Brain and Behavior - University of Texas at Arlington - Chapter Four

Sex-Linked Genes

Genes located on sex chromosomes. Like the gene that causes colorblindness, which is located on the X sex chromosome. This is why colorblindness is more common for males, because having just one affected X chromosome will alter their gene expression.

Sex-Limited Genes

These are genes present in both sexes, but mainly or exclusively have effects in one sex. These genes exert differential effects on males and females, because their effects are activated and regulated by sex hormones.

Heritability

An estimate of how much of the variance in some characteristic id due to genetic variation. Genetic variations depend on combined influence of many genes and environmental changes. Studied in three ways: through monozygotic twins (identical), dizygotic twins (fraternal), and adopted children with their biological parents.

Mutation

A heritable change in a DNA molecule. Might be a result of microduplications or microdeletions of genes.

Epigenetics

A field that is concerned with changes in gene expression without the modification of the DNA sequence, but these are due to interaction with environment.

Embryo Development of The Brain

The humans central nervous system begins to form when the embryo is about two weeks old. Development begins from a neural plate. The dorsal surface folds and thickens forming a neural tube surrounding a fluid-filled cavity. The fluid-filled cavity becomes the central canal and the four ventricles. The neural tube eventually develops into the brain and spinal cord. The neural plate eventually sinks under the surface of the skin.

Proliferation

Refers to the production of new neurons in the brain, which primarily occurs early in life. Early in development from the neural tube, those cells lining the ventricles divide. Most neurons, once produced, migrate to other areas.

Stem Cells

Cells that remain alongside the ventricles and continue to divide, responsible for producing more neurons.

Migration

Refers to the movement of the newly formed neurons and glia to their eventual locations. Most active early in development. Some cells do not reach their destinations until adulthood.

Immunoglobins and Chemokines

Vital in the process of migration. Guide new cells to their eventual destination in the brain.

Differentiation

Refers to the forming of the axons and dendrites that give the neuron its distinct shape. The axon grows first either during migration or once it has reached its target and is then followed by the development of the dendrites.

Myelination

Refers to process by which glia produce the fatty sheath that covers the axons of some neurons. Starts first in the spinal cord then in the hindbrain, midbrain. and forebrain. Begins during the prenatal period and continues throughout life, however, its affected by life experiences via active learning and can be modified.

Synaptogenesis

Refers to the formation of the synapses between neurons; this is the final stage of neural development. Occurs throughout life as new connections are made and old ones are discarded but slows significantly later in life.

Do adult humans continue to proliferate?

Originally thought that proliferation ends in the early stages of development but some exceptions have been found. Stem cells in olfactory cells remain immature throughout life. They occasionally divide and one half differentiates to replace a dying olfactory receptor. Thus, proliferation depends on brain/body regions: different cells have different average life spans. Skin cells tend to regenerate frequently, while heart cells and cerebral cortical cells hardly/don’t regenerate.

The Rule of Differentiation

When a cell differentiates, it will find its way to the correct location. This is done by a process of chemical trails.

Dr. Sperry’s Research

A US neuropsychologist and neurobiologist, conducted a study in 1943 in order to determine how axons found their way to the corresponding structures in the brain. The cortical nerves of newt’s were cute and allowed to regrow to see if they would reconnect in the same place after the eye was rotated 180 degrees. They did, causing the new to see everything upside down and backwards.

Chemical Gradients

Growing axons reach their target area by following a gradient of chemicals in which axons are attracted by some chemicals and repelled by others.

Topography Dorsoventral (TOPDV)

A protein primarily located in the retina and tectum. Likely the chemical gradient by which axons connecting the retina and tectum find their way. Concentrated mostly in dorsal retina axons and the ventral tectum, and least concentrated in the dorsal tectum and ventral retina axons. High concentration areas connect to each other just as low concentration areas connect to each other.

Theory of Competition

Theory that states when axons reach their targets, they form more synapses than they need with many target cells. Over time, some connections are fostered by target cells while others are left to whither away over time. This is likely due to competition with other axons. Referred to as “neural-Darwinism” or “natural bio-evolution”. The number of successful connections would determine the number of synapses.

Determinants of Neuronal Survival

The innervated cells. Rita Levi-Montalcini discovered that target cells do not determine the number of neurons produced, but the number that survive. Target cells, in this case muscles, produce Nerve Growth Factor (NGF). If the axon doesn’t receive enough NGF from the target, it will degenerate and die. All neurons are born with this suicide program and will automatically die if the right synaptic connection is not made.

Apoptosis

Programmed cell death

Nerve Growth Factor (NGF)

A substance which promotes the survival and growth of axons.

Brain-Derived Neurotrophic Factor (BDNF)

A brain-derived protein which determine survival of neurons, specifically sympathetic and sensory neurons. Most abundant neurotrophin in the adult mammalian cortex.

Neurotrophins

Proteins that determine survival, function, and development of sympathetic and sensory neurons. After maturity, neurotrophins are no longer used to trigger apoptosis, and are instead used to increase branches of axons and dendrites throughout life. Decrease of neurtrophins leads to brain shrinkage and is linked to several brain diseases.

Vulnerable Developing (Immature) Brain

During differentiation, myelination, and synaptogenesis. Early stages of brain development are critical for normal development later in life. Much more vulnerable to environmental changes like malnutrition, toxic chemicals, and infections.

Fetal Alcohol Syndrome (FAS)

A condition where children are born and the mother drank heavily during the pregnancy. The condition is marked by hyperactivity, impulsiveness, difficulty in maintaining attention, varying degrees of mental retardation, motor problems, heart defects, and facial abnormalities (wide-set eyes with drooping eyelids, short upturned nose, thin upper lip, and flattened vertical groove between mouth and nose). The dendrites of these children are short with few branches and they experience thinning of the cerebral cortex (this interferes with neuron proliferation early in pregnancy and neuron migration and differentiation later in development). Exposure to alcohol in the fetal brain suppresses glutamate and enhances GABA release. Consequently, many neurons recieve less excitation and less neurotrophins than usual and undergo apoptosis.

What prenatal exposure can increase the likelihood of ADHD developing in children?

Exposure to cocaine.

Differentiation - Passive Experience

Your environment affects how your brain develops. Researchers damaged parts of a young ferret’s brain so that cortical nerves would attach a part of the brain that processes auditory stimulus. This resulted in the auditory processing part of the brain taking on most of the characteristics/functions of a visual processing part of the brain. This suggests that sensory input influences how our brains develop.

Differentiation - Active Learning

Because of the unpredictability of life, we have evolved the ability to redesign our brain in response to actively experiencing. In humans, increased size expansion of neurons has also been demonstrated as a function of physical activity.

Dendritic Development in Response to Learning

Axons and dendrites continue to modify their structure and connections throughout their lifetime. Some dendrites continually grow new spines whereas others retract or disappear. About 6% of dendritic spines appear or disappear within one month. This usually indicates new connections from passive or active learning.

Cortical Development in Response to Environment

Rats raised in an enriched environment develop a thicker cortex and increased dendritic branching. In humans, expansion of cortical neurons has been shown in those people as a function of physical activity. The thickness of the cerebral cortex declines with age but occurs less in those who are physically active.

Cortical Development in Response to Active Learning

Adeptness in a skill usually means enhanced activation of a particular cortical area associated with the behavior. Blind people are better at discriminating objects by touch than others and have increased activation in their occipital cortex while performing touch tasks. The occipital has adapted to process tactile and verbal information. Blind people use their occipital cortex while reading braille and have enhanced verbal skills.

Anatomical and Functional Changes of Musicians’ Cortices

The amplitude of responsive activity in the auditory cortex to pure tones is twice as large for professional musicians as for non-musicians. The temporal and frontal cortices of musicians in the right hemisphere are thicker than those of non-musicians. Violin and piano players specifically, have thicker gray matter in the part of the brain responsible for hand control and vision. Musicians who started playing at age 7 demonstrated advantages over those who started later in life.

Reasons for Impulsivity in Adolescents

It has been widely considered that the immature PFC was responsible for the impulsivity of adolescents due to its importance in inhibiting impulses. However, recent studies have shown that an immature PFC is only partly responsible for the impulsivity exhibited by adolescents. After all, if an immature brain was the cause, why then does risky behavior increase in later teen years? The cause is likely how adolescents respond to rewards, especially anticipation of rewards, which strongly increases in later teenage years.

Behavioral Changes at Old Ages

On average, people’s memory and reasoning fade beyond age 60. This is because neurons alter their synapses and synaptogenesis happens much slower. The size of the hippocampus naturally declines and the frontal cortex begins thinning at age 30. Older adults still show higher performances by activating more brain areas to make up for loss of efficiency.

Plasticity

An ability of the brain to accommodate changes due to environmental effects on the brain, like damage. This only occurs on survivors of brain damage.

Stroke

A cerebrovascular accident. There are two types, both make up the major types of damage most commonly seen in the elderly: ischemia & hemorrhage. Damage leads to temporary loss of blood flow to the brain.

Ischemic Stroke

The most common type, results from blood clot or other obstruction blocking blood flow to the brain. As a result, neurons lose their oxygen and glucose supply.

Hemorrhagic Stroke

A less frequent occurrence, results from a ruptured artery. As a result, neurons are flooded with excess blood, calcium, oxygen, and other chemical.

Edema

Caused by the accumulation of fluid in the brain, leads to increased intra-brain pressure thus increasing the probability of further stroke due to suppression on the brain tissue

Effects of Stroke

Disruption of potassium-sodium pump which leads to the accumulation of sodium ions inside neurons. Increased osmotic pressure inside neurons will lead to rupture and eventually cell death.

Neural Cell Loss from Stroke

Strokes destroy neurons leading to cell loss in three waves. First, edemas and excess intracellular sodium trigger the release of the excitatory neurotransmitter glutamate. Then the overstimulation of neurons by glutamate leads to excessive amounts of ions, particularly calcium and sodium, entering the neuron and causing excitotoxicity. Lastly, excessive positive ions in the neuron block metabolism in the mitochondria and kill neurons.

Thrombolytic Therapy

Using drugs that dissolve blood clots after a stroke.

Tissue Plasminogen Activator (tPA)

Clot-busting drugs that break up blood clots and restore blood flow after an ischemia.

Neuroprotectives

Substances that are able to prevent neuron damage/death through several means, such as: blocking glutamate synapses, blocking calcium entry, and lowering brain temperature (cools brain to 29 degrees celsius which lowers metabolic rate and minimizes consumption of nutrition and O2). Cannabinoids have been used to treat strokes because of their anti-inflammatory effects and decrease in glutamate release by activating cannabinoid receptors expressed presynaptically.

Take-Over

After brain damage, one surviving area with the same function more or less takes over the function that is lost.

Compensation

After brain damage, surviving areas do not take over brain functions of damaged areas but compensate in other ways.

Diaschisis

A phenomenon that refers to suddenly decreased activity of surviving neurons after damage to other neurons. This contributes to behavioral deficits following brain damage and increased stimulation should help.

Regrowth of Axons

Destroyed cell bodies cannot be replaced, however, damaged axons do grow back under specific circumstances. The fact is that regeneration is minimal in the mature mammalian central nervous system. Regrowth is affected by: scar tissues, which is more helpful than harmful, and astrocytes, which release chemicals that keep nearby neurons alive. Chances for regrowth are limited in the peripheral nervous system. If an axon in the PNS is crushed, the axon will regrow starting from the target and grow back toward the periphery at a rate of 1 mm a day. If the axon is cut, the myelin sheath may not reconnect accurately and the axon may not have a sure path to follow, this can result in a misaimed axon which can mess up coordination of movements.

Axon Sprouting

After a postsynaptic neuron loses their input from an axon, it releases neurotrophins that induce neighbor axons to form new branches called collateral sprouts that take over the vacant synapses. This can take months or years. This can be helpful or harmful depending on whether the sprouting axons have a similar function to the damaged part. If they are similar this can result in a successful takeover which will restore function. However, if they are not, this can result in compensation of other areas which actually interferes with behavior and prevents recovery.

Denervation Super-sensitivity

Developed in the post-synaptic cell. If some synapses become inactive or die, the remaining synapses in that area become more responsive and more easily stimulated. This is done in order to compensate for lack of axons, so sensitivity increases to get more out of remaining axons. Leads to increased number of receptors and increased effectiveness of receptors. This can sometimes lead to phantom limb pain.

Phantom Pain or Phantom Limb

Involves combination of collateral sprouting and denervation super-sensitivity which contributes to reorginization of sesory representation cortex. For example, the axons that usually correspond to a the fingers next to the middle finger, grow into the space left by the axons connected to the middle finger. This, combined with increased sensitivity of receptors nearby, leads to sensations from the surrounding areas to be registered as sensations felt from the missing limb, and this is usuall painful, again, because of the super-sensitivity. This can be helped by use of a prosthetic.