Unit 2 review Flashcards
1
Q
if cell reaches wrong target
A
- feels like its in the right spot
- not active when others are active
- apoptosis
2
Q
stem cell
A
- embryonic
- totipotent
- regenerates
3
Q
travel to target
A
- migrate by chemical road signs
- when get close, connect and interact with other neurons
- if other neurons activated at same time, happy and fit in
- use nerve growth factors to determine if in right spot
4
Q
why don’t neurons regenerate
A
- don’t have maternal chemical road signs
- complicated connections
- isolated from outside world, so not exposed to chemical or physical insults
- shielded by BBB
5
Q
3 epochs characterized by apoptosis
A
- ) paranatal- around birth
- ) around 5 yrs old- language cortex killed (Genie)
- ) around 21 yrs old- frontal cortex with cells associated with identity
6
Q
NGF antagonist
A
- bad if inject into brain
- cells kill themselves b/c no brain damage
7
Q
how can lethal gene be dominant
A
- by selfish gene theory doesn’t make sense
- only makes sense if gene kicks in after genes are spread (given to offspring)- Huntington’s
8
Q
L dopa
A
- effective temporarily for parkinsons
- chemical precurser to dopamine- don’t have to wait around for synthesis
- unlike dopamine crosses BBB
9
Q
glutamate
A
- aggravates already hurting cell b/c Na/K pumps not working right
- Glu opens more channels -> bad
- leads to cell death
10
Q
stroke and stimulant
A
- give after penumbra cells have recovered
- worse thing to do immediately
11
Q
severed sensory nerve from brains perspective
A
-identical to missing limb
12
Q
phantom limb
A
- missing extremity which no longer sends input to the brain
- theory- brain interprets noise as sensation
- theory- adjacent nerves connect
13
Q
layout of somatosensory and phantom limb
A
- head next to hand
- if lose part of hand, head area can invade hand area
14
Q
SZ symptoms not until after 20
A
- frontal cortex hasn’t kicked in yet
- if already have preexisting damage from prenatal stress, together with post-adolescent apoptsis leads to frontal lobe damage
15
Q
anti-psychotic drug
A
-targets dopamine receptor and holds on
-dopamine can’t bind
Ex: Haldol
16
Q
overabundance of dopamine
A
- can produce psychotic symptoms
- and can induce parkinsons?
17
Q
positive symptoms
A
- not pleasant
- just means presentation of symptoms normal people don’t have
18
Q
negative symptoms
A
-missing something that other people have
19
Q
what remains in tact for H.M
A
- short term
- everything that paying attention to now
- all implicit in tact
- can learn new skills and retrieve old skills
20
Q
What is lost in H.M
A
- explicit long term
- could not store explicit
21
Q
explicit memories
A
- things you can talk about in words
- storage
- retrieval
22
Q
implicit memories
A
- conditioning
- skill learning
- storage
- retrieval
23
Q
benzodiazepines
A
Ex: Valium
- ease anxiety
- turn down amygdala
- amygdala connected to hippo so hippo suppressed too
- suppressing long term memory
- reversible hippocampus lesion (long term memory deficit)
24
Q
Brenda Milner and mirror drawing
A
- wanted to show he could learn new things
- had to be something H.M did not know at all in past
- demonstrates that he starts out badly and improves with practice
25
london cab drivers and bigger hippo
- drive cabs longer have bigger hippo
| - implies hippo can grow and regenerate
26
fear and sensorimotor conditioning
- different behaviorally
- acquisition of fear is fast b/c associated with danger
- acquisition of sensorimotor is slower
27
extinction
-break connection of neutral and unconditioned stimulus
28
acquisition
-association of neutral and unconditioned stimulus
29
cooling brain
- slowing brain processes and reactions
| - suppression of cerebellum
30
suppression of cerebellum
- GABA, freeze, or poke
- previously learned sensorimotor memories are abolished
- restored after GABA diffuses or brain cools
31
where does sensory motor conditioning reside
cerebellum
32
where does fear conditioning reside
-amygdala
33
Lashley
learning -> damage to lateral temporal -> intact memory
34
Morris
- damage to hippo (also had control group) -> damaged swims around to find island; control swims right to island
* shows hippo damage abolishes storage of a map
35
perseveration
-behavior of Wisconsin card task associated with frontal lobe syndrome
36
Korsakoff's
- lack of impulse control
- widespread lateral temporal damage
- loss of all memories- losing connections (complete)
- can store some memories
- old memories gone, so when answer questions about themselves based on whatever pops in their head
37
frontal cortex in normal individual
- impulse control
| - sculpting identity
38
time course retrograde amnesia
- 2 yrs
- but can remember from 2 years before surgery and back
- due to lateral temporal damage
39
hit head
-lose 2 hrs retrograde amnesia
40
working memory
- associated with flexibility and control
- Phineas Gage (frontal cortical syndrome)
- embodied in frontal cortex
41
explicit long term memories
- H.M and water maze rats suggest medial temporal is implicated in STORAGE of explicit long term memories
- Korsakoff shows that enough damage to lateral temporal leads to loss of actual explicit long term memories
- Lashley showed that memories are spread across lateral
42
cerebellum
-Thompson's blinking bunnies showed that sensorimotor storage in cerebellum
43
output of amygdala
-motor response
| Ex: running away
