Neurodevelopment 2 Flashcards Preview

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Flashcards in Neurodevelopment 2 Deck (19):
1

What can cause degeneration of Neuroplasticity?

Traumatic head injury, Tumour, Infection, Toxic substances (drugs), Radiation, Degenerative conditions, Aging.

2

Post Birth Neurogenisis

In humans majority of neurones have been created at birth

Exceptions:

Cerebellar cells – neurogenesis continues for a few months after birth

Olfactory receptors neurones – replaced throughout life

Hippocampus and some cortical areas – allows lifetime plasticity

3

Neuroplasticity: Degenration Types

Axonal damage – anterograde and retrograde degeneration

Anterograde degeneration: (towards terminals)
decrease connectivity

Retrograde degeneration: (towards soma)
can lead to cell death

4

Neuroplasticity: Regeneration (Neurotrophine)

Family of neurotrophins called nerve growth factor (NGF)

During development - match the correct number of neurons with their targets.

Regulate axonal and dendritic growth, the formation of synaptic structure and connections, and neurotransmitter release.

Promote neuronal cell survival, or cell death, depending on the environment.

5

What is collateral axonal sprouting?

If neurones are stimulated they can form new connections. May be activity dependant because electrical stimulation leads to sprouting.

6

Transplant Neuronal Tissue with Parkinsons

Foetal transplants have been used to restore some motor function. Because the tissue has not been differentialised yet so you can transplant it into the substansia nigra cell so it thinks that it is one of those.

7

What is brain plasticity?

Brain plasticity: capacity of the brain to change in response to chemicals, activity or experience. Donald Hebb said that environmental richness maximises intelligence.

8

Experience and Brain Development

Experience changes the structure of the neurones in the hippocampus and cortex. Animals who live in enriched conditions have larger dendritic fields, more neurones and greater connectivity.

9

The critical period - Konrad Lorenz

A period which the brain is most sensitive to a specific experience. e.g. imprinting. First 6 months after birth are important for a baby's occipital lobe to develop.

10

What can neglect and trauma do?

A child raised in an environment characterized by persisting trauma (e.g., domestic violence, physical abuse) will develop an excessively active and reactive stress-response apparatus. The majority of the stress response systems reside in the brainstem and midbrain (e.g., locus coeruleus). Overdevelopment of these areas, even in the presence of optimal emotional or cognitive experience will result in an altered Cortical Modulation ratio and, a predisposition to act in an aggressive, impulsive, behaviorally reactive fashion.

11

Injury and Brain Development: Vulnerable times in utero

Most vulnerable time is the second/third trimester. Neurotoxic damage in utero: foetal alcohol syndrome. Anoxia in utereo or during birth: cerebral palsy

Early life

Stroke

Intracerebral bleeding

Collision injuries can show some recovery of function

12

FAS - Foetal Alcohol Syndrome

Babies born with this have a particular look, sunken nasal bridge and they have a lack of a philtrum (the gap under your nose)

13

ADHD

Genetic component (multifactorial – many genes involved) – lot of genetic variability
- Distractibility, hyperactivity, impulsivity
- 5% children (greater in boys than girls)
- Smaller brain volumes (especially PFC and cerebellum)
- Delayed cortical thinning
- Reduced signalling in reward pathways

14

Autism

Characterised by rapid brain development within the first 6th months. Increase in both grey and white matter across the brain lobes.

15

What is happening during adolescence?

New synaptic connections are forming, pruning and myelination occurring. The prefrontal cortex is immature: decision making task. Well-developed nucleus accumbens: pleasure and reward
compared to children and adults:
no response to small reward
larger response to medium and large rewards

16

Age-associated memory impairment (AAMI) deficits

NO DEFICITS IN
Implicit memory tasks
Short-term memory tasks
Recognition memory tasks

DEFICITS IN
Free or cued recall
Recollection of original context in which an event occurred
Prospective memory tasks
Working memory tasks

Tasks which require manipulation of information held in the mind while dealing concurrently with further incoming information.

17

Alzheimers Disease

Progressive cognitive decline. Cortical atrophy: frontal , temporal and parietal lobes. Neurofibrillary tangles: breakdown of cytoskeleton.

18

What can reduce AAMI?

Exercise leads to an increase in hippocampal volume and improved spatial memory (Erikson 2011) Drugs/cognitive enhancers, can increase performance on a spatial memory. (Trofimiuk 2010)

19

Genetics and Aging Telemores

Found at the end of a chromosome.
Protect chromosomes (stop them fusing or binding with other DNA).
Cell division - DNA unwraps and is copied - telomere loses a little bit of length. When the telomere becomes too short that cells stop replicating (period of cell senescence). Humans: a cell replicates about 50 times before the telomeres become too short - Hayflick limit.