Exam 2

Front 1

sensitive period

Back 1

plastic changes ties into relevant goals and brain distributes its functions according to the availability territory

Front 2

hemispherectomy

Back 2

complete removal of half of the cerebrum

empty half filled filled with cerebrospinal fluid

Front 3

homunculus

Back 3

"little man"

map of the body

Front 4

myasthenia gravis foundation

Back 4

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

Front 5

Parkinson's Disease

Back 5

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

Front 6

Huntington's Chorea

Back 6

-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

Front 7

Amphetamines

Back 7

make you very awake and alert

increases release of dopamine

Front 8

Cocaine

Back 8

alertness

DA, SHT, NE (dopamine, serotonin, and epinephrine)

blocks reupatke mechanism = more molecules in the synapse = find receptors

Front 9

LSD

Back 9

alters reality

SHT (class of serotonin receptor)

increases it's function

Front 10

Heroin/morphine

Back 10

opids

attaches to endorphine receptors

exagonist =????

Front 11

Tranquilzers

Back 11

Benzodiazepines gaba urgeis cell (less GABA), more inhibition

=fire effect post facilitate function of GABA urgic cells, more inhibition

facilitate more hyperpolarization

Front 12

Prozac/SSRI

Back 12

selective serotonin reuptake inhibitors

-inhibit reupatke of serotonin = more in synapse =increase in functioning

Front 13

Agonists

Back 13

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

Front 14

Antagonists

Back 14

1. Decrease production (block choline)

2. Block release of neurotrasmitters (curare - can't bind = postsynamptic muscles relaxed)

(botox)

3. Block receptors

Front 15

proliferation

Back 15

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

Front 16

Migration

Back 16

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

Front 17

Differentiation

Back 17

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 )

Front 18

Cell Death

Back 18

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

Front 19

synaptogenesis

Back 19

formation of synapses between neurons in the nervous system. explosion of synapse formation (millions per second) occurs during early brain development, known as exuberantsynaptogenesis.

Front 20

WT Greendough

Back 20

rats in impoverished and rich environments - bigger neurons

any age

Front 21

deafferation

Back 21

when nerves severed from lost/damaged associated areas

brain area gets taken over b neighboring neurons

Front 22

phantom limb pain

Back 22

"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

Front 23

Sensory input effect on on brain circuity

Back 23

short and long term changes in output

flexibility = optimize allocation of neaural resources

increased sensitivity @ loss of other

Front 24

tinnitus

Back 24

illusionary, constant ringing in ears w/out input

auditory phantom sensation

Front 25

adaptive coding

Back 25

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

Front 26

constraint theory

Back 26

constraining function side = forced to use

weaker side

-strengthen and build those circuits and healthy side can't take over neural resources

Front 27

gating

Back 27

ability to allow change only when it is important

-new stimulus, what calls for your attention,

Front 28

neuromodulators

Back 28

chem signals that gate plasticity

Front 29

cholinergic neurons

Back 29

located in the subcortical basal forebrain and releases acetycholine

active with learning NOT already established tasks

modulated by other neurotransmitters

Front 30

cortex maps

Back 30

auditory - tonotopic

vision - retinotopic map

touch - somatopiic

taste

smell

Front 31

optic tectum

Back 31

visual cortex that connects to the eye

connects in prewired way (see world upside down)

Front 32

Adjustment to available brain tissue

Back 32

- 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

Front 33

aphasia

Back 33

language lost/damaged after stroke

can recover by language transferring to the right hemisphere NOT b/c left heals

Front 34

neurons function

Back 34

depends on connections

NOT identity. location

One can pick up function of one call that was damaged, although harder second time

Front 35

sensitive period

Back 35

young age = permanent changes

window of time

language: birth to 7, 8-10 harder, after 17 low --proficiency

---bootstrapping from input, - lang acquisition = babbling

Front 36

more plasticity in people with younger ages

Back 36

more helpless because so flexible, but have caretakers to help them

-more cholinergic transmitters (few inhibitory ones)

- "research and development" stage

Front 37

phenomes

Back 37

perceptually distinct units of sounds

as you have more exposure to mother language, harder to hear/distinguish between those of another culture

Front 38

Roger Sperry

Back 38

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

Front 39

experiences on brain circuits

Back 39

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

Front 40

stabismus

Back 40

lazy eye

cells involved in binocular vision don't develop = no stereo vision

Front 41

Neuron competetion

Back 41

if the cannot find niche, they die; one one can survive

Front 42

ocular dominance columns

Back 42

alternating stripes in visual cortex where cells respond to signals from eyes

wide -> segreagate into patches

synaptic competition

Front 43

pruning

Back 43

retraction of axonal branches

necrosis uncontrolled fashion of death

apoptosis: deliberate, controlled fashion; avoids collateral damage, common embryonicaly

-massive die off from competition

Front 44

nerotrophins

Back 44

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

Front 45

rapid versus slow plasticity changes

Back 45

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

Front 46

bionic retinal implant (BRI)

Back 46

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

Front 47

damages to visual areas

Back 47

V1 - scotomas - diminished vision/blindness

V2 - visual agnosias - recognition, meaning

Tertiary - inferior temporal and parietal - lead to specific deficits

Front 48

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Back 48

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