Psyc 215A Unit 2 Lecture 1: Brain Development

Front 1

Genie

Back 1

Denied normal human interactions during a critical period, never learned to speak or be 'normal'.

Front 2

Prenatal Stages and Times

Back 2

Zygote (0-2 weeks)
Embryo (2-8 weeks)
Fetus (9-birth)

Hint 2

3

Front 3

Phases of Brain Development

Back 3

Induction of Neural Plate
Neural Proliferation
Migration and Aggregation
Axon Growth and Synapse Formation
Neuron Death and Synapse Rearrangement

Hint 3

5

Front 4

What becomes the neural plate?

Back 4

Patch of tissue on the dorsal surface of the embryo.

Front 5

How is neural plate induction induced and when is it visible?

Back 5

By chemical signals, and at three weeks after conception.

Front 6

Neural Plate Cells

Back 6

Toti- into multi-potent, often referred to as embyonic stem cells, have an unlimited capacity for cell renewable.

Hint 6

3

Front 7

How is the neural tube formed?

Back 7

Neural plate folds to form the neural groove, which then fuses to form the neural tube.

Front 8

What is inside the neural tube?

Back 8

Cerebral ventricles and central canal.

Front 9

How do neural tubes proliferate in humans?

Back 9

Three swellings at the anterior end in humans will become the forebrain, midbrain, and hindbrain.

Front 10

Migration

Back 10

Once cells have been created through cell division in the vebtricular zone of the neural tube, they migrate.

Front 11

Migrating cells

Back 11

They lack dendrites and axons.

Front 12

Types of neural tube migration

Back 12

Radial (moving out, usually via radial glial cells)
Tangential migration (moving up)

Hint 12

2

Front 13

Methods of migration

Back 13

Somal (extension develops and shoots out, drags cell body behind it)
Glial-mediated (cell moves along a radial glial network)

Front 14

Aggregation

Back 14

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

Front 15

Cell-Adhesion Molecules

Back 15

CAMs aid in migration and aggregation. They recognize and adhere to molecules.

Hint 15

2

Front 16

Axon Growth and Synapse Formation

Back 16

Once migration is complete and aggregation has began, axons and dendrites begin to form.

Front 17

Growth Cone

Back 17

At the growing tip of each extension during AGSF, extends and retracts filopodia as if finding its way.

Front 18

Chemoaffinity Hypothesis

Back 18

Hypothesis that says that during AGSF, axons grow and find their way due to postsynaptoc targets release of chemicals. Does not explain circuitous routes that are often taken.

Front 19

The role and origin of chemical signals during axonal growth.

Back 19

Chemical signals exist across the way, attracting and repeling. Such molecules are often released by glia. Adjacent growing axons also provide signals.

Hint 19

3

Front 20

Are mechanisms underlying axonal growth different across species?

Back 20

Nope.

Front 21

What is needed during synapse formation?

Back 21

The presence of glial cells, especially astrocytes. Chemical signal exchange between pre- and post-synaptic neurons.

Front 22

Neuron Death and Synapse Rearrangement

Back 22

50% more neurons than needed are produced; death is normal.

Front 23

Neural Darwinism

Back 23

Cell death and synaptic pruning are like natural selection, the outcome of competition for neural connections and metabolic resources.

Front 24

How do neurons die during NDSR?

Back 24

Failure to compete for chemicals provided by targets. More targets, fewer cell deaths, etc...

Front 25

What happens to cells that fail to establish connections?

Back 25

Neurons that fail to establish connections are likely to die. They undergo apoptosis and are thus pruned in an experience-dependent manner.

Front 26

Synapse Rearrangement

Back 26

Space left after apoptosis is filled by sprouting axon terminals of surviving neurons. This leads to an increased selectivity of transmission.

Front 27

What is postnatal cerebral growth and consequence of?

Back 27

Synaptogenesis, increased dendric branches, different myelination times.

Hint 27

3

Front 28

Possible reason for greater plasticity of younger brains?

Back 28

Overproduction of synapse.

Front 29

Does every area take the same amount of time to myelinate?

Back 29

No. Myelination of sensory areas then motor areas; myelination of prefrontal cortex continues into adolescence.

Hint 29

3

Front 30

What can experience effect in neural development?

Back 30

Early development, maintenance, and reorganization of neural circuits.

Hint 30

3

Front 31

Are effects of experience on development time-dependent?

Back 31

Yes. Critical period and sensitive period.

Front 32

Critical Period

Back 32

Development 'window' during which some event has a long-lasting influence on the brain. eg, imprinting.

Front 33

What doe enriched environments produce?

Back 33

Thicker cortexes, greater dendritic development, more synapses per neuron.

Front 34

Early deprivation of sensory/social experience causes what:?

Back 34

Sensory: Atrophy of dendrites
Social: Negative affect on intellectual and social behavioursn

Front 35

Stress in early life has been associated with?

Back 35

Bigger amygdala, smaller hippocampus, anxiety/depression later in life.

Front 36

Can deprivation be overcome?

Back 36

Only if it is short, eg a few months.

Front 37

Problems with neural development and include and can cause

Back 37

Austism, mental retardation, injury during development causing FAS.

Front 38

Romanian Orphanage Study

Back 38

Dr. Nathan Fox followed a group of children who lived as babies in orphanages around Romania. Kids in orphanages had less gray/white matter, and lower quality brain activity. Also discovered the sensitive period for social development.

Hint 38

4

Front 39

When are behavioural effects of brain damage to a certain area seen?

Back 39

Not until that particular area fully matures, ex: becomes myelinated, etc.

Front 40

What is there evidence of, regarding drugs on a prenatal brain?

Back 40

Psychoactive drugs may increase later drug use. Nicotine/caffeine increase change of learning disabilities and hyperactivity. Drugs also increasr birth defects and produce lower birth weights.

Front 41

Worst and better times for brain injury in humans

Back 41

Worst: Last half of fetal period and first few months after birth.
Better: First few years after birth.

Front 42

Fetal Alcohol Syndrome

Back 42

Causes learning disabilities, hyperactivity and social problems. Varies depending on when and how much alcohol is consumed.

Front 43

Mental Retardation

Back 43

Impaired cognitive functioning due to abnormal brain development.

Front 44

Causes of mental retardation

Back 44

Genetic abnormalities, prenatal exposure to infections/toxins, birth trauma, malnutrition, environmental abnormalities.

Front 45

Three core symptoms of autism

Back 45

Reduced ability to interpret emotions/intentions.
Reduced capacity for social interactions.
Preoccupation with a single subject/activity.

Front 46

Autism facts

Back 46

Intensive behavioural therapy may improve function.
Often considered a spectrum disorder; heterogenous.

Hint 46

2

Front 47

Autistic Savants

Back 47

Intellectually handicapped individuals who display cognitive or artistic abilities.

Front 48

Neural machanisms of autism has implicated:

Back 48

Cerebellum, amygdala, frontal cortex.

Front 49

Lines of research on cortical involvement in autism

Back 49

Possibly dificient in mirror neuron function.
Abnormal response to faces.

Front 50

How do any of us develop a normal brain?

Back 50

Plasticity.
Range of normality.
Plasticity occurs jnto older adulthood.