Brain Development and Neuroplasticity

How much does the brain weight at birth?

~350 grams

How much does the brain weight around the first year?

~1000 grams

How much does an adult brain weight?

~1200-1400 grams

Neurulation

neural plate forms a tube during the early embryonic stage, around 3 weeks after conception

Process of neurulation

The dorsal surface thickens forming a neural tube surrounded by a fluid filled cavity

The forward end enlarges & differentiates into the hindbrain, midbrain & forebrain

The rest of the neural tube becomes the spinal cord and the ventricles (filled with CSF)

What is the last part of the brain to develop?

The telencephalon develops last and encases the diencephalon

Gyri and sulci form around week 40

Spina bifida

a disorder which the embryo's neural tube does not close properly during the first stage of pregnancy

Anencephaly

congenital deformity in which some or all of fetal brain is missing

Stages of neurulation

Proliferation, Migration, Differentiation, Myelination, Synaptogenesis

PMDMS (please make delicious muffins soon)

Proliferation

production of new cells

~125,000 cells in neural tube divid, so ~250,000 new cells born every minute

Migration

the movement of neural cells along radial glial cells in the growing embryo to the correct parts of their body to determine their function

Occurs via chemical paths of guidance proteins (like Hansel and Gretel)

Growth cone

the tip of the growing axon that follows the chemical paths

Some chemicals work by attracting the growth cone at the tip of the axon and others by repelling it

Differentiation

the forming of the axons and dendrites that gives the neuron its distinctive shape and function

Myelination

the process by which glial cells (oligodendrocytes and Schwann cells) produce the fatty sheathe that covers the axons of the neurons

This process occurs throughout life

Synaptogenesis

formation of synapses

Occurs throughout life as we learn, we form new synapses and strengthen existing ones

Neurotrophins

nerve growth hormone factor, promote the survival and growth of neurons

Pruning

cell death, the neurons that do not form functional connections do not survive

The embryo produces many more neurons than it needs

Apoptosis/cell death

any neurons growing toward established connections will die

Teratogens

environmental agents that disrupt a baby's development during prenatal development

Toxic chemicals, radiation, viruses, alcohol, smoking, certain drugs

How do teratogens affect systems

Different systems have different affects to teratogenic interference due to time and type of teratogen

Fetal alcohol syndrome (FAS)

birth defects resulting from excessive maternal drinking (symptoms depending on amount of drinking)

Facial abnormalities

Cognitive issues (maintaining attention, hyperactivity, slower development)

How does FAS interfere with development?

Effects the migration period as the neurons migrate past their points of destination

Suppresses glutamate and enhances GABA release

Neurons receive less excitation

Microcephaly

abnormally small head

Critical period

experience or activity that is ongoing creates the condition where functional maturation connections occur

Lack of stimulation leads to a shrinking of the nervous system

Need to be exposed to stimulus that stimulate pathways or they deteriorate

Critical period for vision

Circuits connecting the eyes to the brain mostly wire up during the first few weeks after birth

Amblyopia/lazy eye

may occur when a child is more than 18 months and has a cataract that goes untreated for more than 1-2 weeks, affected by deprivation of visual field

Harlow's maternal attachment studies and emotional critical period

Critical period for proper emotional development and interpersonal interaction

Baby monkeys taken from their mothers and placed with a wire mother with milk and a soft mother

Genie and language critical period

Lack of stimulating environment for language development decreased the area dedicated for language acquisition therefore Genie could never fully learn to talk

Lasting cognitive effects as a result of missing critical period for language acquisition

Synaptic pruning

elimination of excess cells and neuronal networks that are non-functional or less functional

More efficient cognitive process Too many unnecessary connections are less efficient

After ~10 years until our brain matures, brain circuits are drastically pruned

Neuroplasticity

the brain's ability to change throughout life

Types of neuroplasticity

Immature brain organizes itself

In brain injury, compensates for lost functions/maximize remaining functions

Whenever something new is learned and memorized

Stroke

occurs when blood flow to the brain is disrupted, causing brain cells to die

Infection

encephalitis, exposure to toxic substance

Degenerative disease

Alzheimers, Parkinson's

Types of damage that warrant plasticity

stroke, infection, degenerative disease, Closed/open head injuries, tumor, cerebral edema

Cerebral edema

brain swelling due to an excess of water permitted to flow into the brain extra-cellular space resulting in a loss of BBB integrity

A damaged junction allows for any molecules to pass through the BBB

the injured tissue releases inflammatory mediators that act on the tight junctions of the endothelial cells of the BBB

Diaschisis

decreased brain activity following an injury due to the resting membrane potential becoming messed up if all sorts of molecules go into the brain and neurons cannot generate electrical responses

Penumbra

area around dead cells that is at risk as the BBB is disrupted in that area

Excitoxicity

disruption of the potassium and sodium pump leading to the accumulation of potassium ions inside the penumbral area, too positive inside

toxic positivity

External mechanisms of recovery

Drugs and surgical procedures such as clot blusters to removes clots brain and returns blood to a certain part of the brain

Restore resting membrane potential

Silent / redundant neural pathway

a system of duplicated pathways in the brain that control the same function

Mechanisms of neuroplasticity

if injury occurs the primary axons will

sprout

unmask

Sprouting

new axons grows and re-establishes synaptic connection

Unmasking

silent axon becomes active

Happens faster, pathway is already there

Reorganization of cortical function

neighboring regions are co-opted to compensate for the loss of other regions

The brain reorganizes itself by forming new connections between neurons

Recovery

a combination of injury reversal and neuroplasticity

Injury reversal

Resolution of penumbra area (BBB recovers)

Resolution of diaschisis (capacity to generate electrical responses)

Resolution of edema

Neuroplasticity in recovery

Unmasking

Synaptogenesis

Neurotransmitter alterations (more released)

Rasmussen's Syndrome

chronic focal encephalitis, a rare inflammatory neurological disease in children

Frequent & severe seizures, loss of motor skills & speech, hemiparesis (paralysis on one side of the body), encephalitis, and dementia

Plasticity and experience

Brain uses neuroplasticity to enhance its function in reaction to experience

You use it, or you lose it

Experiences influences the structure of your brain

Enriched environment experiments

Skills training → increase in neuronal network density, but no change in vascular supply to brain

Exercise → increase in vascular supply to brain, no change in neuronal network density

Need both! Stimulating and challenging environments

Stimulating and challenging environments lead to

Greater synaptic density

Increased dendritic branching

Improved cognitive skills

Enhanced recovery from brain injury

Study comparing London bus drivers and taxi drivers

Taxi drivers had a larger posterior hippocampus Used for complex spatial navigation

Taxi drivers have to workout their hippocampus to figure out how to navigate each new path

What drives and stimulates neuroplasticity?

The work is what drives and stimulates neuroplasticity

"Exercising" those areas

Musician studies

Professional musicians have larger motor function and auditory processing areas (30% larger)

Blind studies, braille tactile discrimination test

Parietal activation in sighted people

Occipital lobe activation in blind people Not just for encoding of braille (tactile), but also with auditory recognition and language decoding