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48 Cards in this Set
- Front
- Back
sensitive period |
plastic changes ties into relevant goals and brain distributes its functions according to the availability territory |
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hemispherectomy |
complete removal of half of the cerebrum empty half filled filled with cerebrospinal fluid |
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homunculus |
"little man" map of the body |
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myasthenia gravis foundation |
autoimmune disease (destroys things) - destroys acetycholine = post synaptic receptors break down = less muscle movement prob - problems w/ coordination, muscle weakness, and eventually diaphram stops = death - couple years |
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Parkinson's Disease |
substantia nigra (black body) in basal ganglia, produces dopamine = caudate/putamen -loose dop projection w/ age (80-90% gone) -hard time moving/movement poor : shuffle, rigid muscles, postural imbalance, tremor when limbs innactive - resting , stops in action =dimension (over 65 yrs) -Treatment: L-Dopa (precursor from what DA made from) help ramaining DAs, MAO reduces reuptake of dopamine (less effective w/ age) & deep brain stimulation of nigra |
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Huntington's Chorea |
-genetic disease, dominant: 30s/40s, found in defective gene huntingtin protein (can test) -basal ganglia: dopa CAG repeats when should have been cut off = toxic gain of function - too sensitive to neurotrasmitters - over fired and worked = die = can't select proper movement or suppress wrong movement -=uncontrollable, explosive, movement |
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Amphetamines |
make you very awake and alert increases release of dopamine |
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Cocaine |
alertness DA, SHT, NE (dopamine, serotonin, and epinephrine) blocks reupatke mechanism = more molecules in the synapse = find receptors |
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LSD |
alters reality SHT (class of serotonin receptor) increases it's function |
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Heroin/morphine |
opids attaches to endorphine receptors exagonist =???? |
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Tranquilzers |
Benzodiazepines gaba urgeis cell (less GABA), more inhibition =fire effect post facilitate function of GABA urgic cells, more inhibition facilitate more hyperpolarization |
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Prozac/SSRI |
selective serotonin reuptake inhibitors -inhibit reupatke of serotonin = more in synapse =increase in functioning |
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Agonists |
increase synapse functioning 1. increase production og neurotransmitters (more precursor molecholine) 2. promote release of neurotransmitter (venoms) 3. stimulate receptors (nicotine, muscarine) 4. Block breakdown 5. Block re uptake |
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Antagonists |
1. Decrease production (block choline) 2. Block release of neurotrasmitters (curare - can't bind = postsynamptic muscles relaxed) (botox) 3. Block receptors |
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proliferation |
on the wall of neural tube germinal zone: where neurons are made - 9 months for gestation, after a couple weeks - 250,000 (x2) per minute |
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Migration |
radial glia cells: move neurons inside to outside- pass each other @ midline = "talk" and become a functional unit when the settle-move past older neurons = form colums that communicate |
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Differentiation |
produces axon, extends, synapse, then dendrite (wiring program of brain) -rowth cones**: end of axons, check environment 1. substrate: axons looking for certain things it an stick to = their direction 2. Chemical clues: "smells" molecules that are attractive or repulsive (Sperry expirment - point to point map; retina to sup. colliculus ) |
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Cell Death |
x2 more neurons produced than needed - die as you age, = dev normal and expected more neurons in larger, complex environment trophic factors: spinal cord doesn't know where axon go, so 2 targets if postsynaptic receptor already full = neuron dies, connect and send trophic factors |
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synaptogenesis |
formation of synapses between neurons in the nervous system. explosion of synapse formation (millions per second) occurs during early brain development, known as exuberantsynaptogenesis. |
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WT Greendough |
rats in impoverished and rich environments - bigger neurons any age |
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deafferation |
when nerves severed from lost/damaged associated areas brain area gets taken over b neighboring neurons |
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phantom limb pain |
"takeover" not complete, still and expectation of sensor input from that body area magnitude of pain correlated eith the extent of remodeling and reodereing - more change = more pain perception |
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Sensory input effect on on brain circuity |
short and long term changes in output flexibility = optimize allocation of neaural resources increased sensitivity @ loss of other |
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tinnitus |
illusionary, constant ringing in ears w/out input auditory phantom sensation |
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adaptive coding |
more/less neural activity to a function depending on needs - actions fine themselves as required to reflects goals -changes: cell body size, new glia cells/neurons, or more dendrites |
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constraint theory |
constraining function side = forced to use weaker side -strengthen and build those circuits and healthy side can't take over neural resources |
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gating |
ability to allow change only when it is important -new stimulus, what calls for your attention, |
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neuromodulators |
chem signals that gate plasticity |
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cholinergic neurons |
located in the subcortical basal forebrain and releases acetycholine active with learning NOT already established tasks modulated by other neurotransmitters |
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cortex maps |
auditory - tonotopic vision - retinotopic map touch - somatopiic taste smell |
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optic tectum |
visual cortex that connects to the eye connects in prewired way (see world upside down) |
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Adjustment to available brain tissue |
- removed tectum = compressed, normal retinotopic map -new inputs (3rd eye) = shared tectum = shared om strips on retinotopic map - extra brain territory available (1/2 retina) = map spread to use entire tectum |
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aphasia |
language lost/damaged after stroke can recover by language transferring to the right hemisphere NOT b/c left heals |
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neurons function |
depends on connections NOT identity. location One can pick up function of one call that was damaged, although harder second time |
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sensitive period |
young age = permanent changes window of time language: birth to 7, 8-10 harder, after 17 low --proficiency ---bootstrapping from input, - lang acquisition = babbling |
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more plasticity in people with younger ages |
more helpless because so flexible, but have caretakers to help them -more cholinergic transmitters (few inhibitory ones) - "research and development" stage |
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phenomes |
perceptually distinct units of sounds as you have more exposure to mother language, harder to hear/distinguish between those of another culture |
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Roger Sperry |
cut optic nerve and rotated eye 180 degrees -reconnect in original pattern/address versus matching the world chemoaffinity hypothesis incoming axons matched to molecule expressed by destination cell in tectum (wrong - too many) ->tuned for a combination of concentrations experience independent - molcules vs. environment |
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experiences on brain circuits |
genome (coding genes) - rough draft of general circuit (doesn't encode everything) experience fortifies and completes it kitten expereince: needs to be actively involved, paired with movement |
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stabismus |
lazy eye cells involved in binocular vision don't develop = no stereo vision |
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Neuron competetion |
if the cannot find niche, they die; one one can survive |
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ocular dominance columns |
alternating stripes in visual cortex where cells respond to signals from eyes wide -> segreagate into patches synaptic competition |
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pruning |
retraction of axonal branches necrosis uncontrolled fashion of death apoptosis: deliberate, controlled fashion; avoids collateral damage, common embryonicaly -massive die off from competition |
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nerotrophins |
life-preserving chemicals, drives competition -protein factors secreted by neurons target that lead to development, survival, and functioning 1. allows cell to differentiate into next stage of dev or 2. prevents apoptosis- cell death synaptoxins eliminates synapses that fall below a threshold |
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rapid versus slow plasticity changes |
A. already many inhibited neural connections that can take over when original connections loose input B. growth of axons to new places, deafferated areas have new connections to target replacing original ones |
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bionic retinal implant (BRI) |
gas permeable patch, sensitive to light w/ mini electrodes plugged into the back of the eye -for disease where photoreceptors damaged but ganglion cells still function |
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damages to visual areas |
V1 - scotomas - diminished vision/blindness V2 - visual agnosias - recognition, meaning Tertiary - inferior temporal and parietal - lead to specific deficits |
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