Chapter 5 Development And Plasticity Of The Brain Flashcards

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1
Q

What are the three main divisions of the brain?

5.1

A

5.1
hindbrain
midbrain
forebrain

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2
Q

What are the four major stages in the development of neurons?
Describe the process in each.
5.1

A

5.1
-forms axons then dendrites
-myelination-glia produce the insulation
forms first in spinal cord then hindbrain, midbrain and forebrain
This process continues for decades.
-Final stage synaptogenesis-formation of synapses. which continues throughout life.

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3
Q

What technical development by LaMantia and Purves increased our understanding of brain development?
What was their major finding?
5.1

A

5.1

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4
Q

What is apoptosis?
What type of chemical can prevent apoptosis?
5.1

A

5.1
Is programmed cell death
Nerve growth factor promotes survival and growth of nerve cells prevents apoptosis.

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5
Q

List five neurotrophins.
What three functions do they serve?
5.1

A

5.1 neurotrophin- chemical that promotes the survival and activity of neurons.
NGF nerve growth factor
BDNF- brain-derived growth factor

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6
Q

What did Weiss observe in his experiments on salamanders’ extra limbs?
What principle did he conclude directed the innervation of the extra limb?
Is this principle still believed to be correct?
5.1

A

5.1
Grafted extra leg onto salamander-in time extra limb moved in synchrony with normal limb
-nerves attach to muscles at random and then send a variety of messages each one tuned to a different muscle.
The muscles like radians tuned into their messages

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7
Q

What did Sperry observe when he damaged the optic nerve of newts?
What happened when he rotated the eye by 180 degrees?
How did the newt with the rotated eye see the world?
5.1

A

Normal- the nerve found its way to attach to the correct target of the nerve (the tectum)
the axon that was previously attached to the dorsal area grew back to dorsal area of retina (ie. they grow back to original target)
Now newt saw things upside down.
5.1

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8
Q

What conclusion did the results from Weiss (salamanders’) and Sperry’s (newts) experiments suggest?
5.1

A

5.1
Weiss analogy/theory is wrong and nerves/axons do find their way to attach to attach to their correct target
preprogrammed to regenerate to the same place where it had originally been.

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9
Q

What is TOPdv?
What is its role in directing retinal axons to the tectum?
5.1

A

TOP-topography DV-dorsal ventral
is a protein found in the amphibian tectum
As axons grow from retina toward tectum Retinal axons with greatest concentration of TOPdv
5.1

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10
Q

What happens to axons that form active synapses?
What happens to axons that do not form active synapses?
5.1

A

they proliferate and survive but others fail

5.1

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11
Q

Describe the principle of neural Darwinism.
How does this relate to the initial overproduction and subsequent death of large numbers of neurons?
5.1

A

neural darwinism-start with more connections than you need.
Stronger ones survive and weaker connections die
5.1

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12
Q

Describe the effects of environmental “enrichment”.

5.1

A

rats in the enriched environment had more stimulation and then developed a thicker cortex more dendrite branches and had improved learning.

5.1

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13
Q

What physiological process appears to be correlated with song learning in mynah birds?
5.1

A

New neurons form in an area of songbirds brain in the spring
Then area loses neurons in thhe fall and winter, then regains in the spring.
5.1

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14
Q

In what brain areas have new neurons been found in adulthood?
What are stem cells and where are they found?
5.1

A

5.1
grey natter
fine gyro of the cerebral cortex and parts of the corpus callosum

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15
Q

What is a brain correlate of absolute pitch?
What evidence suggests that this may result from extensive early musical training?
5.1

A

area subcortical brain structures to musical sounds
Also area around temporal lobe
5.1

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16
Q

What brain area is frequently larger in people who had extensive experience playing stringed instruments?
5.1

A

post central gyrus

5.1

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17
Q

How does a lateral geniculate neuron “know” which axons originated near one another in the retina?
5.1

A

5.1

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18
Q

What two factors determine the development of each brain area?
5.1

A

5.1

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19
Q

Describe the neural development across various brain areas.
Is this relationship linear or logarithmic?
5.1

A

5.1

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20
Q

Describe the evidence for a correlation between brain size and intelligence in humans.
How does this apply to men vs women?
To short people vs tall people?
5.1

A

5.1
not much correlation between head size and intelligence but moderate correlation between brain size and intelligence
-does not apply to men vs women cause on average mens brains are larger but not necessarily skater in general

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21
Q

What are the effects of thyroid deficiency in adulthood?
Compare these with the effects of thyroid deficiency in infancy.
5.1

A

5.1`
lethargy in adults
mental retardation in infants

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22
Q

Describe fetal alcohol syndrome.
How are dendrites affected?
How much alcohol is necessary to produce the syndrome?
5.1

A

condition marked by hyperactivity, impassiveness, difficulty maintaining attention, varying degrees of mental retardation
5.1

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23
Q

What are the effects of prenatal cocaine exposure?
Cigarette smoking during pregnancy?
5.1

A

increased risk of ADD and other behavioural defects.

5.1

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24
Q

What types of behavioural and physiological abnormalities are associated with ADHD and ADD?
5.1

A

5.1

Impulsiveness

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25
Q

What are the two types of stroke and the cause of each?

5.2

A

5.2
ishemic-clot
hemorragic-bleed

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26
Q

In what two ways does a stroke kill neurons?
Describe the sequence of destructive processes in the penumbra.
5.2

A
  1. 2
    - neurons deprived of blood or flooded with blood
    - increased brain pressure
    - impaired Na/K pump=>accumulation of Na inside cells.
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27
Q

What are six treatments that may minimize damage from stroke?
5.2

A

.5.2

  • TPA-breaks up blood clots (need it within 3 hours)
  • cool the brain
  • exposure to cannabinoids (marijuana)=decreases release of glutamate
  • blocking glutamate synapse,
  • blocking Ca entry
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28
Q

list six potential mechanismsm for recovery from brain damage.
5.2

A
  1. 2
    - increased stimulation
    - stimulant drugs such as GABA
    - inject amphetamines but risky
    - block dopamine synapses
    - regrowth of axons
    - axon sprouting aka collateral sprouts
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29
Q

How may learned adjustments in behaviour be promoted?

5.2

A

5.2
practice skills that are impaired by not lost
need to practice soon after damage

30
Q

What is diaschisis?
How is recovery from diaschisis affected by amphetamine or haloperidon?
5.2

A

5.2
decreased acidity of surviving neurons after damage to other neurons
amphetamines enhances movements after damage to cortical region in rats and cats

31
Q

How may crushed, but not cut, axons in the peripheral nervous system form appropriate connections when they regenerate?
Why don’t axons in the central nervous system regenerate?
How might this lack of regeneration be overcome?
5.2

A

5.2
it follows its myelin sheath to the original target.
-CNS-glia cells that rest to CNS damage release chemicals that inhibit growth plus scar formation creates a mechanical barrier. Scientist are working on developing a protein bridge or injecting neurotrophins.
-mTOR deleting gent that inactivates mTOR.

32
Q

Under what conditions is sprouting most likely to be useful?
What evidence suggests that sprouting produces beneficial results?
5.2

A

5.2
axons sprouting
-if the area around damage convey the same/similar information to those that they replace.
-eg if entorhiral cortex is damaged in one hemisphere the axon from the antennal cortex of the hemisphere sprout and take over vacant synapses and take over behaviour however if both sides damaged=>other areas taking over (BAD)

33
Q

What is denervation supersensitivity?

5.2

A

5.2
Process of enhanced response or receptor super sensitivity (dendritic)
Helps compensate for decreased input
can help people with near normal behaviour but sometimes can cause chronic pain.

34
Q

What evidence is there that sensory representations may be reorganized during recovery?
What surprised investigators about the brain of a monkey whose limb had been deafferented 12 years earlier?
5.2

A

5.2

stretch of cortex previously responsive to the limb is now responsive to the face

35
Q

What are some sources of sensory input that can give rise to phantom limbs?
What is the relationship between reorganization of somatosensory cortex and the likelihood of phantom sensations?
5.2

A

5.2
axons that represent the face come to activate the cortical area previously devoted to amputated hand. A touch on the face now produces a sensation in the hand.

36
Q

Why is recovery from brain damage more difficult in old age?
What sometimes happens in old age to functions that had been recovered in young adulthood?
5.2

A

5.2

as we are –we decline however we have a bigger knowledge base

37
Q

What is the Kennard principle?
What evidence supports or refutes it?
5.2

A

5.2

??

38
Q

What are some factors that may determine whether an infant brain is better or less able to recover from brain damage, compared to an adult brain?
5.2

A

5.2

? better able cause axons are still young if minor damage is done

39
Q

How may behavioural interventions facilitate recovery from brain damage?
5.2

A

5.2

practice behaviours not completely list and keep practicing also start as soon as possible

40
Q

What are three potential drug therapies for brain damage?
How may they work?
5.2

A

5.2
TPA for strokes (clot busting)
GABA
Cannabinoids for strokes but best if used before stroke happens.

41
Q

How successful have brain transplants for Parkinson’s disease been?
5.2

A

5.2

not very successful

42
Q

What does the magnetoencephalograph (MEG) measure?
What is an advantage and a disadvantage of MEG?
5.2

A

5.2
Measures faint magnetic fields generated by brain activity
-locates approx activity to within 1 cm
-has excellent temporal resolution showing changes from one to the next

43
Q

What is the principle behind magnetic resonance imaging (MRI)?
What is and advantage and a disadvantage of this technique?
5.2

A

5.2I
standard MRI scans and reord water malice after removal of magnetic field
FMRI modified version of MRI is based on hemoglobin instead of water

44
Q

What is a stereotaxic instrument?
Why is it important to compare sham lesions with actual lesions?
5.2

A

5.2

a device for the precise placement of electrodes in the brain.

45
Q

Antisaccade task

A

a voluntary eye movement away from the normal direction

46
Q

Tissue plasminogen activator (tPA)

A

drug that breaks up blood clots

47
Q

Stroke

A

a temporary loss of normal blood flow to a brain area

48
Q

Stem cells

A

undifferentiated cells that divide and produce daughter cells that develop more specialized properties

49
Q

Proliferation

A

production of new cells

50
Q

Phantom limb

A

a continuing sensation of an amputated body part

51
Q

Neurotrophin

A

a chemical that promotes the survival and activity of neurons

52
Q

Neural Darwinism

A

principle of competition among axons

53
Q

Ischemia

A

type of stroke resulting from a blood clot or other obstruction in an artery

54
Q

Migration

A

movement of brain neurons or glia

55
Q

Nerve growth factor (NGF)

A

a protein that promotes the survival and growth of axons in the sympathetic nervous system and certain axons in the brain

56
Q

Myelination

A

process by which glia produce the insulating fatty sheaths that accelerate transmission in many vertebrate axons

57
Q

Apoptosis

A

a programmed mechanism of cell death

58
Q

BDNF (brain-derived neurotrophic factor)

A

a neurotrophin similar to nerve growth factor

59
Q

Cannabinoids

A

chemicals related to D9-THC

60
Q

Hemorrhage

A

type of stroke resulting from a ruptured artery

61
Q

Focal hand dystonia (musician’s cramp

A

a disorder where one or more fingers is in constant contraction or where moving one finger independently of others is difficult

62
Q

Fetal alcohol syndrome

A

a condition resulting from prenatal exposure to alcohol and marked by hyperactivity, impulsiveness, decreased alertness, varying degrees of mental retardation, motor problems, heart defects, and facial abnormalities

63
Q

Edema

A

accumulation of fluid

64
Q

Closed head injury

A

a result of a sharp blow to the head that does not puncture the brain

65
Q

Collateral sprouts

A

newly formed branches of an axon

66
Q

Deafferent

A

to remove or disable the sensory nerves from a body part

67
Q

Dendrites

A

branching fibers from a neuron that receive information from other neurons

68
Q

Denervation supersensitivity (receptor supersensitivity)

A

increased sensitivity to neurotransmitters by a postsynaptic neron after loss of input

69
Q

Diaschisis

A

decreased activity of surviving brain neurons after damage to other neurons

70
Q

Differentiates

A

to develop the axon and dendrites that give a neuron its distinctive properties

71
Q

Describe the formation of the central nervous system in the embryo. What happens to the fluid filled cavity?

A

embryo is 2 weeks old-the central nervous system begins to form
dorsal surface thickens then long thin lips rise curl and merge forming a neural tube that surrounds a fluid filled cavity.
As the tube sinks under the surface of skin. forward ends enlarges and differentiates into hind brain, midbrain then forebrain.
rest becomes spinal cord fluid filled cavity becomes central canal of the spinal cord and the 4 ventricles of the brain containing CSF.