Development of the Nervous System Flashcards

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1
Q

Introduction - Development of the Nervous System

A

The brain undergoes considerable development through its lifetime. Process starts with a single fertilised egg, ends with a functional adult brain. The brain is plastic, continuously changing in response to its genetic programs and environment. It is altered both by experience and as the brain develops throughout time. Neurodevelopment refers to the development of the brain and is influenced by many factors. Developing neurons undergo 5 different phases in order to become the human brain we know of. Some of these happen in order, whereas others are more long-term or overlap.

  1. Induction of the neural plate
  2. Neural proliferation
  3. Migration and aggregation
  4. Axon growth and synapse formation
  5. Neuron death and synapse rearrangement

A fertilised egg is totipotent, meaning that is has the ability to become any type of body cell. However, 4 days after embryological development, newly created cells lose their totipotency and begin to specialise. At this stage, developing cells are pluripotent, they can give rise to many different types of body cell and have unlimited capacity for self-renewal and become any type of mature cell. As the embryo develops, new cells become increasingly specialised. New cells are multipotent, can only develop into one class of cells e.g. blood cells. Most developing cells eventually become unipotent, they can only develop into one type.

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2
Q

Describe the process of Induction of the Neural Plate (First stage in dev of NS)

A
  • 3 weeks after conception, patch of tissue on dorsal surface of embyro becomes neural plate.
  • NP = Tissue going to develop into nervous system
  • Development induced by chemical signals from mesoderm layer
  • As pulled together, broader areas fuse. Neural tube forms basis of CNS. Neural crest forms basis of PNS.
  • Cells of neural plate often refered to as stem cells which are pluripotent and have unlimited capacity for self-renewal.
  • Growing neural plate folds to form neural groove. Lips of this form the neural tube which becomes the cerebral ventricles and spinal canal.
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3
Q

Describe the process of neural proliferation (2nd stage in neural development)

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  • Tissue which develops into neural tube. recognisble as fluid filled tube. Cells of this increase in species specific ways which results in characteristics.
  • 3 swellings appear at end of neural tube - become the forebrain, midbrain and hindbrain.
  • Pattern controlled by chemical signals from organiser areas of the neural tube - floor plate and roof plate.
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4
Q

Describe the process of migration (Third stage of neurodevelopment)

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  • Cells migrate to the target location by moving through cells already formed.
  • Two types of neural tube migration
  1. Radial Migration = Moving out by moving along radial glial cells in straight line to outer wall of tube
  2. Tangenetial Migration - Moving up, occurs at righ angle ro radial.
  • Two types of migration for developing cells
  • Somal transolation - Growth of extension in direction of migration
  • Glia-mediated migration - Temporary network of radial glia cells appear in developing neural tube and move along radial glia network.
  • Movement guided by environment

Neural crest migration

  • Travels along further distance
  • Guided by chemical signals
  • Glial cellls involved in release of chemical signals
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5
Q

Describe the process of aggregation (third stage in neurodevelopment)

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After migration, cells need to align themselves with other cells and form structures.

Both processes mediated by cell-adhesion molecules.

No synpases or dendrite yet, so have narrow gap junctions.

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6
Q

Describe the process of axon growth (fourth stage of neurodevelopment)

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Once migration complete and structures formed, axons and dendrites begin to grow.

Sperry (1963) tested the chemoaffinity hypothesis which is the hypothesis that postsynaptic surfaces release specific chemical labels which attract target axons in both dev and regeneration.

Found out that axons capable of precise growth by rotating eyes of frogs.

  • When rotated 180 without cutting optic nerve, frog misdirects tongue strikes by 180.
  • Optic nerve cut and eye rotated 180 = first blind, once nerve regen frog misdirects strike by 180. Axons grow back to original synaptic sites.
  • Series of chemical signals attract and repel axonal growth
  • Pioneer growth cones = First travel to route and interact with guidance molecules
  • Fasiculation - Tendency of developing axons to grow along paths established by preding neurons

Topographic Gradient Hypothesis of Axonal Migration

  • Axon targets arrange same way on terminal surface as original
  • Growing axons guided to their target by 2 intersecting chemical gradients
  • Axons maintain spatial relationships with neighbours due to chemical gradients on target cell body
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7
Q

Describe the process of synapse formation (4th stage in neurodevelopment)

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  • Once reached site, need to establish pattern of synapses
  • Need coordinated activity of 2 neurons to create synapse between
  • Depends on prescence of glial cells
  • High levels of cholestrol needed
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8
Q

Describe the process of neuron death & synapse rearrangement (5th stage in neurodevelopment)

A

More neurons are produced than required.

Necrosis - Passive cell death

Apoptosis - Active cell death

  • Safer than necrosis
  • Structures pulled apart carefully
  • Inflammation prevented
  • Consequence of cancer

Triggered by..

  • Some genetically programmed for early death
  • Failure to obtain chemicals, competition

Promoted by neurotrophins which promote growth and survival.

Synapse Rearrangement

  • Space is left when neurons die. Filled by axon terminals.
  • Rearrangement of synaptic connections leading to increased selectivity of transmission
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9
Q

Explain how the human brain is not fully developed at birth

A
  • Find out from animal models. Develops slowly which is unique.

Focus on the Prefrontal cortex

  • Age-related changes in cog function.
  • Role in working memory - Keeping releavnt info accesible for short periods of time while completing task.
  • Planning and carrying out sequences of actions
  • Inhibiting responses inappropriate for current context
  • Following rules of social behaviour
  • Infants don’t display certain cog functions e.g. Piaget.
  • Diamond (1991) says because neural circuity of prefrontal cortex not developed yet. Synaptogenesis not maximal until early in 2nd year.

The brain increases in size due to

  • Synaptogenesis. Differs between regions.
  • Myelination of sensory and motor areas - Increases speed of axonal conduction.
  • Increased dendritic branches - Pattern progresses from deeper to more superficial layers.
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10
Q

Name the types of experience affecting early development

A

Two types of experience

  1. Permissive = Necessary for info in genetic program to be manifiested
  2. Instructive = Contribute to direction of development
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11
Q

Explain how experience affects neuroplasticity in adults

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The mature brain can still change and adapt. Changing the way humans think about selves and those with brain damage.

Hertzog et al. (2008) - Exercise may reduce or delay memory problems.

Muhlnickel et al. (1998) - Tinnitus produces reorganisation of primary auditory cortex.

Elbert et al. (1995) - Musicians who played with left hand have enlarged hand rep area in right somatosensory cortex.

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12
Q

Describe autism and attempts to identify its neural mechanisms

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  • Apparent before age of 3, hetereogenous disorder (impaired in some things, superior in others) with genetic basis
  • Neural mechansims - Damage to some neural structures. Fusiform face area shows less fMRI activity in response to faces. Mirror neurons - role in understanding intentions of others.
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13
Q

Describe Williams Syndrome and attempts to identify its neural mechanisms

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  • People sociable and empathetic, Good language skills, low iq
  • Serious cognitive deficits such as attentional problems and spatial abilities.
  • Missing one of the copies of chromosome 7
  • Thinner cortex and white matter. Thinning in orbiotofrontal cortex and boundary of pariertal and occipital cortex.
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14
Q

Discuss brain tumors as a cause of brain damage and the different types

A

Meningiomas Tumours – Grow between the meninges and 3 membranes covering the CNS.

  • Are also encapsulated tumours – Grow within own membrane, but usually benign.

Infiltrating Tumours – Grow through surrounding tissue.

  • Usually malignant – difficult to remove

Gliomas Tumours – Develop from glial cells and rapidly infiltrate.

Metastatic Tumours – Grow from being transported to the brain through the bloodstream.

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15
Q

Discuss strokes as a disorder of brain damage

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Produce dead tissue area called infarct. Surrounded by dysfunctional area called penumba which is the goal of stroke treatment.

Two types

  • Cerebral Hamemorrhage: Cerebral blood vessel ruptures and blood seeps in and destroys surrounding tissue
  • Cerebral Ischemia: Disruption of blood supply to brain. 3 causes, thrombosis - plug blocks blood, embolism, plug carried and ecomes lodged, Arteriosclerosis, walls of blood vessels thicken and create blockage.

Glutamate important

  • NDMA most involved
  • NA+ and CA2 enter postsynaptic triggering release of glutatame, spreading toxin
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16
Q

Discuss closed-head injury as a cause of brain damage

A

Brain injury which does not penetrate skill.

Contustions - Damage to cerebral circulatory system. Brain bashes against skill. Blood collects in sudural space

17
Q

Discuss infections as a cause of brain damage

A

Invasion of the brain by microorgansisms resulting in infalmmation called encephalitis.

Two types of viral infections

  1. Affinity for neural tissue e.g. rabies
  2. Attack neural tissue, but no special affinity e.g. herpes
18
Q

Discuss neurotoxins as a cause of brain damage

A

E.g. mercury led

Produce toxic psychosis

Some produced by body

19
Q

Discuss and provide examples of neurological diseases associated with brain damage

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Epilepsy - Faults at inhibit synapses causing many neurons to fire in bursts.

Parkinson’s Disease - Movement disorder of old age. Associated with degenration in substantia nigra and little dopamine

Huntington’s Disease - Motor disorder associated with severe dementia.

MS - Attacks myelin of axons in CNS

20
Q

Explain the process of neural degeneration in response to nervous system damage

A

Antereograde degeneration

  • Degeneration of distal segment between cut and synpatic terminals. Swells and breaks off due to being cut off from metabolic centre

Retrograde Degeneration

  • Degeneration of proximal segment between cut and cell body.
  • Slower as regenerating axon makes new synaptic contact
21
Q

Explain the process of neural regeneration in response to nervous system damage

A
  • Non-existent in CNS, but possible in PNS
  • If original Schwann cell myelin sheath intact, regenerating axons may grow through to reach orginal target
  • If nerve severed, may grow into incorrect sheaths
  • If ends widely separated - no meaningful regeneration
  • Schwann cells promote regeneration by producing neurotopic factors which stimulate growth cones, axons and cell adhesion molecules.

Collateral Sprouting = Axon degenerates, axon branches grow out from healthy neurons and synapse at sides vacted by degenerating axon.

22
Q

Explain the process of neural reorganisation in response to nervous system damage-

A
  • Pons et al. (1991) - Mapped primary somatosensory cortex of monkeys whose contralateral arm sensory neurons cut 10 yrs before. Cortical face rep had expanded into orginal arm area.

Investigated in humans using the blind.

Mechanisms of Neural Reorganisation

  • Strengthening of existing connections
  • New connections established by collateral sprouting.
23
Q

Explain how to promote recovery of function after brain damage

A

Difficult to compenstate between true recovery and compenstatory changes as things such as brain swellings can make it look as if there has been an improvement.

Neurotransplantation

  • Transporting foetal tissue, but has limited success in humans
  • Transporting stem cells e.g. embyronic stem cells into damaged rat spinal cord. Those with damage showed improved mobility.

Rehabilitative Training

  • Weiller et al. (1999) - Constaint-induced therapy. Tied down arm for 2 weeks while affected one got training. Increase in performance.
  • Cognitive and physical exercise - Active individuals less likely to get neurlogical disorders. However, problems in measurement.

Promoting Regeneration

  • Induce in the CNS but directing growth of axons by Schwann cells.
  • Also by neuroprotective molecules
24
Q

Describe Phantom Limb syndrome and adult plasticity

A
  • Claims that it is due to reorgnaisation of the somatosensory cortex
  • Feels touch on face and phantom limb due to proximity on somatosensory cortex
  • 20% of those born without limbs report this
  • 50% of ppl experience severe pain in limbs
25
Q

How is development time-dependent?

A

Critical period - If occur without, have no effect

Sensitive period - Period when most sensitive

26
Q

What are Topgraphic Sensory Cortex Maps and what do they show?

A

Knudsen & Brainard (1991) - Owls with vision deplacing prisms on eyes. Led to change in auditory spatial map in tectum. Owl with prisms that shifted visual world to 23 degrees to right had auditory map which shifted 23 to right.

Shows how experience can affect early development

27
Q

How can early experience affect songbirds?

A

Bolhuis, Okanoya & Scharff (2010)

  • Songbirds produce 2 classifications of vocalisations, calls and songs.
  • If reared in isolation with no tutor, birds sing abnormal songs in subsong period.
  • Defeanded birds after critical period: Abnormal song
  • Defended birds after crysallised song: Normal singing
28
Q

How can experience affect deprivation of the eye?

A

Deprivation on ocular dominance columns in PVC

  • Depriving one eye of input for early days of life has lasting adverse effect, but doesn’t happen if other eye also blindfolded
    • 1 Blindfolded = Ability of eye to activate VC reduced, ability of other eye increased. Early deprivation changes pattern of synpatic input into layer IV of PMC. Reorganises the system.
  • Width of clums of input from deprived eye is decreased and width from non-deprived increased