Week 5: Neurodevelopment and Neuroplasticity Flashcards

1
Q

Development

A

A change in a property of neurobiology over time (ex: myelination, brain growth, etc)

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2
Q

Prenatal development stages

A

1: Induction of the neural plate
2: Neuronal Proliferation
3: Migration
4: Axonal growth
5: Cell death

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3
Q

Stage 1

A

Layers develop 18 days after conception (ecto-, meso-, and endoderm). Stem cells accumulate en mass in the neural plate on the ectoderm. Neuronal tube and basic brain structures form after 24 days

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4
Q

Stem cells

A

Can generate sub-types of cells. Are highly able to differentiate, but after they differentiate they can only produce that type of cell

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5
Q

Stage 2

A

Rapid neuron creation; more than we need. Made in the ventricular zone before migrating to final destination

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6
Q

Stage 3

A

Cells move either radially (out from the center) or tangentially (any other pathway). Deep layers form first, then cells move outwards. Follows aggregation

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7
Q

Aggregation

A

Migrating cells organize themselves in a particular way; mishaps in alignment could correspond to disorders

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8
Q

Stage 4

A

When cells reach their final point, their axons grow toward biologically predetermined destinations. The growth cone at the end of the axon is guided by attractive and repulsive chemicals.

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9
Q

Fascigulation

A

Pioneer axons will blaze a trail that other axons will follow when growing. Leads to the formation of tracts.

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10
Q

Sperry frog experiment

A

Examining if spatial proximity determined axon growth. Cut axons in a frogs eye, then rotated it to see if the axons would reconnect differently. Found that they will still grow toward their original target, even when rotated

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11
Q

Chemoaffinity theory of axon growth

A

Growth patterns are guided by one growth factor per growth pattern.
DISPROVEN: lesion studies found that axons are sensitive to more than one chemical

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12
Q

Topographic gradient hypothesis

A

Concentration of chemicals guides axon growth. Arguing topographic gradient of chemicals

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13
Q

Synaptogenesis

A

Formation of synapses. Facilitated by glial cells. Weaker connection will be pruned or die. Occurs very rarely past a certain developmental point

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14
Q

Neurotrophin hypothesis of synaptogenesis

A

There is a competition for neurotrophin signals; the more you get the more likely you survive

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15
Q

Stage 5

A

Cell death. Apoptosis is programmed and clean; neurosis is spontaneous and messy
Strongest cells are selected for due to limited brain resources

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16
Q

Synapse elimination

A

Facilitated by glial cells. With repeated activation, synapses can get weaker or stronger over time

17
Q

Causes of change in synaptic density

A

The brain grows x4 in size over life (synaptogenesis, dendritic growth, myelination); brain areas mature at different rates

18
Q

Critical period

A

A period of development where stimulus is required for development. End due to limitations on growth and/or myelination

19
Q

Sensitive period

A

A period where stimulus is more powerful in affecting development. Has environmental and psychological factors that motivate or inhibit learning

20
Q

Adult neurogenesis

A

Very rare; only occurs in the hippocampus and the olfactory bulb. New cells take 4-6 weeks to develop and are more plastic and more excitable

21
Q

Benefits of Hippocampal neurogenesis

A

Has been found to improve memory and reduce anxiety. Consistent with the link btw the hippocampus and mood

22
Q

Traits of Neurodevelopmental disorders

A

High heritability; emerge early in life; high comorbidity rate

23
Q

Schizophrenia

A

Symptoms: positive and negative (adding sensation or loss of sensation)
Causes: dopamine transmission defects; excessive pruning of cortical areas; abnormal cell organization
Physiological: reduced grey matter in hippocampus and orbitofrontal cortex
Heterogenous disorder

24
Q

DA Hypothesis of Schizophrenia

A

Too much dopamine in specific pathways (high in mesolimbic, low in mesocortical) correlates with positive symptoms

25
Q

Autism Spectrum Disorder (ASD)

A

Symptoms: poor social interaction, repetitive behaviors, slow language development
Causes: Unknown. Diagnoses are increasing due to awareness and advancements in technology
Physiological: high number of synapses/too much gray matter
Heterogenous disorder

26
Q

Attention Deficit Hyperactivity Disorder (ADHD)

A

Symptoms: inattentive and hyperactivity (can be solo or combined)
Causes: maturational delay in the prefrontal cortex; affects 6-10% of the population; lower dopamine levels
Physiological: reduced cortical volume in the prefrontal cortex
Treatment: icrease dopamine and noradrenergic transmission

27
Q

Psychopathy and Anti-social Personality Disorders (ASPD)

A

Traits: guiltless, manipulative, aware of actions and not changing or caring; typically charismatic and popular
Genetic and environmental risks; difficult to study due to ethics
Physiological: reduced function in frontal cortex and amygdala

28
Q

Low arousal theory of ASPD

A

Reduced response to threats which decreases impulse control and causes a continual need for stimulation