Genetics, Evolution, Development and Plasticity Flashcards

1
Q

• Does human behavior depend on genetics, environmental influences, or both?

A
  • The Nature-Nuture Issue
  • A review of genetics provides a springboard for evaluating this controversial question
  • Conclusion: BOTH genes and environment affect us, question really is to what degree they do so separately (e.g. sexual orientation and intelligence, is it nature or nurture, and how much?).
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2
Q

Genetic Contribution to Facial Expression

A

Consider facial expressions. A contribution
of the environment is obvious: You smile more when the world
is treating you well and frown when things are going badly.
Does heredity influence your facial expressions? Researchers
examined facial expressions of people who were born blind
and therefore could not have learned to imitate facial expressions.
The facial expressions of the people born blind were
remarkably similar to those of their sighted relatives

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3
Q

Mendelian Genetics

A
  • Mendel demonstrated that inheritance occurs through discrete units of heredity, called genes (19th century munk Mendel)
  • Prior to mendel, thought that inheritance was blending process of egg and sperm (blending process), like mixing paint.
  • Mendel demonstrated that inheritance occurs through genes, and Genes come in pairs, called alleles (one from each parent, e.g. one for blue and one for brown eyes from mom and dad, and are aligned along chromosomes (46, form 23 pairs)
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4
Q

DNA, RNA, Proteins

A

Classically, a gene has been defined as part of a chromosome composed of the double-stranded molecule deoxyribonucleic acid (DNA). However, many genes do not have the discrete locations we once imagined (Bird, 2007). Sometimes several genes overlap on a stretch of chromosome.

Sometimes a genetic outcome depends on parts of two or more chromosomes.
- Often, part of a chromosome alters the expression of another part without coding for any protein of its own.
• A gene is defined as a portion of a chromosome and is composed of deoxyribonucleic acid (DNA)
• DNA serves as a model for the synthesis of ribonucleic acid (RNA)
• RNA is a single strand chemical that can serve as a template/model for the synthesis of proteins (messenger RNA)

DNA contains four “bases”—adenine, guanine, cytosine, and
thymine. The order of those bases determines the order of corresponding
bases along an RNA molecule—adenine, guanine,
cytosine, and uracil. The order of bases along an RNA molecule
in turn determines the order of amino acids that compose
a protein. For example, if three RNA bases are in the order cytosine,
adenine, and guanine, then the protein adds the amino
acid glutamine. If the next three RNA bases are uracil, guanine,
and guanine, the next amino acid on the protein is tryptophan.
- Any protein consists of some combination of 20 amino acids.

  • Proteins determine the development of the body by:
  • Forming part of the structure of the body
  • Serving as enzymes, biological catalysts that regulate chemical reactions in the body

Not all RNA molecules code for proteins. Many RNA molecules perform regulatory functions

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5
Q

• Homozygous gene

A
  • identical pair of genes on the two chromosomes
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6
Q

• Heterozygous gene

A

unmatched pair of genes on the two chromosomes (e.g. one for blue eyes, and one for brown)

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7
Q

• Genes are either dominant, recessive, or intermediate

A
  • A dominant gene shows a strong effect in either the homozygous or heterozygous condition
  • A recessive gene shows its effect only in the homozygous condition
  • The gene for high sensitivity to the taste of phenylthiocarbamide (PTC) is dominant, and the gene for low sensitivity is recessive.
  • An intermediate gene occurs in a phenotype where there is incomplete dominance in the heterozygous condition
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8
Q

• Autosomal genes:

A

all other genes except for sex-linked genes. The autosomal genes are found on autosomal chromosomes (which are all chromosomes except the sex chromosomes)

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9
Q

• Sex-linked genes

A

genes located on the sex chromosomes
• In mammals, the sex chromosomes are designated X & Y
• Females have two X chromosomes (XX)
• Males have an X and a Y chromosome (XY) (contributes either with an X or a Y  determines sex of child)
When biologists speak of sex-linked genes, they usually
mean X-linked genes. The Y chromosome is small, with relatively
few genes of its own, but it also has sites that influence the functioning of genes on other chromosomes.

One sex-linked gene (recessive version) controls red-green color vision deficiency – found on X chromosome – if man has gene = he has deficiency (since he only has one X chromosome) = why more males than females have the deficiency (men have 0.08 probability, but women have 0.08*0.08 probability = very low).

different from sex LIMITED genes (mainly active in one sex, but present in both)

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10
Q

sex-limited genes

A

present in both sexes but active mainly in one sex. Examples
include the genes that control the amount of chest hair in
men, breast size in women, amount of crowing in roosters,
and rate of egg production in hens. Both sexes have the genes,
but sex hormones activate them in one sex and not the other,
or one sex much more than the other. Many sex-limited genes
show their effects at puberty

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11
Q

Genetic Changes

A
  • Genes change in several ways:
  • Mutation: a heritable change in a DNA molecule
  • Microduplication/microdeletion: (During the process of reproduction) part of a chromosome that might appear once might appear twice or not at all
  • Researchers think schizophrenia might be due to microduplication/microdeletion in brain-relevant genes.
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12
Q

Mutation

A

a heritable change in a DNA molecule

Changing just one base in
DNA to any of the other three types means that the mutant
gene will code for a protein with a different amino acid at one
location in the molecule. Given that evolution has already
had eons to select the best makeup of each gene, a mutation
is rarely advantageous. Still, those rare exceptions are important.
The human FOXP2 gene differs from the chimpanzee
version of that gene in just two bases, but those two mutations
modified the human brain and vocal apparatus in several ways
that facilitate language development

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13
Q

Microduplication/microdeletion:

A

(During the process of reproduction) part of a chromosome that might appear once might appear twice or not at all
• Researchers think schizophrenia might be due to microduplication/microdeletion in brain-relevant genes.

When this process happens to just a tiny portion
of a chromosome, we call it a microduplication or microdeletion.
Although it is possible for a microduplication to be helpful,
most are not. Microduplications and microdeletions of
brain-relevant genes are responsible for several psychological
or neurological disorders, probably including some cases of
schizophrenia.

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14
Q

Epigenetics

A

Changes in gene expression can occur without changes in our DNA – what you do any moment affect you now, but also produces epigenetic effects that affect your gene expression for a longer period of time.

A gene may be active in one person and not another. After all, monozygotic (“identical”) twins sometimes differ in handedness, mental health, or other aspects.

Examples:

  • Mice not used to fat food  higher probability of heart disease if exposed to fatty food later.
  • Fear of odor in parent mice  higher sensitivity to odor in offspring.
  • Father mice stress  offspring weakened hormonal response to stresses and altered gene expression in part of the brain.

Epigenetic mechanisms:
e.g. most widely studied: DNA methylation + histone remodelling

chromosomes are found in nucleus – we need to unravel chromosome into chromatim fibers. – chromtin is made up of DNA, which is wrapped around histones (which are proteins).

DNA methylation is the action that occurs when a methyl molecule attaches to a DNA strand. (usually at adenine nucleotide bases I think) – DNA methylation tends to decrease the expressions of adjacent genes on the DNA

Histone remodelling occurs at level of histones. = it is the action that occurs when histones change their shape, and in doing so, changes the shape of adjacent DNA. – histone remodelling can decrease or increase gene expression. (when histone “loosens” = more gene expression)

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15
Q

DNA methylation

A

is the action that occurs when a methyl molecule attaches to a DNA strand. (usually at adenine nucleotide bases I think) – DNA methylation tends to decrease the expressions of adjacent genes on the DNA

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16
Q

Histone remodelling

A

Histone remodelling occurs at level of histones. = it is the action that occurs when histones change their shape, and in doing so, changes the shape of adjacent DNA. – histone remodelling can decrease or increase gene expression. (when histone “loosens” = more gene expression)

An acetyl group loosens histone’s grip and increases gene activation

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17
Q

Heretability

A

• Refers to how much characteristics depend on genetic differences (between 0 (no contribution of genes) to 1 (all contribution of genes))
• Researchers have found evidence for heritability in almost every behavior they have tested
• Almost all behaviors have both a genetic and an environmental component
• Study monozygotic and dizygotic twins
• Study adopted children and their resemblance to their biological parents and adoptive parents (genes vs environment influence) – but beware, biological mother’s prenatal environment can also be of influence, which is still environment, not genetic.
• examine “virtual twins”—children of the same age, adopted at the same time into a single family. They grow up in the same environment from infancy, but without any genetic similarity. Any similarities in behavior imply environmental influences.
• In twin and adoption studies researchers have found evidence for some amount of heritability in basically any characteristic besides religion.
Any estimate of heritability applies only to a particular population at a particular time. (e.g. alcohol abuse may have high heritability in US, but in country with strict norms/prohibited alcohol consumption, heritability might not be expressed much)

Candidate gene approach:
researchers test a hypothesis, such as “a gene that increases the activity of the serotonin transporter may be linked to an increased risk of depression.”

genome wide association study:
examines all the genes while comparing two
groups, such as people with and without schizophrenia. The
problem with that approach is that it tests thousands of hypotheses
at once (one for each gene) and therefore has a risk
of seeing an apparent effect by accident – especially problematic in small samples, but also ethnic groups (some ethnic groups might have higher prevalence of a behavior, and also a gene, possible tagging that gene as a risk factor, without it actually being so)

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18
Q

genome wide association study:

A

examines all the genes while comparing two
groups, such as people with and without schizophrenia. The
problem with that approach is that it tests thousands of hypotheses
at once (one for each gene) and therefore has a risk
of seeing an apparent effect by accident – especially problematic in small samples, but also ethnic groups (some ethnic groups might have higher prevalence of a behavior, and also a gene, possible tagging that gene as a risk factor, without it actually being so)

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19
Q

Environmental Modification

A
  • Traits with a strong hereditary influence can be modified by environmental intervention
  • e.g., PKU: a genetic inability to metabolize the amino acid phenylalanine
  • Environmental interventions can modify PKU by diet (and diet alone)  important to show, even if there are hereditary influences, it can be modified through environment.
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20
Q

How Genes Affect Behavior

A
  • Genes do not directly produce behaviors
  • They produce proteins that increase the probability that a behavior will develop under certain circumstances
  • Genes can also have an indirect affect, e.g. altering your environment, by producing behaviors that alter how people in your environment react to you. (e.g. making you attractive = more people contact you  your genes affected you, by affecting your environment)
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21
Q

The evolution of behavior

A

Evolution is a change over generations in the frequencies of various genes in a population.

We distinguish between two questions: How did some species evolve, and how do species evolve?
Did = from what to what
Do = the process
• Principles: offspring resemble parents,
• Mutations, recombinations, and microduplications of genes introduce new heritable variations
• Certain individuals reproduce more than others do, thus passing on their genes to the next generation. Any gene that is associated with greater reproductive success will become more prevalent in later generations
Breeders choose individuals with a desired trait and make
them the parents of the next generation through a process
called artificial selection. Over many generations, breeders
have produced exceptional e.g. racehorses.
Darwin original idea: nature selects individuals/genes that are more successful (e.g. good at finding food)

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22
Q

Common Misunderstandings about Evolution

A

Does the use or disuse of some structure or behavior cause an evolutionary increase or decrease in that feature?
• Lamarckian evolution: According to this idea, if you exercise your arm muscles, your children will be born with bigger arm muscles  no evidence for this!

Have humans stopped evolving?
• Because modern medicine and welfare can keep almost anyone alive  Flaw: evolution depends on reproduction, not just survival. If people with certain genes have more than the average number of children, their genes will spread in the population.

Does “evolution” mean “improvement”?
• Evolution improves fitness, which is operationally defined as the number of copies of one’s genes that endure in later generations.  if you reproduce and your children survive, then you increase your fitness. – does not directly mean improvement (example: colorful peacock atracs females (adaptive), but in face of a new predator, it becomes maladaptive)

Does evolution benefit the individual or the species?
• Neither, it benefits the genes (e.g. a gene that makes you sacrife yourself for your children benefits the genes, as your children carry them on and reproduce)

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23
Q

Does evolution benefit the individual or the species?

A

Neither, it benefits the genes (e.g. a gene that makes you sacrife yourself for your children benefits the genes, as your children carry them on and reproduce)

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24
Q

Does “evolution” mean “improvement”?

A

• Evolution improves fitness, which is operationally defined as the number of copies of one’s genes that endure in later generations.  if you reproduce and your children survive, then you increase your fitness. – does not directly mean improvement (example: colorful peacock atracs females (adaptive), but in face of a new predator, it becomes maladaptive)

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25
Q

Have humans stopped evolving?

A

• idea: Because modern medicine and welfare can keep almost anyone alive  Flaw: evolution depends on reproduction, not just survival. If people with certain genes have more than the average number of children, their genes will spread in the population.

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26
Q

Does the use or disuse of some structure or behavior cause an evolutionary increase or decrease in that feature?

A

Lamarckian evolution: According to this idea, if you exercise your arm muscles, your children will be born with bigger arm muscles  no evidence for this!

27
Q

Why might altruistic behavior occur?

A

an action that benefits someone other than the actor. A gene that encourages
altruistic behavior would help other individuals survive and spread their genes, at a possible cost to the altruistic individual.
• real altruism, in the sense of helping a nonrelative without quickly getting something in return, is unusual for nonhumans, but common in humans.
• Should altruism reproduce? In theory no - A gene that benefits the species but fails to help the individual dies out with that individual.
• A better explanation is kin selection—selection for a gene that benefits the individual’s relatives. A gene spreads if it causes you to take great efforts, even risking your life, to protect your children, because they share many of your genes, including perhaps a gene for protecting their own children.
• Another explanation is reciprocal altruism, the idea that individuals help those who will return the favor. We tend to be more altruistic to other we have seen help others.
• A third hypothesis is group selection. According to this idea, altruistic groups thrive better than less cooperative ones
o problem: Even if cooperative groups do well, wouldn’t an uncooperative individual within the cooperative group gain an advantage?
o But nonetheless, it works – especially in humans – we can punish or expel uncooperative people.

28
Q

Evolutionary psychology

A

Evolutionary psychology concerns how behaviors evolved.–> how our genes reflect those of our ancestors and why
natural selection might have favored the genes that promote certain behaviors.
Underlying assumption: a behavior ”surviving” natural selection must have some advantage.

e.g. Some animal species have better color vision than others, and some have better peripheral vision. Species evolve the
kind of vision they need for their way of life
e.g. goosebumps – little effect in humans, but in other animals come when cold/frightened  make them look bigger + beter insulation.

29
Q

Maturation/development of the Vertebrate Brain

A
  • CNS begins to form when an embryo is 2 weeks old
  • Most primitive neural tissue is the neural plate – which fold to form the neural groove  neural groove curls around neural tube – something enlarges, form hind mid and form brain – rest becomes spinal tube
  1. The dorsal surface thickens, and then long thin lips rise, curl, and merge, forming a neural tube that surrounds a fluid-filled cavity.
  2. As the tube sinks under the surface of the skin, The forward end enlarges and differentiates into the hindbrain, midbrain, and forebrain
  3. The rest of the neural tube becomes the spinal cord

The fluid-filled cavity within the
neural tube becomes the central canal of the spinal cord
and the four ventricles of the brain, containing the cerebrospinal
fluid (CSF). The first muscle movements start at age
7,5 weeks, and their only accomplishment is to stretch the
muscles. At that age, spontaneous activity in the spinal cord
drives all the muscle movements, as the sensory organs are
not yet functional.

Brain mass:
At birth: 350 grams – 1 year: 1000 g – adult 1300-1400 g

In infancy, primary sensory cortices are the most developed parts. Gyri and sulci mostly formed + their connectionswith the thalamus are fairly well established.

the greatest changes over the first couple of years happen in the prefrontal cortex and other cortical areas responsible for attention, working memory, and decision making - the brain areas that are slowest to develop, such as the prefrontal cortex, are the ones most likely to deteriorate in conditions such as Alzheimer’s.

Nervous system changes rapidly at 3-7 week period, at 7 weeks resembles a person, brain looks like human brain at 11 weeks, at 7 month gyri and sulci, looks pretty much like adult brain at birth (but cellular structures are quite different)

30
Q

The Development of Neurons

A

The development of neurons in the brain involves the following processes:

  1. Proliferation
  2. Migration
  3. Differentiation
  4. Myelination
  5. Synaptogenesis
31
Q
  1. Proliferation
A
  • The production of new cells/neurons
  • Early in development, the cells lining the ventricles divide
  • Some cells become stem cells (and stay where they are) that continue to divide (other cells remain and stay the same, other may become glia, some may migrate)
  • Humans vs chimpanzees: human neurons proliferate for longer
32
Q
  1. Migration
A
  • The movement of the newly formed neurons and glia to their eventual locations (some don’t reach locations until adulthood)
  • Occurs in a variety of directions throughout the brain
  • Chemicals known as immunoglobulins and chemokines guide neuron migration
  • Migration Mostly occurs pre birth, but some also after
33
Q
  1. Differentiation
A
  • The forming of the axon and dendrites that gives the neuron its distinctive shape
  • The axon usually grows first (e.g. during migration, or when its reached the target location), followingly dendrites develop.
34
Q
  1. Myelination
A
  • The process by which glia produce the fatty sheath that covers the axons of some neurons
  • First occurs in the spinal cord and then in the hindbrain, midbrain and forebrain
  • Occurs gradually over time (and decades)

myelination, the process by which glia produce the insulating
fatty sheaths that accelerate transmission in many vertebrate
axons. Myelin forms first in the spinal cord and then in the
hindbrain, midbrain, and forebrain. Myelination continues
gradually for decades and increases as a result of learning a
new motor skill.

35
Q
  1. Synaptogenesis
A
  • The formation of the synapses between neurons
  • (begins before birth) Occurs throughout the life as neurons are constantly forming new connections and discarding old ones
  • Slows significantly later in the lifetime
36
Q

New Neurons Later in Life

A
  • Originally believed that no new neurons were formed after early development
  • Later research suggests otherwise
  • Stem cells: undifferentiated cells found in the interior of the brain that generate “daughter cells” (aka progenitor cells or precursor cells) that can transform into glia or neurons
  • New olfactory receptors also continually replace dying ones (happens in mammals, only in humans early in life)
  • Stem cells differentiate into new neurons in the adult hippocampus of mammals and facilitate learning (1996: sam weaze – even in aging brain, stem cells are capable of making new neurons  neurons can be replaced! But currently very active research area, we don’t know HOW stem cells can replace a dying neuron)
37
Q

How could researchers determine whether new neurons form in the adult brain in humans?

A

radioactive isotope of carbon, 14C. – content (in air) changed after nuclear bombs - Researchers examined
carbon in the DNA of various human cells. Every cell acquires
DNA molecules when it forms and keeps them until it dies.
When researchers examined people’s skin cells, they found a
concentration of 14C corresponding to the year in which they
did the test. That is, skin cells turn over rapidly, and your skin
cells are less than a year old. When they examined skeletal
muscle cells, they found a 14C concentration corresponding
to 15 years ago.
In cerebral cortex: 14C concentration corresponding to the year of the person’s birth  14C concentration of the human hippocampus indicates that we replace almost 2 percent of neurons in that area per year (also happens in striatum/basal ganglia)

38
Q

Pathfinding by Axons

A
  • Axons must travel great distances across the brain to form the correct connections
  • Weiss experiment and theory: The salamander’s extra leg moved in synchrony with its neighbor because each axon found the correct muscle.
  • Research question: Did they (axons) grow at random, or did they grow to a specific target?
  • Sperry’s (1954) research with newts indicated that axons follow a chemical trail to reach their appropriate target – took out newts’ eyes, rotated 180 degrees, put back in – newt had time to recover – then cut optic nerve – allowed newt to recover – the axons reconnected, the newt was able to regrow nerves (newts can do this)  about a month later, newt could see.
  • When sperry dangled food near them, newt would launch in wrong direction = showed newt could regrow axons to reach original target area, and the regrowth happen by a chemical trail to reach appropriate target – what is important: animals wire themselves with precisions = this is how axons choose which path to grow in.
39
Q

Chemical Gradients (axon pathfinding)

A

? We have too few genes for each to code a target location for axon.
A growing axon follows a path of cell surface molecules, attracted
by certain chemicals and repelled by others, in a process
that steers the axon in the correct direction = follow gradient of chemicals

e.g. One
protein in the amphibian tectum is 30 times more concentrated
in the axons of the dorsal retina than of the ventral retina and
10 times more concentrated in the ventral tectum than in the
dorsal tectum.
As axons from the retina grow toward the tectum,
the retinal axons with the greatest concentration of this
chemical connect to the tectal cells with the highest concentration.
The axons with the lowest concentration connect to the
tectal cells with the lowest concentration

40
Q

Duane syndrome

A

When we have abnormal axonal growth, we can have disorders that manifest from this, e.g. duane syndrome.
• 1:1000 births
• the nerves controlling the eye muscles send some of their axons to the wrong destinations (instead of growing to muscles INSIDE, may grow to muscles on OUTSIDE (contract/flex goes wrong = individuals have trouble with orienting their eye placement)

41
Q

Competition Among Axons

A
  • When axons initially reach their targets, they form synapses with several cells
  • Postsynaptic cells strengthen connection with some cells and eliminate connections with others (this depends on pattern of input from axon)
42
Q

Neural Darwinism

A

We are born with overabundance of neurons and connections.
• Some theorists refer to the idea of the selection process of neural connections as neural Darwinism
• In this competition among synaptic connections, we initially form more connections than we need
• The most successful axon connections and combinations survive while the others fail to sustain active synapses (= apoptosis = preprogrammed mechanism of cell death)
• The pruning away of axons happen in experience dependent manner (don’t use it = you lose it)
• But be cautious in analogy to evolution: Mutations in the genes are random events, but neurotrophins steer new axonal branches and synapses in approximately the right direction

43
Q

Neurotropins

A
  • Neurotrophins = Chemicals that promote the survival and activity of neurons - Neurotrophins are essential for growth of axons and dendrites, formation of new synapses, and learning
  • Example: Nerve growth factor (NGF) – type of protein released by muscles that promotes the survival and growth of axons
  • In addition to NGF, the nervous system responds to brain-derived neurotrophic factor (BDNF) and several other neurotrophins
  • (brain has overproduced neurons  applies apoptosis)
  • Axons that are not exposed to neurotropins after making connections undergo apoptosis
  • This is important, results in healthy brain that contains no neurons who has failed to make (necessary) connections.
44
Q

The Vulnerable Developing Brain

A
  • Early stages of brain development are critical for normal development later in life – highly vulnerable to malnutrition, toxic chemicals, and infections that would produce milder problems if occurring at later ages.
  • A mutation on one gene can lead to many defects
  • Chemical distortions in the brain during early development can cause significant impairment and developmental problems
45
Q

Fetal Alcohol Syndrome

A

Developing brain vulnerable to many chemicals, especially alcohol.

A condition that children are born with if the mother drinks heavily during pregnancy
Marked by the following:
• Hyperactivity and impulsiveness
• Difficulty maintaining attention
• Varying degrees of intellectual disability
• Motor problems and heart defects
• Facial abnormalities
Drinking during pregnancy leads to thinning of the cerebral cortex that persists to adulthood – more drinking = larger effects

Physiologically, alcohol exposure causes:
• Short dendrites with few branches
• Suppression of glutamate and enhancement of GABA release
• Less excitation and exposure to neurotrophins than usual and undergo apoptosis

Exposure to alcohol damages the brain in several ways. At
the earliest stage of pregnancy, it interferes with neuron proliferation.
A little later, it impairs neuron migration and differentiation.
Still later, it impairs synaptic transmission - Alcohol kills neurons partly
by apoptosis. To prevent apoptosis, a brain neuron must receive
input from incoming axons (and if more GABA and less glutamate = less input = apoptosis! this NT alteration happens WHILE drinking – AFTER drinking, brain has compensated by building MORE glutamate receptors  when alcohol leaves, glutamate overexcites its receptors, bringing excess sodium and calcium into the cell and poisoning the mitochondria.  cell death)

46
Q

Differentiation of the Cortex

A

Neurons differ in shape and chemistry. When and how does a neuron “decide” which kind of neuron it is going to be?

Immature neurons experimentally transplanted from one part of the developing cortex to another develop the properties characteristic of their new location, but those transplanted later does less so.

Destrying visual part of thalamus in one side of ferrets  the rewired temporal cortex, receiving input from the optic nerve, produced visual responses.

The overall conclusion is that to some extent, the sensory input instructs the cortex about how to develop.

47
Q

Fine-Tuning by Experience

A

• The brain has some ability to reorganize itself in response to experience
• Axons and dendrites continue to modify their structure and connections throughout the lifetime
• Dendrites continually grow new spines (allowing for more surface area)
• The gain and loss of spines indicates new connections are being formed, which relates to learning (new connection = biological basis of learning)
What we see on picture: fish neuron on left = isolation = fewer branches, than on right side (more dendritic branches from enriching environment) -> environment has biological impact (but it looks like the right has more dendrites?)
Example form humans:
humans in a normal environment do better intellectually than children in orphanages where the staff provides little more than minimum care.

Question remains: how much we could increase intelligence beyond normal by providing special training or enhanced experiences.
e.g. teaching children something difficult, like latin, has been assumed to make them smart in other ways too. =
far transfer. (Near transfer occurs if training on one task produces improvement on a similar task.)
 but the effect of far transfer is often week.

effects of computerized programs to practice memory skills may induce Temporary improvement of the skills that were
practiced (near transfer far transfer effects highly debated)

48
Q

Blind people reorganization

A
  • Blind people improve their attention to touch and sound, based on practice.
  • The occipital lobe can adapt to also process tactile and verbal information
  • E.g. blind people processing of Braile in occipital lobe
  • Discriminating Braile during temporary inactivation of the occipital cortex  interferes with blind people’s ability to identify Braille symbols, whereas it does not affect touch perception in sighted people.
49
Q

Music Training and reorganization

A

• The temporal lobe of professional musicians in the right hemisphere is 30% larger than non-musicians
• Thicker gray matter in the part of the brain responsible for hand control and vision of professional keyboard players
• Results suggest that practicing a skill reorganizes the brain to maximize performance of that skill
Studies with MEG, fMRI have shown stronger responses to tones, sounds, speech, etc in musicians compared to nonmusicians. Musicians also tend to have better speech perception, and musicians can quicker learn to distinguish sounds in tonal languages than Chinese.

50
Q

When Brain Reorganization Goes Too Far - musicians cramp

A
  • Focal hand dystonia or “musicians’ cramp” refers to a condition where the reorganization of the brain goes too far
  • The fingers of musicians who practice extensively become clumsy, fatigue easily, and make involuntary movements
  • This condition is a result of extensive reorganization of the sensory thalamus and cortex so that touch responses to one finger overlap those of another
  • Things like changing your position might help alleviate focal hand dystonia – previously thought is was a disorder in the hand (treated with surgery/drugs)
51
Q

Brain Development and Behavioral Development - adolescents

A
  • Adolescents tend to be more impulsive than adults – they also tend to “discount the future” (taking immediate, lower rewards than waiting for higher ones)
  • Adolescents are not equally impulsive in all situations – often depend on (the presence of) peers
  • The prefrontal cortex of adolescents is relatively inactive in certain situations, but this may or may not be the cause of impulsivity

although the prefrontal cortex is indeed not quite
mature in adolescents, its immaturity is only a small part
of the explanation for impulsivity. In laboratory tests most
adolescents inhibit impulses just as well as adults. Most of
the riskiest behaviors, especially antisocial risky behaviors,
come from individuals with a lifelong history of troublesome
behaviors, beginning in childhood and extending into
adulthood (Bjork & Pardini, 2015). Furthermore, if risky,
impulsive behavior were the product of an immature
prefrontal cortex, we should expect it to decline over the
teenage years as the cortex gradually matures. In fact, most
types of risky behavior become more common toward the
later teenage years
A more likely explanation for risky adolescent behaviors is that the brain’s response to rewards, especially anticipation of rewards, increases strongly during the teenage years  seek excitement, especially when trying to impress peers.

52
Q

Brain Development and Old Age

A
  • Some neurons lose their synapses, and the remaining synapses change more slowly than before in response to experiences
  • Brain structures begin to lose volume (frontal volume declines by half a percent each year, starting around 30 years – this is an average, not same for everyone)
  • People decline differently – often those who remain physically fit also retain their cognitive abilities.
  • Old people often have a rich knowledge bank = compensation.
  • Often older people find ways to compensate for this loss of volume (e.g. by activating more widespread brain areas to compensate for decreased arousal in one or two areas)
  • Experiment: blood transfusion from young to old mice increased growth of dendritic spines. (but vice versa slowed synaptic plasticity)
53
Q

Plasticity after Brain Damage

A
  • Almost all survivors of brain damage show behavioral recovery to some degree
  • Some recovery relies on the growth of new branches of axons and dendrites
  • Understanding the processes of recovery will give us new and improved therapies
54
Q

Examples of Brain Damage

A
  • Tumors (abnormal proliferation – CAN be cancerous)
  • Infections
  • Exposure to toxic substances or radiation (e.g. carbonmonoxide poisioning)
  • Degenerative diseases (e.g. parkinson’s, death of dopaminergic neurons in tissues in subcortical structures + Alzheimer’s, destruction of cells/cell death leading to memory impairments)
  • Closed/open head injuries (open = e.g. shot wound, closed = e.g. a fall, hiting your head)
  • A closed head injury refers to a sharp blow to the head that does not puncture the brain
  • One of the main causes of brain injury in young adults
  • After a severe injury, recovery can be slow and incomplete
  • One cause of damage after closed head injury is the rotational forces that drive brain tissue against the inside of the skull. Another cause is blood clots that interrupt blood flow to the brain
  • A stroke/cerebrovascular accident (CVA) is temporary loss of blood flow to the brain
  • Common cause of brain damage in elderly
  • Effects of strokes vary from barely noticeable to immediately fatal
55
Q

Types of TBI (traumatic brain injury)

A
  • A closed head injury refers to a sharp blow to the head that does not puncture the brain
  • One of the main causes of brain injury in young adults
  • After a severe injury, recovery can be slow and incomplete
  • One cause of damage after closed head injury is the rotational forces that drive brain tissue against the inside of the skull. Another cause is blood clots that interrupt blood flow to the brain
  • A stroke/cerebrovascular accident (CVA) is temporary loss of blood flow to the brain
  • Common cause of brain damage in elderly
  • Effects of strokes vary from barely noticeable to immediately fatal
56
Q

Types of Strokes

A

Ischemia: the most common type of stroke, resulting from a blood clot or obstruction of an artery = stop in blood supply.
• TIA: transient ischemic attack “mini-stroke” = really a warning sign of a potential larger ischemic stroke.
• But often they are permanent.
Hemorrhage: a less frequent type of stroke resulting from a ruptured artery  neurons are flooded with excess chemicals.

57
Q

Edema

A

Both ischemia and hemorrhage lead to many of the same problems, including edema

How does stroke cause brain damage at cellular level?
• Edema = The accumulation of fluid in the brain resulting in increased pressure on the brain and increasing the probability of further strokes
• Disruption of the sodium-potassium pump = K+ inside neurons
• Edema and K+ = release of glutamate
• Over excitation  Na+ and other cations to enter cells
• Blocks metabolism in the mitochondria
• Kills the neuron

58
Q

Acute Stroke Treatment

A
  • A drug called tissue plasminogen activator (tPA) breaks up blood clots and can reduce the effects of an ischemic strokes
  • Has to be delivered within a few hours after stroke onset. (4.5 hours) – but often patients don’t realize they have stroke  don’t get there in time.

It is difficult to determine whether a stroke was ischemic or hemorrhagic. Given that tPA is useful for ischemia but could only make matters worse in a hemorrhage, what is a physician to do?
 An MRI scan distinguishes between the two kinds of stroke, but MRIs take time, and time is limited. The usual decision is to give the tPA. Hemorrhage is less common and usually fatal anyway, so the risk of making a hemorrhage worse is small compared to the hope of alleviating ischemia.

Other short-term interventions: block excitation by blocking glutamate receptors – alternatives: cooling the brain, antioxidants, antibiotics, albumin, and treatments affecting the immune system. = good effects in animals, not much in humans (possible because animals were young and healthy, human stroke patients often older and sick).

Exposure to cannabinoids (the chemicals found in marijuana) minimizes the damage caused by strokes in laboratory animals.
• Rationale: cannabinoids decrease the release of glutamate + cannabinoids exert anti-inflammatory effects and alter brain chemistry in several ways that might protect against damage (mostly effective if just before stroke, or shortly after)

  • Research has begun to attempt to save neurons from death by blocking:
  • Glutamate synapses
  • Calcium entry
  • Therapeutic hypothermia
  • Cooling protects the brain after ischemia by reducing overstimulation, apoptosis, and inflammation
  • Often used in cardiac arrest (heart doesn’t pump blood to brain)
59
Q

Later Treatment from Brain Damage

A
  • Following brain damage, surviving brain areas (can) increase or reorganize their activity
  • But sometimes: Diaschisis: decreased activity of surviving neurons after damage to other neurons – occurs really because activity in one area normally stimulates others, so when this activity is removed, the spread of activity is reduced.
  • Drugs (stimulants) may stimulate activity in healthy regions of the brain after a stroke
60
Q

Axonal regrowth

A
  • Damaged axons do not readily regenerate in a mature mammalian brain or spinal cord (a damaged axon cannot regenerate) – (not in CNS, but in PNS axons can regrow.)
  • Collateral sprouting - After a cell loses input from an axon, it secretes neurotrophins that induce other axons to form new branches, or collateral sprouts, that take over the vacant synapses - formation of new branches (from an INTACT axon (as long as it had same job as the now deceased axon) can result in recovery
61
Q

Denervation Supersensitivity

A

if a certain set of synapses
becomes inactive—perhaps because of damage elsewhere in
the brain—the remaining synapses become more responsive,
more easily stimulated. This process of enhanced response,
known as denervation supersensitivity or receptor supersensitivity,
has been demonstrated mostly with dopamine synapses

Denervation supersensitivity helps compensate for decreased
input. However, when either collateral sprouting
or denervation supersensitivity occurs, it can strengthen
not only the desirable connections, but also undesirable
ones, such as those responsible for pain.

  • The heightened sensitivity to a neurotransmitter after the destruction of an incoming axon
  • Can cause consequences such as chronic pain
62
Q

Phantom Limb

A
  • Phantom limb: the continuation of sensation of an amputated body part
  • Supernumerary phantom limbs – illusion of having an extra limb (can feel quite painful)
  • The cortex reorganizes itself after the amputation of a body part by becoming responsive to other parts of the body
  • Original axons degenerate leaving vacant synapses into which other axons sprout – this can lead to the sensation in amputated body part, when other body parts are stimulated – e.g sensation in amputated arm, when cheek is stimulated)
63
Q

Learned Adjustments (when losing sensation of a limb)

A
  • Deafferentated limb: limbs that have lost their afferent sensory input (injury to dorsal root ganglion = deaffrination, brain doesn’t get afferent info)
  • Limb can be used but other mechanisms easier (still has intact ventral motor root, efferent info still possible) – monkey with connection to one afferent connection severed = walked using 3 legs. If both forelimb connections severed = used all 4 (despite not getting afferent input)  they can do it, its just easier not to use damaged limb if it is possible to accomplish task with just the working limbs.
  • Therapy techniques to improve functioning of brain damaged people