Lecture9 Flashcards

1
Q

What 2 factors are depended on for maintenance & reorganisation of neural circuits?

A

Time-dependence (critical & sensitive periods) & Experience/Use (use it or lose it)

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2
Q

In deprivation & enrichment experimental manipulations, what has been discovered when rats are in a deprived environment?;
What about in an enriched environment?;
Which brain region does this occur in?

A

Fewer synapses & dentritic spines & poor depth & pattern perception;
More dendritic spines & synapses;
Layer 3 of the somatosensory cortex

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3
Q

In enriched environments, what has been found to increase in adult rats?;
What is this associated with?

A

Neurones in the dendate gyrus of the hippocampus (60% more) & in olfactory bulbs;
Exercise interaction with the enriched environment

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4
Q

What did Bechera & Kelly find about exercise in cognitively enriched rats?;
Exercised & enriched rats were also found to…

A

It improves object recognition memory & induces brain derived neurotropic factor (mRNA) expression & cell proliferation;
Preferentially explore novel objects

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5
Q

In a study on ocular dominance, when kittens had one eye sutured (leading to monocular deprivation), what was found?;
How did this differ with adult cats?

A

No cells were activated by the deprived (contralateral) eye - critical period;
There was little effect on ocular dominance but overall cortical activity was diminished (not as catastrophic)

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6
Q

After a week of monocular deprivation in the critical period, what did Antonini & Stryker find was reduced in the deprived eye?;
What about long term deprivation?

A

Axonal branching in axons from the lateral geniculate nuclei (layer IV in primary visual cortex);
Changes were not comparably greater

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7
Q

What does evidence regarding vision suggest about Competition in neural development?;
What suggests this is not just a single process & that shifting & balancing occurs?

A

Selective deprivation - ocular dominance columns (layer IV) in many species are developed at birth; deprivation of one eye during sensitive period leads to reduced activation of layer IV of the corresponding visual cortex; That activation of the other cortex by the intact eye increases

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8
Q

What does evidence regarding motor control suggest about Competition in neural development?

A

In newborns, each muscle cell is innervated by several motor neurons but only 1 survives development; in in-vitro studies, when 1 developing muscle cell is innervated by 2 motor neurons, electrical stimulation (or activation) of 1 neuron, led to degradation of the other

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9
Q

What did Knudsen & Brainard find when they placed prisms over the eyes of barn owls?

A

Prisms displaced visual field x degrees to the left or right; vision mapping shifted in the direction of the prism; auditory map also shifted in the tectum in the corresponding direction & to the same extent

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10
Q

With the cutting of nerves or sewing together the fingers of one hand, altering demands on the system by increased use, what changes in the somatosensory maps occur?;
What does this suggest about the adult cortex?

A

The relevant part of the cortex no longer responds to the touch of that finger, but that now defunct area starts to respond to stimulation of the adjacent finger (it fills in the silent area & takes over);
That it is a dynamic area & changes can still happen

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11
Q

What have single unit recordings revealed about individual digit representations in the somatosensory area of monkeys if the 2 fingers of one hand are sewn together?

A

Months later the cortical map changes so that the sharp border once present between the fingers is now blurred; fingers don’t behave individually anymore

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12
Q

When thumbs & fingers have been stimulated in young string players, what was found?;
What was the size of the effect correlated with?

A

Responses were higher, suggesting that a larger cortical area is dedicated to touch in musicians;
The age at which they’d begun their musical training (larger responses before 12 yrs)

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13
Q

fMRI scans in adults performing a simple motor task a few minutes each day (touching finger to thumb) showed what?; What does this suggest?

A

Speed & accuracy improved with practice & greater changes in corresponding motor cortex after a few weeks;
That training can induce rapid changes in brain organisation that reflect plasticity

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14
Q

In Karni et al.’s study, how long did the primary motor cortex show increased activation for in participants who had engaged in training of repeated motor sequences?

A

Up to 8 weeks, even when no training ensued on the task in the interim

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15
Q

For people with phantom limbs, after time elapses…;

If the amputated part is hurt…;

A

They still feel it exists & is reduced in size (telescoped); The limb can feel enlarged again

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16
Q

What did Ramachandran find with his patient who had an amputated left arm?;
How can this be explained?

A

When part of his cheek was stroked, he reported sensations in his missing left hand;
Hand & face representations on the somatosensory map are close together so the face representation can expand & encroach on the hand representation

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17
Q

Where & how does Anterograde neural degeneration occur after brain damage;

A

From point of disruption forwards to the synaptic terminals (distal segment); happens fast because of separation from metabolic centre

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18
Q

Where & how does Retrograde neural degeneration occur after brain damage?;
What may increase in this case?

A

From point of disruption backwards to the cell body (proximal segment); happens slow, over days; reduction in size, then death;
Production of proteins (but no guarantee of regeneration)

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19
Q

How does Transneural degeneration occur?

A

Damage spreads to neurones that are linked synaptically

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20
Q

Concussion occurs when the force from the impact causes the brain to…;
In severe concussions, as the brain rebounds it…;
Then the brain swells, which puts pressure on the…

A

Strike the inner surface of the skull & rebound against the opposite side;
Twists;
Brain stem, which controls breathing & other basic life functions

21
Q

Describe the symptoms of a concussion following a blow to the head;
What cumulative effects can occur?

A

Brief loss in consciousness (or none at all); temporary confusion; behavioural, affective & cognitive problems; no evidence of structural (neuronal) damage;
Internal bleeds; linear & rotational forces can lead to cell death

22
Q

Describe the effects of Punch-drunk syndrome in boxers; What did EEG recordings of uni footballers show?

A

General cognitive deterioration & eventual scarring after repeated concussions (effects are cumulative);
Alterations even after 2 years of sustaining a concussion

23
Q

With a Closed brain injury, although the blow doesn’t penetrate the skull, what can it cause?;

A

Contusions (bruises) when the brain slams against the skull (coup & contracoup); haematomas - bleeds due to shearing of the blood vessels (alcohol is anti-coagulant); oedema - swelling due to fluid (from pressure); loss of consciousness (downward pressure & twisting on brain stem); epilepsy (disrupted tissue can impair neural activity)

24
Q

What occurs with a Subdural Haematoma?

A

There’s a midline shift (oedema gets pushed to the side)

25
Q

Explain the biomechanics of Traumatic Bran Injury at a neuronal level;
Neurones that are not completely ruptured may…;
But they may also form…

A

With either anterograde or retrograde degeneration, the neuron is not activated by the post-synaptic axon which can cause a domino effect of metabolic changes;
Re-sprout axonal projections (restoration);
Unwanted connections resulting in behavioural disturbances

26
Q

When a blow penetrates the skull (penetrating brain injury), what can occur?

A

Bleeding, infections, scarring (thus epilepsy) & oedema

27
Q

Skull fractures can be…;

Which one is more complicated?

A

Linear or Depressed;

Depressed, because impact drives fragments into dura & brain leading to infection & epileptic activity

28
Q

Post-traumatic epilepsy occurs due to what?;

What do these patients typically receive?

A

The presence of scar tissue (changes in membrane structure & function);
Anticonvulsants prophylactically

29
Q

Sudden disruption to the brain’s blood circulation result in what?;
Abnormalities of the brain resulting from pathology of blood vessels include…

A
Cerebrovascular damage (or strokes); 
Lesion of the vessel wall; occlusion of lumen due to thrombus/embolus; rupture/altered permeability; increased viscosity or other changes of the blood
30
Q

The brain receives 15% of the…; & accounts for…

A

Resting cardiac output; 20% of the oxygen consumption

31
Q

What is a haemorrhage?;

Why may it happen?

A

Bleed into the brain when a blood vessel ruptures (leading to stroke);
Congenital weakness in blood vessel wall, or because of an aneurysm (arteries are most vulnerable at the forks & may swell up until they burst)

32
Q

Where does bleeding occur with a haemorrhagic stroke?

A

Inside or around brain tissue

33
Q

What is Ischaemia?;
An Ischemic stroke results from what?;
How long do the consequences of this typically take to develop?

A

Disruption in blood supply (thrombus, embolus or arteriosclerosis);
A blood clot which stops the flow of blood to an area of the brain;
A few days

34
Q

What are Infarcts?;

What are they surrounded by?

A

Areas of dead tissue caused by stroke;

The Penumbra which is alive but dysfunctional & may recover depending on treatment

35
Q

What are Mitochondria?;
What does Cerebral Hypnoxia lead to?;
What happens on reperfusion (oxygen supply)?;
What can ongoing destruction of Mitochondria lead to?

A

Sites of aerobic metabolism, converts food energy into useful form;
Mitochondrial dysfunction;
Dysfunction is partially & transiently reversed;
Secondary energy failure, neurotransmitter dysfunction & neurone death

36
Q

Explain why the PNS is more capable of regeneration than the CNS

A

Schwann cells (in PNS) produce neurotropic factors to stimulate growth, & cell adhesion molecules on their membrane provide paths for growth; oligodendroglia (in CNS) don’t have these qualities & actually release factors which inhibit growth

37
Q

In the PNS, regeneration from the proximal stump of the nerve starts when?;
If the Schwann cells are not damaged or severed, what can happen?

A

2 - 3 days after damage;

Individual axons can re-grow & reach their correct targets

38
Q

When a nerve is damaged & the severed ends of Schwann cell sheaths are slightly separated, what happens?;
What if there is a complete & large separation?

A

Axons may regenerate into the wrong sheathes & reach incorrect targets leading to poor coordination;
The re-growing of axons may become a tangle with no destination & there’ll be no functional regeneration

39
Q

When an axon degenerates, what might axons from neighbouring intact neurones do?

A

Grow to synapse at the vacated sites (collateral sprouting) establishing new connections;

40
Q

What are two mechanisms of re-organisation?;

A

Collateral sprouting (long-term re-organisation can be too great to be explained by changes to existing connections only) & Strengthening of existing connection due to release from inhibition by original connections (can be rapid but restricted & can’t be explained by normal growth, rather a change in balance of maintenance)

41
Q

If the cerebral cortex is damaged while Neurogenesis is still ongoing, what is the brain able to do?;
What happens if there is damage during the time of Neural Migration?

A

Compensate by making neurons & there is a better functional outcome than if the injury is in adulthood; There is poor functional outcome (connections to targets won’t happen)

42
Q

Injury during the peak time of Synaptogenesis allows for what?;
When does this peak time occur?;
An injury during the 3rd trimester & birth will lead to what?;

A

Compensatory synaptogenesis & correlated functional improvement;
During 18 months after birth;
Poor functional outcome because this is the time of maximum migration

43
Q

What did Teuber show with soldiers suffering neural lesions?;
What did Milner report about patients aged over 40?

A

Those at age 17-20 years showed a greater recovery than those aged 26 & over;
Less recovery than younger patients

44
Q

How are intelligence & cognitive reserve correlated?;

What could possibly explain this?

A

Higher premormid intelligence leads to better recovery; More education more synapses (greater plasticity) & generating more strategies to solve problems

45
Q

What did Barulli & Stern show about how cognitive reserves may mediate Alzheimer’s disease pathology?

A

People with higher cognitive reserves will show a later decline, but once it begins it declines more rapidly

46
Q

Why do females & left-handers show more functional recovery after brain injury?;
What do optimistic, extroverted & easygoing individuals tend to have following brain injury?

A

They have less functional lateralisation than males or right-handers;
A better prognosis, possibly due to compliance with rehabilitation programs

47
Q

When monkeys with ischaemic lesions in the hand area of the motor cortex, underwent rehabilitation by training them to pick up pellets, what was found?

A

The penumbra reduced; the extent of digit representation was altered

48
Q

How can Competition, where neurones compete for synaptic sites & neurotrophins, be used as an advantage for stroke victims?

A

Increased training with affected limb, or by constraining the intact limb will force the use of the affected limb

49
Q

In an experiment, participants attended to 1 of 2 visual stimulus streams adjacent to each hand, whilst repeated pairing of peripheral nerve stimulation & transcranial magnetic stimulation was used to alter functional responses in the left thumb area of primary motor cortex. What occurred?;
What does this mean?;
What does this suggest about voluntary visual attention?

A

When they attended to visual stimuli located near the left thumb, increases in excitability were enhanced, as measured with evoked responses;
That neurones had becomes more connected around the cortical area of the thumb during the attention manipulation; It can exert an important influence on the functional organisation of the motor cortex