acid decarboxylase - GAD) ;
or grafting immature inhibitory neurons into visual cortex of mature mice

42
Q

How do environmental factors influence the recovery of juvenile plasticity?
What are those factors??

A

By modifying cortical inhibition

  • > non-invasive approaches
  • dietary restriction
  • dark exposure
  • environmental enrichment
  • perceptual learning
  • physical exercice
43
Q

Which category of antidepressants restores critical period plasticity?

A

SSRI (e.g. Fluoxetine - Prozac), reduces inhibition

44
Q

How does dark exposure (DE) reduce visual cortical inhibition?

A

> DE can recover cortex to critical period levels of inhibition
- DE on adult animals - after critical period - reduces amplitude of inhibitory post-synaptic currents (IPSCs)

> DE alters the modification threshold for synaptic plasticity: (in DE exposed animals)

  • Low frequency stimulation produces less LTD
  • High frequency stimulation induces more LTP

=> Dark exposure could reduce the impact of monocular deprivation
<=> binocular deprivation does not induce a shift in ocular dominance in the brain
or DE could reverse lost visual function in adult animals after extended monocular deprivation

45
Q

What is the effect of continuous dark exposure on cats that underwent monocular deprivation as kittens through the critical period?

A

10 days of continuous dark exposure in the adult cat recovers visual function in the deprived eye

46
Q

The effect of dark exposure on monocular deprivation make it a strong candidate for what?

A

For recovery of function in the visual system by modifying inhibition

47
Q

What is amblyopia?

A

Disorder of the brain’s response to visual input
- resulting from monocular deprivation occurring during childhood as a result of one of several repairable ocular conditions

48
Q

What are the causes of amblyopia?

A 
Repairable ocular conditions:
- strabismus
- cataracts
- corneal scarring
(easy to detect - physical manifestation - likely remedied in UK but less in developing world)
  • anisometropia
  • astigmatism
    (subtle defects less often notice -> often not treated even in countries with available treatment)
49
Q

What is the best clinical practice for treating amblyopia?

A

Use surgery to return the defective eye back to normal and then patching or using eyedrops on the good eye

50
Q

What are the implications of the research on deprivation in the visual cortex, dark exposure, and other non-invasive novel treatments for amblyopia?

A

> Major societal impact

> Insight into the consequences of deprivation in other sensory systems

51
Q

How do neurodevelopment disorders influence the excitatory-inhibitory (E-I) balance?

A

Highly penetrant genetic causes of neurodevelopment disorders disrupt the E-I balance by altering synaptic development

52
Q

What are the risk factors for E-I imbalance?

A

> Mutation of the genes that code for neurexins and neuroligins

> Critical receptors for Hebbian plasticity
- inhibitory neurons in cortex are reduced in number and in production of GABA

> Disruption of Fragile X Mental Retardation Protein (FMRP) function
- Fragile X syndrome exhibits a clear E-I imbalance at various stages of development

> Mutation in other highly penetrant genetic causes of neurodevelopmental disorders
- e.g. MeCP2 disruption causes Rett’s syndrome ; critical role in production of enzymes necessary for GABA production in inhibitory neurons -> major E-I imbalance

53
Q

What are the variations of critical periods?

A
  • Differ by region and function

- Can be disrupted in various ways

54
Q

What can the disruption of the critical period plasticity development cause?

A

Contribute to numerous psychiatric disorders

> Delayed/exaggerated critical period plasticity
or deprivation/aberrant experience occurring during the critical period
-> neurodevelopmental disorders

Biological Foundations of Mental Health (15 decks)

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