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Psych 270 - Midterm 2 > Neural Development > Flashcards

Neural Development Flashcards

1
Q

Genes

A
  • Units of heredity that maintain their structural identity from one generation to another
  • As a rule, genes come in pairs because they are aligned along chromosomes (strands of genes) that also come in pairs
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2
Q

Homozygous

A

-If you have the same genes on your two copies of some chromosome, you are homozygous for that gene

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3
Q

Heterozygous

A

-If you have an unmatched pair of genes, you are heterozygous for that gene

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4
Q

Dominant gene

A

-Shows a strong effect in either the homozygous or heterozgyous condition

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5
Q

Recessive gene

A

-Shows its effect only in the homozygous condition

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6
Q

Sex-linked genes

A

-Are the genes on the sex chromosomes designated X and Y

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7
Q

Autosomal genes

A

-All other chromosomes that aren’t X or Y are called autosomal chromosomes

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8
Q

Sex-limited genes

A
  • Genes that are present in both sexes but that exert their effects primarily in one sex because of activation by androgens or estrogens
  • Examples are 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
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9
Q

Epigenetics

A
  • A field that deals with changes in gene expression without modification of the DNA sequence
  • Epigenetic changes can be inherited, at least for a generation or two
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10
Q

Histones

A
  • Proteins called histones bind DNA into a shape that is more like string wound around a ball
  • The histone molecules in the ball have loose ends to which certain chemical groups can attach
  • To activate a gene, the DNA must partially unwind from the histones
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11
Q

Adding or removing an Acetyl group to histone tails does what?

A
  • Adding an acetyl group to histone tails causes the histones to loosen their grip on the DNA, and therefore facilitates expression of that gene
  • Removing an acetyl group from histone tails causes them to tighten their grip on the DNA, and therefore turns the gene off
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12
Q

Add or removing a methyl group to histone tails does what?

A
  • Methyl groups are usually added or removed at the promoter regions of the beginning of a gene
  • Adding methyl groups (CH3) to a promoter turns OFF a gene
  • Removing a methyl group from a promoter turns ON a gene
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13
Q

Heritability

A
  • Estimate of the degree to which variation in a characteristic depends on genetic variations in a given population
  • Heritability ranges from zero, indicating no genetic contribution to the variation, to one, indicating complete control
  • Remember, any estimate of heritability applies only to a particular population at a particular time
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14
Q

What 3 ways do researchers use to determine the heritability of a characteristic?

A
  1. Twin studies:
    - Monozygotic twin studies = from one egg
    - Dizygotic twin studies = from two eggs
    - “Virtual twin” studies = children of the same age, adopted at the same time into a single family
  2. Adoption studies
  3. Candidate gene approach
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15
Q

Proliferation

A

-The production of new cells

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16
Q

Migrate

A
  • Movement of brain neurons or glia
  • Chemicals known as “immunoglobulins” and “chemokines” guide neuron migration
  • A deficit in these chemicals leads to impaired migration, decreased brain size, and mental retardation
17
Q

Synaptogenesis

A
  • Is the formation of synapses

- It begins long before birth but continues throughout life, as neurons form new synapses and discard old ones

18
Q

Myelination

A
  • 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
19
Q

Neural Darwinism

A

-In the development of the nervous system, we start with more neurons and synapses than we can keep, and then a selection process keeps some of the synapses and rejects others

20
Q

Nerve growth factor (NGF)

A
  • A protein that promotes the survival and growth of the axon
  • An axon that does not receive NGF degenerates, and its cell body dies
21
Q

Apoptosis

A

-A programmed mechanism of cell death

22
Q

Neurotrophin

A
  • A chemical that promotes the survival and activity of neurons
  • Neurotrophins are essential for growth of axons and dendrites, formation of new synapses, and learning
23
Q

Fetal alcohol syndrome

A
  • Children of mothers who drink heavily during pregnancy
  • A condition marked by hyperactivity, impulsiveness, difficulty maintaing attention, varying degrees of mental retardation, motor problems, heart defects, and facial abnormalities
24
Q

Far transfer

A
  • Improvement of a skill due to practice at a dissimilar skill
  • In general, far transfer is a weak effect
25
Q

Near transfer

A

-Occurs if training on one task produces improvement on a similar task

26
Q

Autism Spectrum Disorder

A
  • Family of psychological disorders marked by impaired social and emotional exchange and other symptoms such as:
  • deficits in gestures, facial expressions, and other nonverbal communication
  • stereotyped behaviours, such as repetitive movements
  • resistance to a change in routine
  • unusually weak or strong responses to stimuli, such as indifference to pain or a panicked reaction to a sound
27
Q

Focal hand dystonia (AKA “musicians cramp”)

A

-A disorder where one or more fingers is in constant contraction or where moving one finger independently of others is difficult

28
Q

Korsakoff’s syndrome (AKA Wernicke-Korsakoff syndrome)

A
  • Is brain damage cause by prolonged thiamine deficiency
  • The brain needs thiamine (vitamin B1) to metabolize glucose, its primary fuel. Sever thiamine deficiency is common among people with sever alcoholism who go for weeks at a time on a diet of nothing but alcoholic beverages, lacking in
  • Prolonged thiamine deficiency leads to a loss or shrinkage or neurons throughout the brain, especially in the dorsomedial thalamus, the main source of input to the prefrontal cortex
  • Symptoms include apathy, confusion, and memory loss
29
Q

Confabulation

A
  • A distinctive symptom of Korsakoff’s syndrome, in which patients fill in memory gaps with guesses
  • They tend to confabulate about their own lives (ex. “what did you do last weekend?”) rather than semantic questions like “What is the capital of Russia?”
30
Q

Alzheimer’s Disease

A
  • Condition characterized by memory loss, confusion, depression, restlessness, hallucinations, delusions, sleeplessness, and loss of appetite
  • Alzheimer’s disease becomes more common with age, affecting almost 5% of people between 65-74, and almost half of people over 85.
31
Q

Amyloid-B

A
  • The genes controlling early-onset Alzheimer’s disease cause a protein call amyloid-B to accumulate inside and outside neurons and spread from cell to cell
  • The protein damages axons and dendrites, decreases synaptic input, and decreases plasticity
  • The damaged axons and dendrites cluster into structures called PLAQUES that damage the cerebral cortex, hippocampus, and other areas
32
Q

Tau protein

A
  • Part of the intracellular support structure of axons
  • High levels of amyloid-B cause more phosphate groups to attach to tau proteins
  • The altered tau cannot bind to its usual targets within axons, and so it starts spreading into the cell body and dendrites
  • The areas of cell damage in the brain correlate better with tau levels than with amyloid-B levels
  • The altered tau is principally responsible for TANGLES, structures formed from degeneration within neurons
33
Q

Infant amnesia

A
  • Is the universal experience that older children and adults remember very little of what happened in their first few years of life
  • Early in life the hippocampus rapidly forms new neurons and replaces old ones with new ones. The formation of new neurons facilitates new learning, but as the new neurons and synapses displace old ones, the new learning weakens old memories

Psych 270 - Midterm 2 (3 decks)

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