B. A neural tube forms around a fluid-filled cavity; develops into hindbrain, midbrain, and forebrain, the central canal, ventricles

C. human brain: 350 grams at birth ,1000 grams at age one, 1,200- 1,400 g as adult

D. The four steps of neuron development:

1. Proliferation: Production of new cells; cells along the ventricles of the brain divide to become neurons and glia

2. Migration: Movement of primitive neurons and glia toward their final destination

3. Differentiation: Neurons developing an axon and dendrites

4. Myelination: In humans: first in the spinal cord then brain. Begins during prenatal

period,continues into adulthood

E. Determinants of Neuron Survival

1. Rita Levi-Montalcini : muscles produce and release nerve growth factor (NGF)

Axons that don't receive enough NGF degenerate and their cell bodies die.

Programmed cell death: apoptosis.

2.. Neurotrophin: a chemical that promotes the survival and activity of neurons. Ex: NGF, brain-derived neurotropicfactor (BDNF). They prevent apoptosis, increase axonal branching, decrease pain and increase regrowth in damaged axons.

3. The developing nervous system produces two or three times as many neurons as will survive. This allows for errors, and to compensate for unpredictable body size variations

F. Pathfinding by Axons

1. Sperry (1943) :severed optic nerve axons will grow back to their original targets in tectum; process depends on chemical gradients in target cells

2. ex: TOPDv : more concentrated in axons of dorsal retina and in ventral tectum

3. Competition among axons in the developing nervous system

Postsynaptic cells strengthen the synapses of some cells and weaken synapses

with others

Neural Darwinism: During development, synapses form randomly before a

selection process keeps some and rejects others (also influenced by chemical

guidance and trophic factors)

G. Fine-tuning development by experience

H. Proportional Growth of Brain Areas

1. Rate and duration of development in one area are closely proportional to the rate and duration in others. In general, the greater the total mass of brain the greater the mass in any given brain area.

2. The relationship between brain size and IQ is unclear.

Developing brain is more vulnerable to malnutrition, toxic chemicals, and infections.

Fetal alcohol syndrome (FAS): Symptoms include decreased alertness, hyperactivity, facial abnormalities, and mental retardation

Prenatal exposure to cigarette smoking is associated with:

· low birth weight and other illness early in life

· Sudden Infant Death Syndrome

· long-term intellectual deficits

· Attention Deficit Hyperactivity Disorder (ADHD)

· impairment of the immune system

· delinquency and crime later in life (sons especially)

A. Causes of Human Brain Damage

1. Closed head injury: A sharp blow to the head that does not actually puncture the brain. The most common cause of brain damage in young people.

2. Stroke (cerebrovascular accident): A temporary loss of blood flow

Ischemia: most common type of stroke; loss of blood flow caused by obstruction of

an artery.

Hemorrhage: Less common type of stroke, bleeding due to the rupture of an

artery.

Cells in immediate vicinity die quickly. Later cells in penumbra die. Reason:

- tissue plasminogen activator (tPA) clot-busting drugs (restore blood flow), or

- drugs that antagonize glutamate activity.

- lower brain temperature to 29 deg Celsius within 30 minutes after stroke

B. Mechanisms of Recovery:Brain-damaged individuals often learn to make better use of unimpaired abilities; many also learn to use abilities that appeared to be completely lost after injury but were only impaired.

Deafferented: Removing the sensory nerves (afferent nerves) from a body

part. Monkeys with a deafferented limb fail to use it because walking on three

limbs is apparently easier than trying to move the impaired limb. However, if

forced they can learn to use the deafferented limb.

Diaschisis: Decreased activity of surviving neurons after other neurons are

destroyed. Behavioral deficits due to diaschisis can sometimes be improved

with the use of stimulant drugs.

Damaged axons hardly regenerate in the mammalian central nervous system

possibly because of too much scar tissue or the presence of growth-inhibiting

proteins.

Collateral sprouts: A newly formed branch from an uninjured axon that attaches

to a synapse vacated when another axon was destroyed. The brain is constantly

losing old synapses and sprouting new ones to replace them.

Denervation supersensitivity: Heightened sensitivity to a neurotransmitter after

the destruction of incoming axons. Heightened sensitivity as a result of inactivity

by an incoming axon is called disuse supersensitivity.

After an injection of 6-OHDA which destroys dopamine neurons, postsynaptic cells

react to the decreased dopamine input by increasing their number of dopamine

receptors. If the 6-OHDA is injected on the left side only, amphetamine

(which increases dopamine release) will work only on the right intact side and

will result in movement on the left. If apomorphine (a morphine derivative

that directly stimulates dopamine receptors) is given the movement will be to

the right as the receptors on the left will be supersensitized.

5. Reorganization of sensory representations

Monkeys that had an entire limb deafferented twelve years previously had a

large stretch of their cerebral cortex (which was previously responsive to that

limb) become responsive to the face. Later researchers found that after

amputation of a limb axons form sprouts not only in the cortex, but also in the

spinal cord and brainstem potentially leading to a phantom limb, a continuing

sensation of an amputated body part.

1. Kennard principle: Recovery from brain damage early in life is more extensive

than after similar damage later in life.

2. The Kennard principle does not apply to many cases; the effects of early brain damage may be greater than, less than, or the same as the effects of later damage (depending on the location of the damage and the tested behavior).

3. Damage to the orbital frontal cortex (an anterior area of the prefrontal cortex) in

monkeys produces deficits on the delayed alternation task at age ~t, but at age 2 the

behavior improves considerably. In contrast, damage to the dorsolateral prefrontal

cortex produces only a moderate deficit on the delayed alternation task in infants;

however, when tested 2 years after the lesion, brain-damaged monkeys exhibit clear

deficits. The apparent reason for this phenomenon is that the dorsolateral prefrontal cortex does not do much during early infancy, but by age 2 (when it

starts assuming important functions) the damage begins to affect behavior.

1. At present therapy consists mainly of supervised practice of the impaired

behaviors. The therapist tries to help the brain-damaged person find their lost skills

or learn to use remaining abilities more effectively.

2. Several drugs have aided recovery from brain damage in animals; so far, we do not know their effect on humans.

Nimodipine is a drug that prevents calcium from entering cells.

Gangliosides (a class of glycolipids---combined carbohydrates and fat molecules) promote restoration of damaged neural tissue.

3. Brain grafts: Replacing dead brain cells with healthy ones from a donor. This

technique has been used most frequently in Parkinson's disease but is still in the

experimental stage.