Week 3-Brain Communication And Development Flashcards

1
Q

What’s resting potential?

A

-The opening of ion channels makes the inside of
the neuron more negative than the outside ‘extracellular’ space.
-This is primarily due to the action of ion channels (leak and pump) which allow and maintain a graded difference in prevalence of charged ions from inside, to outside, the cell.
Typically:
* 3 Na+ ions out
* 2 K+ ions in

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2
Q

How can the typical resting membrane potential
inside the neuron (-70 mV) be influenced?

A

This can influenced by incoming signals from other cells which can either:
* Further polarise the cell (more negative) this inhibits the likelihood of an action potential occurring
* Else it can depolarise the cell (make it more
positive, i.e., towards neutral) which is excitatory
and increases the chance of the cell generating an
action potential.
* We call these events post-synaptic potentials

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3
Q

What are some features of postsynaptic
potentials?

A
  • Post synaptic potentials travel across the
    neuron almost instantaneously (rapid)
  • But as they travel they decrease in size (decremental)
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4
Q

How does depolarisation affect postsynaptic potentials?

A
  • If the cell receives excitatory input it will
    depolarise.
  • If the membrane potential at the Axon
    Hillock (red square) achieves the threshold of excitation (commonly -50 to -55 mV) the cell will fire.
  • However, remember that the incoming signals can only travel short distances before they expire (decremental)
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5
Q

How does hyperpolarisation affect postsynaptic potentials?

A
  • If the cell receives inhibitory input it will hyperpolarise to become even more negative.
    -If the inside of the cell is more negative you’ll
    need a bigger stimulus to reach the threshold.
    -Therefore the cell is inhibited from firing by
    hyperpolarisation.
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6
Q

How do signals integrate?

A
  • The resting potential of post-synaptic cell is polarised (-70mV).
  • Cells are usually contacted by many incoming PSPs.
  • Each PSP could have excitatory or inhibitory influences (usually many of each), by depolarising or hyperpolarising the post-synaptic neurone (respectively).
  • The effect of these PSP’s transmit across the neuron decrementally.
  • The balance between excitatory and inhibitory input (the net effect) determines whether an action potential fires
  • If the net effect transmitted to the axon hillock results in depolarisation to the threshold of excitation then an action potential will fire.
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7
Q

How are action potentials all or nothing?

A

-In some ways the firing of a neurone is like
the firing of a gun
-As the trigger is squeezed it gradually moves
back (depolarising potential)
-Until it causes the gun to fire (action potential)
Like a gunshot, an action potential is an all or none phenomena
-Squeezing the trigger harder won’t make the bullet travel faster or further

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8
Q

How are action potentials generated?

A

When the integration of inputs achieves the
threshold of excitation at the axon hillock, it
initiates the generation of an action potential
(AP).
The AP itself is described according to various
components or phases:
1. Depolarisation: Na+ channels open, influx of Na+ into cell.
2. K+ channels open, K+ begins to leave cell.
3. Peak : Na+ channels begin to close, K+ channels still open.
4. Repolarization: Na+ stops entering cell, K+ ions move out.
5. Hyperpolarization: K+ channels start to close but some K+ ions continue to move out of cell.

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9
Q

PSP communication already occurs, so why do we need action potentials?

A

-The axon of a motor neurone is up to 10,000 times as long as the cell body is wide.
-This means that you need a non-decremental way to send information long distances.
* AP are large swings to opposite polarity
* Non-decremental so able to carry the original signal for long distances

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10
Q

How are action potentials able to transverse large distances without losing the integrity of the signal? (the original large swing in polarity is maintained)

A

This is due to a cascading effect whereby the rapid depolarisation at the axon hillock leads to the achievement of the threshold of excitation in the next section of the axon and this continues down the length of the axon.

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11
Q

The speed of transmission is affected by what?

A

The anatomy of the axon
*Myelinated axons (up to 150 m/s)
*Non-myelinated axons (0.5-10 m/s)

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12
Q

How does the axon communicate with other parts of the neuron?

A

-The ways that two cells can synapse are many and varied. Pre-synaptic terminal buttons to post-
synaptic soma, axon or dendrites

Axo-axonic (axon)
Axo-somatic (soma)
Axo-dendritic (dendrites)

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13
Q

What are electrical synapses?

A
  • Electrical synapses are the result of a narrow gap between the pre- and postsynaptic neurons known as a gap junction.
  • The close proximity (e.g., 4 nm {DNA is about 2 nanometers across}) means the cytoplasm of the two cells are interconnected
  • This permits electrical signals (and even small molecules) to pass directly from one cell to the next.
  • This system is FAST
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14
Q

What are electrical synapses part 2?

A

-Electrical synapses in the cerebral cortex allow each network of inhibitory neurons to fire in a
highly coordinated way
-They may relate to rhythmic activity in the cortex.
-The high speed of electrical synapses transmission means they are important for reflexive processes.
-A downside of electrical transmission is that there is no opportunity for ‘gain’ i.e., a small signal cannot bring about a large response.

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15
Q

What are chemical synapses?

A
  • This method of transmission depends on the release of chemicals from presynaptic cell, which are received and have an effect on post synaptic
    cell.
  • In chemical synapses the pre- and post-synaptic membranes are divided by the synaptic cleft (20 nm wide).
  • The post-synaptic membrane contains receptors that can receive the chemical transmitters that will be used to communicate from the pre-synaptic cell.
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16
Q

What are chemical synapses? – transmitter release

A

-Neurones contain bubble-like structures that are filled with chemicals called vesicles.
-The AP stimulates the influx of Ca2+, which causes synaptic vesicles to:
* Attach to the release sites
* Fuse with the plasma membrane
* Expel their contents into the synaptic cleft.
-These chemicals can act as a form of transmission or communication by affecting the post-synaptic

17
Q

What are receptors?

A
  • NT receptors are membrane-spanning proteins.
  • The part exposed to the extracellular space recognises and binds the transmitter to bring about a function that has an effect on the target cell.
  • There are different types of receptor. 2 of the most common:
    Ligand-gated ion channels - direct
    G-protein-coupled receptors - indirect
18
Q

According to the effect on postsynaptic cells, synapses can be what?

A

-Inhibitory (e.g., Cl-, Hyperpolarising) Excitatory (+ e.g., Na+, Depolarising)
* Depending on the type of ion channel which opens, the postsynaptic cell membrane becomes either depolarised or hyperpolarised.
* This decreases or increases the likelihood of the receptor neurone firing with an AP.
* You recognise this because, once again, we are talking about post-synaptic potentials.

19
Q

How is the lock and key theory more complicated?

A
  • Most neurotransmitters can bind to different receptors: one key opens different doors
  • And one receptor can sometimes bind to different substances: one door opened by different keys
20
Q

What’s a neurotransmitter?

A

A neurotransmitter (NT) is a chemical released by the presynaptic neuron to bring about an effect in the post-synaptic neurone.
A NT:
* When released, it must act on a post-synaptic receptor and cause a biological effect.
* If the chemical is artificially applied on the post-synaptic membrane, it should have the same effect as when it is released by a neuron.
* Must be produced within a neuron
* Must be released when the neurone is stimulated
* Once released it must be inactivated.

21
Q

What occurs in the termination of neurotransmitter action?

A

-Receptors cannot withstand exposure to neurotransmitters constantly. If they are overexposed to NT all the time their ability to respond is impaired (desensitise)
-Therefore, a mechanism is required to clear unused NT from the cleft to prevent residual activation
* Enzymatic degradation
* Reuptake
* Diffusion
* Glia

22
Q

What’s colocalisation or coexistence?

A

-It was once believed that each neurone synthesises and releases only ONE neurotransmitter
-Now it is known that many neurones contain more than one neurotransmitter
-Usually one small NT and a neuropeptide

23
Q

What are chemical synapses? - Pharmacology

A

-The introduction of external chemicals (i.e., illicit and licit drugs) can influence and effect the action of endogenous (within the body) NT’s.
-Agonists increase or promote activity
-Antagonists decrease or inhibit the activity

24
Q

What occurs in the development of the central nervous system?

A

The first observable development of the nervous system is the induction of the neural plate.
* 3 weeks after conception, patch of the ectoderm
becomes distinguishable as neural plate.
The neural plate develops to form:
* neural groove
* neural tube

-The anterior end of the neural tube develops 3 swellings that become the forebrain, midbrain and
hindbrain (7 weeks - Day 40)
Neural proliferation:
At this stage rapid cell division occurs in the ventricular zone of the neural tube (nearest the ventricle)

25
Q

What occurs during migration in the development of the CNS?

A

-Once the cells have been created in the ventricular zone they migrate to appropriate location
-During this process they are still immature neurones (no dendrites or axons).
-Glia make scaffolding for migration
-After migration, cells aggregate to form various neural structures.

26
Q

What occurs during differentiation in the development of the CNS?

A

-Once neurones aggregate in the desired location differentiation occurs.
-Axons and dendrites may begin to grow as cells differentiate depending on purpose and location.
-Axon growth is complex

27
Q

What occurs during neuronal death in the development of the CNS?

A

-During gestation, more neurones are produced than required (50%)
-‘Superfluous’ cells die
This can be:
* Pre-programmed (apopstosis)
* Synaptic rearrangement: unnecessary connections die (necrosis)

28
Q

What happens in the development of the CNS by 20 weeks?

A

-By 20 weeks the brain is about 5 cm long and it has the basic shape of a mature brain
-The brain is growing at 250,000 cells a minute in the foetus

29
Q

What happens during postnatal development?

A

-At birth: 350-400 g -Adult: 1300-1400g
-Much of the growth happens in the first 2 years
-This increase in size is NOT due to increase in number of neurones
Three other kinds of growth
1) Synaptogenesis
2) Myelination
3) Increasing branching of dendrites

30
Q

What’s Synaptogenesis?

A

-Synaptogenesis – formation of synaptic connections - is integral to brain connectivity and
communication.
-There is a rapid increase in synaptogenesis in the
cortex after birth.
-But there are differences between regions (i.e., in
visual and auditory cortices proliferate at 4 months
whereas frontal cortex develops more at 2 years)
-Many synapses that form early in development
are eventually lost; overproduction of synapses in
the young brain may contribute to greater plasticity with relevance for learning

31
Q

What’s Myelination?

A
  • Myelination increases the speed of axonal
    conduction and parallels functional development
  • Myelination of sensory areas occurs in first few
    months post-natal.
  • Followed by myelination of motor areas
  • Myelination of prefrontal cortex continues into
    adulthood
32
Q

What’s Dendritic Branching?

A
  • Rapid process
  • Generation of new dendrites which leads to creation of new synapses
  • Changes can be observed in seconds
33
Q

What’s Pruning?

A
  • Pruning: The selection of the pruned terminal arbours follow the “use it or lose it” principle seen in synaptic plasticity.
  • This means synapses that are frequently used have strong connections while the rarely used synapses are eliminated
  • Pruning is carried out by microglia.
34
Q

What are the effects of experience in postnatal development?

A

-Most experiences are time dependent: the effect
of a given experience on development depends
on when it occurs during development
-Leads to the concept of early development as a
‘window of opportunity’
-Sensory deprivation: animals reared in the dark
have fewer synapses in visual areas and as adults have problems perceiving depth.
-Enrichment: thicker cortices with more dendrites
and more synapses per neurone

35
Q

What’s Autism spectrum disorder?

A

Most prevalent childhood neurological disorders (between 1:166 and 1:1000 births):
1. Reduced ability to interpret emotions and intentions of others
2. Reduced capacity of social interaction and communication
3. Preoccupation with a single subject of activity
-Savants: individuals considered by some measures to have diminished intellectual faculties but display amazing and specific cognitive or artistic abilities
-Impaired brain development? There is often a defect in development of brainstem control the muscles of the face in people with autism; suggesting a problem with cerebellar development
(Stephen Wiltshire)

36
Q

What are the neural mechanisms of autism?

A

1- Autistic individuals spend less time looking at faces and remember faces less well. Research has shown that brain areas that respond to faces (fusiform gyrus) are less active
2- Mirror neurones: these neurones fire when you see somebody performing an action. They help one understanding the intentions of others. Children with autism have deficient mirror neurone function

37
Q

What’s Williams Syndrome?

A

-Intellectual disability and heterogeneous pattern of abilities and disabilities (similar to autism)
-In many aspect opposite to autism: Sociable, empathetic and talkative
-Very good linguistic and musical abilities
-Serious cognitive deficits: attention, spatial abilities. -Terrified of apparently mundane
-Engaged storytellers, musicians, loving, trusting, and sensitive to the feelings of others
-Impaired spatial abilities and underdeveloped parietal and occipital cortices; this appears to be due to a major mutation in chromosome 7