Bethany's flash cards for chapter 10-12 biopsych
1
Q
general adaptation
A
three stages:
alarm
resistance
exhaustion
2
Q
2 predictions with James Lange Theory
A
- people with autonomic/skeletel response should feel less emotion
- increasing one’s response should enhannce an emotion
3
Q
sapolsky
A
agues that nature of today’s crises are more prolonged
-accounts for stress related illness and psychiatric problems in industrial societies
4
Q
personality & brain hemispheres
A
right hemisphere: more socially withdrawn, less satisfied with life more prone to unpleasant emotions
left hemisphere: happier, outgoing, friendly
5
Q
ANS & PNS: emotion
A
emotional situations arouse ANS
each situation evokes sympathetic & parasympathetic respones
6
Q
3 components of emotion
A
cognition
action
feeling
7
Q
damage to ventromedial cortex
A
decreased guilt
8
Q
damage to prefrontal cortex
A
impaired & impulsive decision making
9
Q
5-HIAA
A
- serotonin metabolyte found in CSF, blood, urine
- high levels 5-HIAA: more serotonin release & turnover
- low levels 5-HIAA: greater probability that monkey will attack larger monkeys
- monkeys with high5-HIAA more likely to survive but monkeys with low 5-HIAA more likely to have dominant position in the group
10
Q
Urbach-Wiethe Disease
A
causes calcium to build up in amygdala
case study of SIN
- experiences dangerous fearlessness
- experience anger but not fear in response
11
Q
brain areas involved in moral decisions
A
prefrontal cortex
cingulate gyrus
amygdala
12
Q
James Lang Theory
A
autonomic arousal & skeletel action occurs 1st in an emotion
-we label our physiological responses
13
Q
functions of emotion
A
adaptive values (fear-escape & anger-attack)
make quick decision
moral decisions
14
Q
activation of frontal & temporal areas of left hemisphere
A
associated with “approach” and behavioral activation system
- marked by low-moderate arousal
- can characterize either happiness or anger
15
Q
behavoral inhibition system
A
associated with increased activity of frontal & temporal lobe of right hemisphere
- increases attention & arousal
- inhibits action
- stimulates emotion like fear & disgust
16
Q
interoception
A
self monitoring body
patients who could match tones with heart beat had more active right insular area
17
Q
exhaustion
general adaptation
A
after extended exposure to stress, body may begin to shut down
- weight loss
- depletion of adrenal glands
- enlargement/dysfunction of adrenal glands
- delusion/hallucinations
- inappropriate use of defense mechanisms
18
Q
restistance
general adaptation
A
body adapts to stressor (optimal)
- weight returns to normal
- hormones level out
- intensified use of coping
19
Q
attack & brain
A
increased activity in corticomedial area of amygdala
20
Q
localization & disgust
A
brain attends strongly to facial expressions
emotions tend to not be localized to specific parts of cortex
localization exists for feelings of disgust
-insular & primary taste cortex
21
Q
testosterone effects
A
alters way people respond to stimuli
decreases cerebral cortex ability to identify/regulate emotion
22
Q
alarm
general adaptation
A
immediate reaction to stressor (fight or flight)
- weight loss
- increased hormones
- enlarged adrenal cortex & lymph glands
- increased anxiety
23
Q
leukocytes
A
- B cells: leukocytes that mature in bone marrow & secrete antibodies
- antibodies: y shaped proteins that attach to certain antigens
- antigens: surface proteins that are antibody-generator molecules
T cells: attack intrudes directly & help other other T or B cells to multiply
Natural killer cells: leukocytes that attack tumor cells & cells with viruses
24
Q
HPA axis
A
dominant response to prolonged stressors
activation of hypthalamus
-induces pituitary gland to secrete adrenocorticotropic hormone (ACTH)
-ACTH stimulates adrenal cortex to secrete cortisol
25
stress activates 2 systems in body
sympathetic nervous system (fight or flight)
HPA axis
- hypothalamus
- pituitary gland
- adrenal cortex
26
infection & cytokines
- during infection, leukocytes & other cells produce cytokines
- combat infection & communicate with brain to inform of illness
cytokines in brain produce symptoms of illness
- fever, sleepiness, lack of energy
- sleep & inactivity: ways to conserve energy
27
stress & response
nervous system activates immune system
-immune system increases production of natural killer cells, leukocytes, cytokines
cytokines can trigger symptoms of illness as reaction to stress
28
psychoaneuroimmunology
deals with way in which experience alters immune system
| -deals with how immune system influences CNS
29
amygdala damage in humans
- lost ability to detect averse emotional cues in stimuli
- difficulty identifying fearful facial expressions
- trouble recognizing scrary music
30
hypothalamus
stimulates pituitary gland to secrete ACTH into bloodstream which stimulates adrenal gland
31
emotion in brain
limbic system: includes forebrain areas surrounding thalamus which is critical for emotion
frontal & temporal lobes activated during emotional experience
32
mobius syndrome
body's action not required for emotion
33
James-Longe Theory: Brain damage
| subjective & autonomic response
damage to R somatosensory
- normal autonomic response
- weak subjective experience
damage to PEC
- weak autonomic response
- normal subjective response
34
Increased violence
exposure to lead
trauma in childhood
living in violent neighborhood
35
James-Lange Theory Data
paralyzed people feel same emotion prior to injury
people with "pure autonomic failure" still report feeling emotion but less intensity
-Pure Autonomic Failure: output of ANS to body fails
suggest other factors involved in perception
36
James-Lange Theory : Botox
people with botox
- slower time reading sad sentences
- weaker emotional response time to short videos
suggests body change is important to feel emotion
37
Damage to amygdala
interferes with
- learning fear response
- interpretting/understanding stimuli with emotional consequences
38
Low serotonin turnover
history of violent behavior & crime
attempt violent suicide
recurrent violent behaviors
39
role of serotonin
also released during aggression
| high serotonin inhibits impulses
40
2 routes to amygdala
thalamus to amygdala (quick direct)
neocortex to amygdala (more comprehensive)
41
birth control pills
prevent pregnancy by interfering with usual feedback cycle between ovaries and pituitary
combination pill: prevents release of ovum
-thickens mucus in cervix so egg cannot implant in uterus
42
hans seyle
defined stress as non specific response of body to any demand made upon it
threats on body activates general response to stress called general adaptation syndrome
43
right vs left hemisphere & emotion
right more responsive to emotional stimuli
right inactive: don't experience emotion/don't remember emotion
damage to RTC -problem with responsiveness to emotional stimuli
damage to left 3 better at detecting emotion
44
amygdala & memory
strong memory for emotionally charged events
damage to amygdala can reduce this kind of memory info
reward & motivatation
-dopaminergie pathways from ventral tegmental area of midbrain to nucleus acumbens
damage to amygdala
- impairs processing & emotional info
- recognize cognitive aspects of emotion but not feeling
45
triple imbalance hypothesis
violence depends on cortisol & serotinin
- aggression highest: low cortisol, high testosterone
- serotonin inhibits violence
46
wolffian ducts
precursors to other male reproductive organs
| -develop in vas deferen & seminal vesicles
47
absence of sex hormones
female looking genitalia
48
male Y chromosome
includes SRY gene
causes gonads to evolve into testes
developing testes produce androgens that increase growth of testes
testes also produce mullerian inhibiting hormone
49
Hormones: organizing & activating effects
organizing effects: occur mostly at sensitive stages of development (before birth)
-determine whether brain and body will develop male/female characteristics
activating effects: occur at any time of life & activate a certain response
-distinction between organizing & activating effects not absolute
50
pituitary hormone
stimulates contraction of uterus
stimulates mammary gland to release milk
released during orgasm
faciliates formation of pair bonds
recognizing familar faces
matenal behavior & social attachment
51
causes of ambiguous genitalia
born with XX pattern but SRY gene moves to another chromosome
atypical hormone pattern before birth-mutation of testosterone receptors
congenital adrenal hyperplasia : overdevelopment of adrenal glands before birth
genetic defect: cortisol production leads to overstimulated adrenal gland
- leads to extra testosterone production
- female fetus partly masculinized
52
sex hormones increase responses of certain levels of hypothalamus
ventromedial nucleus
medial preoptic area
anterior hypothalamus
53
testosterone & early development
testosterone converted within neurons to estriadol
54
sexually dimorphic nucleus
area in anterior hypothalamus (larger in males) contributes to male sexual behavior
55
sensitive period
early periods when hormones have long lasting effects
- sexual differentiation depends mostly on level testosterone during sensitive period
- sensitive period for genital formation: 3rd & 4th month of pregnancy
56
androgen insensitivty
XY chromosome pattern but genital appearance of female
normal androgen production but lack androgen receptors that enables it to activate genes in cell's nucleus
57
periovulatory period
time of maximum fertility and estrogen levels when ovulation occurs
-studies suggest women become more sexually responsive during this time
58
anatomical differences between males and females
frontal cortex/limpic cortex larger?
prefrontal cortex/amygdala larger?
women: parts of frontal & limbic cortex are larger
men: parts of pariental cortex & amygdala are larger
parts of female hypothalamus generate cyclical pattern of hormone release
59
hormones and dopamine
testosterone & estriadol release dopamine by medial preoptic area
dopamine stimulation by D1 and D5 receptors association with sexual arousal
serotonin activity decreases sexual arousal by blocking dopamine receptors
60
homosexual men and brain
larger anterior commisure & suprachiasmitic nucleus
smaller neurons in 3rd intestitial nucleus of anterior hypothalamus
61
5 alpha reductase
enzyme that converts testosterone to dihydrotestosterone
people deficient in this enzyme look female at birth but develop penis at puberty
brain exposed to testosterone in early development
62
mullerian ducts
precursors to female oviducts uterus upper vagaina
63
steroid hormones
derived from cholesterol & exert their effects in 3 ways
1. binding to membrane receptors like neurotransmitters
2. entering cells and activating certain kinds of proteins in cytoplasm
3. binding to chromosomes where they activate/inactivate certain genes
64
evolutionary explanation for homosexuality
genes maintained by kin selection
genes increase probability of female relatives producing
activation/deactivaton of certain genes
65
studies of twins & sexual orientation
studies show sexual orientation influenced by genetic factors
probability for homosexuality highest in monozygotic twins
66
gender differences in sexual behavior
men more likely to seek multiple partners
women more likely to be concerned with earning potential
men show more jeaolousy with sexual infidelity
women can also gain from multiple sexual partners
men tend to prefer younger sexual partners (more fertile)
women do not
67
sexual selection
genes that make an individual more appealing to the opposite sex will increase probability of reproduction
68
sex & serotinin
males have more serotonin but females remove serotonin more slowly
69
alpha -fetoprotein
found in blood during early sensitive periods
- binds to estrogen & prevents it from entering cells
- doesn't bind to testosterone
70
congenital adrenal hyperphasia & females
brains of genetic females with CAH show greater preference for boy-typical toys
masculinized interests during adolescence
71
estrogens
female hormones
| -progesterone: prepares uterus for implantation of fertilized ovum
72
where do sex hormones bind?
hypothalamus & amygdala
73
amyloid beta & tau protein buildup results in?
neurofibrillary tangles
- twisted pairs of filaments within neurons
- disrupts neuron's structural matrix
amyloid plaques
-deposits containing aluminium silicate & amyloid peptides
build up of proteins
74
curcumin & alzheimer's
curcurmin is component of tumeric that's been shown to inhibit amyloid beta deposits & phosphate attachment to tau proteins
75
association
pairing a weak input with a strong input enhances later responses to a weak input
76
types of brain damage: korsakoff syndrome
caused by prolonged thiamine (B1) deficiency
- impedes brain's ability to metabolize glucose
- loss /shrinkage of neurons in brain
symptoms
-confusion forgetting, taking guesses to fill in memory gabs (confabulation), apathy
77
sensitization
response to mild stimulus as a result to previous exposure to a more intense stimuli
changes identified at synapse
- serotonin released from facilitating neuron blocks potssium channels in presynaptic neuron
- prolonged release of transmitter from that neuron results in prolonged sensitizaton
78
brain areas involved in memory
hippocampus, entorhinal cortex, amygdala, striatum, left parietal cortex, prefrontal regions
79
striatum
primary input to basal ganglia
- caudate nucleus
- putamen
80
karl lashley
searched for "engrams" in brain
-believed he could cut out learned response
discovered that learning and memory did not entirely depend on connections across cortex
also found learning doesn't depend on single area of cortex
equipotentiality
mass action
81
episodic declarative, procedural memory
episodic : ability to recall single personal events
declarative: ability to state memory into words
procedural: ability to develop motor skills
82
properties of LPT suggest it as a cellular basis of learning & memory
(specificity & cooperativity)
specificity: only synapse onto a cell that have become highly active become strengthened
cooperativity: simultaneously stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by a single axon
83
monkey study & damage to dorsolateral PFC
cannot maintain spatial info in working memory
84
parts of basal ganglia
corpus striatum, globus pallidus, substantia nigra, subthalamic nucleus
major inputs: putamen & caudate nucleus
85
habituation
decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli
- change in synapse between sensory & motor neurons
- sensory neurons fail to excite motor neurons as they di previously
86
explicit vs implicit memory
explicit memory: (declarative memory) deliberate recall of info that one recognizes as a memory
implicit memory: the influence of recent experience on behavior without realizing one is using memory
87
patterns of people with amnesia
normal working memory
difficulty forming new declarative memorize
some degree of retrograde amnesia
better impicit than explicit memory
nearly intact procedural memory
88
types of brain damage: alzheimer's
gradual loss of declarative memory
- 50% of people over 85 & 5% of people 65-74
- 49% of cases are late onset
- -50% of patients with late onset have no known relative with the disease
89
hippocampal damage associated with which amnesia?
anterograde
90
delayed response task
common test of working memory
| -responding to something you heard or saw a short while ago
91
explicit (declarative & implicit (procedural) memory
explicit: with conscious recall
- semantic memory: facts & general knowledge
- episodic memory: personally experienced events
implicit memory: without conscious recall
- procedural memory: motor & cognitive skills
- primary: enhanced identification of objects or words
92
basal ganglia & memory
implicit learning/habit learning depends on basal ganglia
- learns a strategy that leads to correct response & develops pattern
- Parkinson's damages basal ganglia-can't develop implicit memory
93
Khadem
patients with early hippocampal damage but intact limbic cortex of MTC could not recall anything that happened to them during the day but did well in school
basal ganglia & motor regions -skills performance & procedural knowledge
94
long term potentiaton
reflects increased activity by presynaptic neuron & increased responsiveness by the postysynaptic neuron
LTP important for certain types of learning, but as time passes, more dependent of cerebral cortex
95
differences between STM & LTM
STM -limited capacity
STM - fades quickly without rehearsal
memories from LTM can be stimulated with cue/hint
retrieval of memories lost from STM do not benefit from presence of a car
research proposes all info enters STM where brain consolidates it in LTM
96
Pavlov's theory
believed that conditioning strengthened connections between the CS center and UCS center in brain
97
Smith et al
used PET to look at ares responsible for storage and rehearsal
- L posterior parietal cortex: storage of verbal material
- rehearsal: broca's area, premotor cortex, posterior parietal cortex
98
working memory
alternative to STM
-proposed by Baddeley & hitch
emphasis on themporary storage of info to actively attend to it and work on it for period of time
99
weakened distinction between STM & LTM
not al rehearsal STM become LTM
time needed to consolidate varies
epinehphrine & cortisol enhance consolidation of experiences
100
Hippocampus function
critical for declarative memory functioning (esp. episodic)
esp important for spatial memory
especially important for contextual learning & binding
important for conextual learning (detail) (context of event)
damage to hippocampus impairs recent learning more than older learning
-more consolidation =less hippocampal reliance
101
entry of calcium through NMDA
| Channel triggers further changes
activism of a protein sets 2 series of events in motion
more AMPA receptors are built and dendrite branching is increased
changes increase later responsivenes of the dendrite to incoming glutamate
102
working memory & prefrontal cortex
storage for working memory
elevated levels of calcium potentiates later responses
103
thompson et al
suggested that the "engram" for classical conditioning is located in cerebellum & not cortex
104
suppression of activity of LIP
led to condition in which subject displayed no previous learning
as suppression wore off, animal began to learn at same speed
later assumed that learning did not occur in LTP
105
differences between STM & LTM
short term memory: limited capacity
short-term memory: fades quickly without rehearsal
memories from long-term memory can
106
lateral interpositus nucleus and memory
changes occur in LTP of cerebellum
- response increases as learning proceeds
- necessary for learning & retention
107
encoding, consolidation, retrieval
encoding
- hippocampus
- prefontal cortex
consolidation
-hippocampus
retrieval
-various
108
brain areas associated with amnesia
```
hippocampus
entorhinal cortex
amygdala
striatum
left parietal cortex
prefrontal regions
```
109
anterograde vs retrograde amnesia
retrograde: cannot remember past
anterograde: cannot form new memories
110
studies show hippocampus critical for which types of memory
declarative memory
| episodic memory
111
prefrontal cortex
learning rewards & punishments
also basal ganglia, ventromedial prefrontal cortex, orbitofrontal cortex
112
parietal lobe & memory
associated with piecing info together
113
associated with encoding but not consolidation
prefrontal cortex
114
aplysia
slug-like invertebrate with big neurons
allows researchers to study
- habituation
- sensitazation
115
Hebb
differentiated beween two types of memories
short term
long term
116
long term depression
prolonged decrease in response at a synapse that occurs when axons have been less active than others
-opposite of LTP - as one synapse strengthens, another weakens
117
hebbian synapse
occurs when successful stimulation of a cell by an axon leads to the enhanced ability to stimulate that cell in the future
- increases in effectiveness occur because of simultaneous activity in presynaptic & postsynaptic neurons
- such synapse may be critical for many kinds of associative learning
118
henry molaison
removed his hippocampi, parahippocampal gyri, amygdala
- inability to form new explicit memories but not implicit
- still able to form procedural memories but no memory of having learned the new task
- working memory intact
- also able to acquire new spatial memories
- difficulty with episode & declarative memory but not procedural memory
119
causes of Alzheimer's
accumulation & clumping of the following
- amyloid beta protein: produces widespread atrophy of cerebral cortex & hippocampus
- abnormal form of tau protein (part of intracelluar support system of neurons)
120
other brain areas important in learning
amygdala associated in fear learning
parietal lobe associted with piecing info together
anterior & inferior region of temporal lobe: semantic memory
-semantic dementia: loss of semantic memory if brain hemispheres damaged
prefrontal cortex: learning rewards & punishments
-also basal ganglia ventromedial prefrontal cortex, orbitfrontal cortex
damage to orbitofrontal cortex: people opting for immediate reward
121
long term potentiation
occurs when one or more axons bombard a dendrite with stimulation
-leaves the synapse "potentiated" for a period of time and the neuron is responsive
122
anterior & inferior region of temporal lobe
involved in semantic memory
semantic memory: long term memory not drawn from personal experience (name of colors, capitals of countries, etc)
semantic dementia: loss of semantic memory if both hemispheres damaged
123
Lashley's two principles
equipotentiality: all parts of cortex contribute equally to complex functioning behaviors
mass action: cortex works as a whole, and the more cortex is better
124
extensive stimulation of postsynaptic cell
causes release of a retrograde transmitter
- decrease in action potential thresold
- increase neurotransmitter release
- expansion of axons
- transmitter release from additional sites
125
Hebb Rule
when 2 neurons are active simultaneously the synapse betwen them will become strengthened
126
biochemical mechanisms of LTP
known to depend on changes at glutamae & GABA primarily in postysynaptic neurons
occurs at several types of receptors sites including the ionotropic receptors
- AMPA receptors
- NMDA receptors
127
Hebbian Learning
long term potentiation -leads to increase in number of receptors and amount of neurotransmitters
128
LTP in hippocampal neurons
repeated glutamate excitation of AMPA receptors depolarizes the membrane
depolarization removes magnesium ions that had been blocking NMDA receptors
glutamate then able to excite NMDA receptors, opening a channel for calcium ions to enter neuron
129
damage to orbitfrontal cortex
people opt for immediate reward
