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163 Cards in this Set

  • Front
  • Back
neural plate
small patch of ectodermic tissue on the dorsal surface of developing embryo; first stage of neural development in all vertebrae
neural tube
Neural tube develops from neural plate; if dysfunction occurs, spina bifada can develop
neural crest
just dorsal to neural tube; formed from cells that break off from neural tube; develop into peripheral nervous system (migrate very far)
the "organizer" cell layer
mesoderm
prenatal brain development phase 1
induction of neural plate
prenatal brain devel phase 2
proliferation
prenatal brain deve phase 3
migration and aggregation
prenatal brain deve phase 4
axon/dendrite growth and synaptogenesis
prenatal brain deve phase 5
cell death and synaptic rearrangement
totipotent
cell has the ability to develop into any type of cell (early stage)
multipotent
neural plate cells can develop into any type of cell in the nervous system
where does cell division occur during proliferation?
ventricular zone
pattern of proliferation is controlled by what?
chemicals released from the organizer areas of neural tube
embryonic cell layers (outer to inner)
ectoderm, mesoderm, endoderm
what form are cells in during migration?
immature (no axons/dendrites)
two directions cells can travel during migration
radially (straight line away from ventricular zone); tangentially (right angle to radial migrations)
two methods of cell migration (in phase 3 of prenatal neural development)
glia-mediated translocation: cells move along glia, looks like a snake swallowing a rat, can only move radially! somal translocation: cell extension reaches out (explorative) and pulls cell along after, retracts extension
why is timing of migration important?
when a cell migrates determines what its role will be; outer layers move first
what guides cells during migration?
chemicals attracting and repelling them
what is aggregation?
migrated cells linking up to form functional relationships
what are cell adhesion molecules? what is a condition that can develop if mutation occurs?
molecules on outer layers of cells that allow cells to recognize and link together; mutation can cause Downe's syndrome
during what phase of prenatal neural development are gap junctions present?
phase three, during aggregation; they don't know why though
what are filopodia?
extensions from growth cones on axons/dendrites
what did sperry's classic study prove?
that neurons have a predetermined way of growing, and do not simply grow in one direction
what are axon and dendrite growth likely guided by?
chemical signals, topographic arrangement (cells in one area grow to same place)
what do we know about synapse formation?
when it occurs (after cell maturity), but not why or how. theory that glia play a role in synaptogenesis
what percentage of neurons die in phase 5 of prenatal neural development? why?
50%! normal and healthy. the extra were redundant and losing them allows the brain more plasticity
two theories of cell death:
necrosis: passive process; cell breaks off and spills contents into extracellular space, causing inflammation
apoptosis: active process; cell without enough neutrophins triggers genetic program that packages up cell material for cell suicide :(, scavenger microglia are alerted and go clean up the mess
why does synapse rearrangement occur?
after cell death, connections are inefficient; rearrangement focus output of neuron onto fewer postsynaptic cells, allowing for more specific and orderly transmission
how does the rate of human brain development compare with other species? how much does brain volume increase after birth?
very slow! volume quadruples from birth to adulthood.
synaptogenesis
creation of new synapses but not new cells; thought to be related to change in function of brain area
differences in rate of synaptogenesis in brain areas:
fastest in primary auditory/visual cortices 7-8mos postnatal; two years for prefrontal cortex
when do primary visual/auditory cortices have the most synapses? prefrontal cortex?
3 years postnatal for prim vis/aud cortices, adolescence for prefrontal cortex
true/false: at adulthood, you have the most synapses and synaptogenesis rate is fastest
FALSE, varies throughout life, adult levels are lower.
increased myelination and increased dendritic branching are responsible for what?
increase in brain volume! (myelination roughly parallels synaptogenesis growth)
describe development of white matter in a lifespan
increases slowly and steadily until adulthood, goes down from there
gray matter development:
happens in an inverted U shape; when a brain area has maximum gray matter (higher than adult levels), this correlates with functional maturity of that brain area
two brain areas that reach functional maturity (maximum gray matter) early:
motor and visual cortices
functions of prefrontal cortex:
-planning/carrying out
-working memory
-decision making
-appropriate social behaviors
what is object permanence? when does it develop?
7-12 months, a baby understands that even if an object is out of sight, it still exists
what is perserverance? when does it develop? what part of the brain is responsible for it?
2nd year of life, baby understands that if an object placed under X several times and then placed under Y once, object will be found under Y. prefrontal cortex!
what are permissive experiences? example?
experiences that trigger genetic programs to be manifested; if experience doesn't happen, gene will not develop. ex) language, as in feral children or Genie's cases.
what are instructive experiences? example?
contribute to the direction of development. ex) language will not develop fully in an unenriched environment, particularly related to wealth.
critical period
if experience does not occur within time frame, skill will not develop. very few true critical periods
sensitive period
if experience does not occur within time frame, will have very weak influence on development. ex) language, specifically grammar
general principle regarding effects of experience on development of neuron circuits:
if neuron circuits, once formed, are not used, they will not survive. if you don't use it, ya lose it, suckaz!
effects of environmental enrichment/deprivation (tested in rats):
enriched environment: perform better on memory and learned behavior tasks, heavier hippocampus, more dendritic branching, more synapses. deprivation: low performance :(
if one area of the brain is not being used, what will happen? example?
another area will take over. if you cover an eye even for a few days during sensitive period of development, there will be permanent synaptic rearrangement
if heavy exposure occurs during development, what effect does this have on brain? example?
brain area will become larger; auditory increases with music exposure
what was the owl experiment? what did it show?
rotated heads 23 degrees, auditory system reorganized 23 degrees to compensate. showed brains plasticity and ability to organize to compensate for changes
when are most neurons formed by? what are the exceptions? what activity possibly influences neurogenesis?
7 months prenatal, except olfactory bulb and hippocampus; physical exercise
monkey experiment:
induced strokes; one monkey was prevented from using "good" arm, the other was not. monkey who couldn't use good arm lost less brain area and recovered more functionality. shows power of cortical rearrangement.
how are skeletal muscles connected to bones? what causes them to move?
connected to bones by tendons, move by contractions,
what are muscles made up of? what controls them?
muscles fibers; innervated by motor axons
how many muscle fibers are controlled by an axon (max and min)?
3 to 1000s.
in absence of stimulus, muscle....
relaxes, duhhh.
how do we get a range of motion?
opposing pairs of muscles at joints
flexor muscles:
bend joints when contracted
extensor muscles:
extend joints when contracted
antagonistic muscles (example too):
opposing sets of muscles, biceps and triceps
what is referred to as the "final common pathway" for movement?
motor neurons, because we only do what they tell us to.
where are cell bodies of motor neurons found?
spinal cord and cranial nerve nuclei (control facial movements)
neuromuscular junctions:
where motor neuron meets muscle fiber
describe acetylcholine's role in neuromuscular junctions
excitatory neurotransmitter; binds to nicotinic acetylcholine receptors on postsynaptic cell, ionotropic and causes sodium channels to open and sodium floods cell, can cause action potential; action potential will produce wave of contractions
what is the activated site on a muscle fiber called?
YOUR MOM. jklolz, motor-end plate
what is a muscle twitch?
a single wave of contractions in the muscle, caused by an action potential arriving in the neuromuscular junction
why does the firing rate of action potential increase in muscles?
to allow an action to have more force
define recruitment
process of increasing the number of motor units firing within muscles to increase force
what type of poisoning causes muscle weakness, paralysis, or even death? what does it do in the neuromuscular junction?
curare poisoning; blocks nicotinic acetylcholine receptors preventing action potentials in neuromuscular junction
what is the disease whose name literally means "muscle weakness"? what type of disease is it? what happens if you have it?
myasthenia gravis, autoimmune disease, immune systems produce protein that attacks nicotinic acetylcholine receptors.
true/false: mary broadfoot walker was the bomb, and the white man screwed her over.
TRUE.
what drug did dr mary walker create? what subsequent drug cures her drug's side effects?
pyridostigmine; atropine (eliminates nausea by blocking acetylcholine receptors in other places)
what do muscle spindles do? where do they send information?
spindles give information about muscle length; attached to a muscle fiber; each sends info to the spinal cord, which sends motor info back to muscle
stretch reflex is:
brief strong contraction of muscle that is temporarily lengthened
how does a reflexive movement work (on knee, for example)?
hit knee, spindle is lengthened causing action potential in sensory neurons, motor neurons have action potentials, muscle contracts
two cortices in the pyramidal system, and their inputs/outputs
secondary motor cortex(made up of supplementary and premotor cortices): sends information to primary motor cortex, gets input primarily from dorsolateral prefrontal association cortex. primary motor cortex: input from secondary, major point of departure for motor signals; the larger the movement area, more skillful the move.
this system crosses over at the medulla.
pyramidal motor system!
what happens if you damage the secondary motor cortex?
difficulty sequencing movements
where does the pyramidal system begin and end?
cortices to spinal cord
name and describe dorsolateral tracts.
dorsolateral cortico spinal tract: direct tract, runs from cortex to spinal cord. dorsolateral corticorubro spinal tract: indirect pathway, go from cortex synapse at red nuclei and then go to spinal cord.
which motor pathway can communicate with the cranial nerves?
dorsolateral corticorubro spinal tract
which set of motor pathways is responsible for the brain's contralateral peripheral control?
dorsolateral tracts (left lobe = right side of body)
name and describe the ventromedial tracts.
ventromedial cortico spinal tract: direct pathway, goes from cortex to both sides of spinal cord. ventromedial cortico brain stem spinal tract: indirect, made up of tectum. tectum colliculi that help process auditory and visual information communicate
true/false: ventromedial tracts are a more concentrated form of communication than the dorsolateral tracts.
false, more diffuse.
loss of skilled voluntary movements; capable of moving with appropriate force/direction/fine tuning, but are unable to sequence properly
apraxia! often not due to damage in motor cortex, sometimes in secondary, but mostly damage is in posterior parietal association cortex
loss of voluntary movement in one side of body, often due to damage in motor cortex
hemiplagia
extrapyramidal systems are primarily composed of _____ and the ______, which help us control _________ and _______ of motions.
basal ganglia, cerebellum, control movements (particularly force), precision
basal ganglia composed of?
caudate and putamen, receptive areas of the basal ganglia. receive info from the substantia nigra (also cortical input). these guys smooth movements out
describe flow of information from substantia nigra to motor cortices, in terms of brain structures.
substantia nigra to basal ganglia (specifically caudate and putamen), send info to globus pallidus, sends info to thalamus, sends info to motor cortices.
what structure degenerates in parkinson's disease, and why does this cause the classic symptoms?
substantia nigra; this is where dopamine is produced, which smooths out our movements.
genetic disorder that begins in basal ganglia; mutated protein kills neurons; affects motor movements and leads to extreme dementia
Huntington's disease :( way way sad
Tourette's syndrome
thought to be a disorder of the basal ganglia; classic symptoms are tics or outbursts.
what do the sensorimotor association areas do?
integrate input from various sensory systems; tell us about our body's surrounding environment so we can move safely
inputs: visual/auditory/somatosensoryoutputs: eye field, secondary motor cortex, dorsolateral prefrontal association cortex
posterior parietal association cortex
dorsolateral prefrontal association cortex
inputs: posterior parietal association cortex
outputs: secondary motor cortex, eye field
inputs and outputs of cerebellum
inputs: vestibular and somatosensory systems, as well as primary and secondary motor cortices
what system is the cerebellum part of?
extrapyramidal system
what does it mean if a function is lateralized?
behavioral and cognitive abilities specialized in one hemisphere
language is lateralized in the ..... (generally)
LEFT hemisphere
true/false: motor abilities and sensation are organized contralaterally
true dat
massive fiber tract bundle that connects hemispheres (though not the only connection)
corpus callosum
t/f: each eye contributes to one visual field
false
left retina receives information from which eye?
right eye
optic chiasm:
place where half of axons from each eye cross over to opposite side of brain
ears are responsible for information only...
from their own side of the head
when you have competing auditory information, what do you pay attention to?
information from opposite side of head
people with severed corpus callosum give us valuable information about what?
asymmetry of the brain
What percentage of people are righties? Of them, how many are life-language dominant? What percentage lefties? How many are left-language dominant? What about the others?
96% righties, 90% of righties left-language dominant. of 10% lefties, 70% left-language dominant. 15% mixed, 15% right-language dominant
Which language dominance test is more reliable? What is the procedure for this test?
Wade test: inject 1/2 brain with tranquilizer and ask patient questions; if she responds, shows which side is dominant
Name the two language dominance tests
Wade's test and the dichotic listening tasks
How do people who speak sign language differ from verbal speakers in hemispheric language dominance?
They don't! Most are left-language dominant. Impairments affect them the same way.
Broca's work indicated what for the first time?
language impairments/disorders are associated with a specific area of the brain
Who is Tan?
Frenchman who could understand well but only verbalize the syllable tan. Broca's patient.
phonemes:
how many does the word "ship" have?
basic speech sounds of a language
3: sh-i-p
morphemes:
how many does "unhappily" have?
smallest unit of language that carries meaning, like root word, prefix, or suffix
3: un happi ly
syntax:
grammatical structure of a language (like where adjectives go in relation to nouns)
semantics:
deepest level of organization in language
Broca's area:
area in left frontal lobe next to motor areas for mouth and tongue, thought to contain programs for speaking words
Wernicke's area:
area in left temporal lobe, thought to contain meaning of all words, immediately adjacent to primary auditory cortex
Arcuate fasciculus:
fiber tract connecting Wernicke's and Broca's areas
Angular gyrus:
involved in reading, connects written words with meaning, located behind Wernicke's area
How does information travel from a heard question in the brain according do the Wernicke-Geschwind model?
question is heard in auditory cortex, info sent to Wernicke's area, then via arcuate fasciculus to Broca's area, then to primary motor cortex
severe language impairment, caused by head injury or stroke
aphasia
impaired language production disorder; name 3 characteristics
Broca's aphasia
1. slow effortful speech
2. syntactically incorrect but with good content words
3. comprehend semantic effects of words, but because of syntax difficulties, can have trouble with simple questions
Wernicke's aphasia characteristics:
1. profound comprehension deficit
2. fluent but meaningless speech
3. phonemic and syntax levels are okay
most debilitating aphasia
global aphasia: all aspects of language function lost
most common aphasia
anomic aphasia: characterized by difficulty finding the right word, not associated with specific brain area
cortical aphasia:
arcuate fasciculus damaged, will understand you but have meaningless yet fluent speech
golgi tendon organs
embedded in tendons, respond to increases in muscle tension, i.e. the pull of the muscle on the tendon
muscle spindle
gives information about muscle length, attached to a muscle fiber
criticism of wernicke-geschwind model
too simplistic; people who have just broca' area removed and no surrounding area have little to no lasting effects
supporters of wernicke-geschwind model
damage done to broca's area that warranted surgery would have resulted in cortical rearrangement of language area
t/f: where a lesion is located in the brain is a stronger determinant of long lasting damage than how much is removed
false, though when more damage is done in the anterior areas of the frontal lobe, that seems to have a large impact.
language deficiency is most pronounced with damage to the...
anterior version of the frontal lobe
t/f wernicke-geschwind model still used today
false
t/f areas of the brain dedicated to language are used exclusively for specialized processes
false, area used for reading also responsible for short term memory
3 components of emotions:
cognitive (feeling or subjective conscious experience), behavioral (overt expression), physical (visceral organs reacting)
emotion:
particular kind of subjective feeling, real or imagined, that has high significance to the individual
3 dimensions of emotions
duration, intensity, and pleasantness
crucial brain area for generating conscious experience
frontal lobe
damage to the ________ cortex can cause flat affect
frontal cortex
two brain areas involved in emotions:
frontal lobe, amygdala
t/f: damage to amygdala prevents someone from making fluid, properly sequenced motor movements
false; amygdala lesion causes difficulty in reading other people's expressions, incapable of forming new fears or aversions
list the brain structures in proper order associated with auditory fear conditioning
natural sound processed by thalamus, sent to auditory cortex and amygdala. from amygdala to hypothalamus, causes sympathetic response. from amygdala to spinal cord, causes behavioral response
what structure causes people to fear a neutral sound after auditory fear conditioning?
the AMYGDALA, ya turkey!
what caused the theory that emotions are on the right side of the brain?
lateralization of expressions (smiles start on the left side of the face!)
t/f the more complex a behavior, the more variability you will find among brain scans
true
James-Lange theory:
object is perceived, physiological response happens, people interpret this response by associating an emotion with it
common sense theory:
object perceived, emotional response, physiological response follows
Cannon-Bard theory:
stimuli perceived, physiological and emotional response happen simultaneously
Modern theory of emotion:
stimuli, physiological response, and emotional response all influence each other equally
What was the Schacter and Singer experiment?
group all given shot of epinephrin, half told to expect feelings of agitation. put in room with rude person; those told about agitation were not bothered by the rude person because they had something to attribute their emotional response to
limbic system:
ring of nuclei and tracts around the thalamus
what did pepez theorize in 1937
that limbic system was the circuitry of emotion; wrong because it's not just one circuitry
when your brain perceives an event that can be interpreted emotionally, it activates these two things:
sympathetic nervous system (fight vs flight response), HPA (hypothalamus pituitary adrenal cortex axis)
what is HPA?
hypothalamus-pituitary-adrenal cortex axis that releases glucocorticoids
most common glucocorticoid in the body:
cortisol
6 universal facial expressions are: ____________ and were theorized by _________ to have come ______ language development
surprise, anger, fear, disgust, happiness, sadness
Darwin
before to give us signaling tools of communication
theory that expression formation influence emotions is called:
facial feedback hypothesis
Duchenne smile and muscle groups:
genuinely happy smile, involved obicularis occuli and zyomaticus major
obicularis occuli
muscles in duchenne smile, involuntary movement
zyomatic occuli
muscles in duchenne smile with voluntary control
facial electromyography studies
tiny little micromovements in face that cannot be controlled give away a poker face if you can perceive them.