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Biopsychology > exam 3 > Flashcards

exam 3 Flashcards

1
Q

advantages of sexual reproduction (2)

A
  1. quick evolutionary adaptations to evolutionary changes
  2. corrects genetic errors and disadvantageous mutations
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2
Q

Mendel’s laws of inheritance (3)

A

law of dominance
law of segregation
law of independent assortment

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3
Q

(mendel) law of dominance

A

some alleles are dominant, some are recessive. dominant alleles overcome the recessive

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4
Q

(mendel) law of segregation

A

each gamete carries only one allele for each gene (because the alleles segregate)

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5
Q

(mendel) law of independent assortment

A

in the formation of gametes, genes of different traits segregate independently

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6
Q

sex-linked genes
(occurs usually on which chromosome?)

A

genes located on the sex chromosomes
usually on the x-chromosome

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7
Q

sex-limited genes
examples?

A

genes present in both sexes, but have a greater effect in only one (occurs due to hormones throughout development)
ex: chest hair, breast size

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8
Q

SRY gene
on which chromosome?
does what?

A

on the y-chromosome
causes gonads to become testes

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9
Q

what hormones do testes produce

A

androgenes

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10
Q

testes producing androgens that in turn increase the growth of testes is known as what kind of loop?

A

positive feedback loop

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11
Q

androgens cause (2):

A

growth of testes
growth of wolffian ducts

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12
Q

what do wolffian ducts develop into (2)?

A

seminal vesicles & vas deferens

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13
Q

what hormone (produced by testes) makes the mullerian ducts degenerate?

A

MIH hormone

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14
Q

what happens if there is no SRY gene (3)?

A

gonads become ovaries
wolffian ducts degenerate
mullerian ducts develop

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15
Q

what hormone do ovaries produce?

A

estrogens

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16
Q

what do mullerian ducts develop into?

A

uterus, oviducts, etc. (female reproductive system)

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17
Q

similarity across all steroids?

A

same chemical backbone, 4-carbon rings

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18
Q

what is a steroid?

A

sex hormones (androgens, estrogens, etc)

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19
Q

where are steroids produced?

A

adrenal glands

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20
Q

organizing effects of hormones
occur when?
determine what?

A

occur during sensitive periods of development (before birth & puberty)
they determine the development of female or male characteristics

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21
Q

activating effects of hormones
occur when?
do what?

A

occur at any time of life
they temporarily activate a particular response (pregnancy, menstruation, etc.)

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22
Q

progesterone
what does it do (2)?

A

prepares uterus for fertilized ovum
promotes maintenance of pregnancy

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23
Q

other word for intersex

A

hermaphrodite

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24
Q

most common cause of intersex

A

Congenital adrenal hyperplasia (CAH)

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25
Q

what happens with CAH (3)?

A

overdevelopment of adrenal glands from birth
extra testosterone production
female becomes partly masculinized
(little effect on males)

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26
Q

androgen insensitivity syndrom (AIS) is a condition of what?

A

intersex

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27
Q

what happens with AIS (3)?

A

lack of receptor that enables chemicals from XY cells (the cells don’t respond to androgens)
males(XY) have smaller penis / female genital appearance
still have testes, so may develop breasts but will not menstruate

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28
Q

sex difference in the medial preoptic area (hypothalamus)?

A

more dendritic spines and synapses in males
BECAUSE: testosterone and estradiol increase production of prostaglandin E2

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29
Q

sex difference in the ventromedial nucleus (hypothalamus)?

A

more widely branched dendrites in males
BECAUSE: estradiol activates P13 kinase, which increases glutamate release

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30
Q

sex difference in arcuate nucleus and anteroventral periventricular nucleus (hypothalamus)?

A

more dendritic spines and synapses in females
BECAUSE: estradiol increases GABA production, which acts on astrocytes to decrease dendritic branching

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31
Q

alpha-fetoprotein
found where and when?
binds to?
prevents?

A

found in the blood during sensitive periods
binds to estradiol
prevents estradiol from entering developing cells

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32
Q

alpha-fetoprotein during pregnancy
(to males and females)

A

females are not exposed to the protein because estradiol binds to it
males receive masculinizing effects as the alpha protein freely enters cell and gets converted to estradiol

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33
Q

what controls menstrual cycle?

A

the ovaries, which are controlled by the hypothalamus & the pituitary gland

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34
Q

what hormone is released at the end of a menstrual period?
where is it released from?

A

follicle-stimulating hormone (FSH)
released from anterior pituitary

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35
Q

what does FSH do?

A

promotes growth of follicles in ovary

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36
Q

what do follicles in the ovaries do (2)?

A

nurtures ovum
produces estrogen

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37
Q

what increases in the middle of the menstrual period?

A

estradiol

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38
Q

what hormones are released after there is an increase in estradiol?
where do these hormones come from?

A

FSH and LH (luteinizing hormone)
released from anterior pituitary

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39
Q

what do FSH and LH do?

A

cause follicles to release ovum

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40
Q

what is the periovulatory period

A

ovulation, middle of menstrual cycle
highest level of fertility

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41
Q

brain regions important for male sexual arousal (3)?
they are all a part of what?

A

ventromedial nucleus (VMH)
medial preoptic area (mPOA)
anterior hypothalamus (AH)
all: hypothalamus

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42
Q

what does testosterone do for male sexual arousal?

A

it triggers the release of dopamine by the mPOA and other areas

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43
Q

how does serotonin decrease sexual activity?

A

serotonin inhibits dopamine release

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44
Q

what hormones increase gradually throughout pregnancy (2)?

A

estradiol and progesterone

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45
Q

what is prolactin necessary for?

A

milk production and general maternal behavior

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46
Q

oxytocin during pregnancy?

A

can improve contractions for birth
increases throughout pregnancy

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47
Q

what mating behavior does vasopressin promote?

A

monogamy

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48
Q

4 components of emotion

A

cognition
action
feeling
physiological changes

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49
Q

James-lange theory

A

autonomic arousal & skeletal actions come first (emotion is the label of such aka the person’s perception)

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50
Q

schacter & singer’s theory

A

physiological arousal is cognitively interpreted with context, which produces the emotional experience
(assess situation, emotion is called-upon, autonomic responses determine the intensity of this emotion)

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51
Q

what’s the general area of the limbic system?

A

the forebrain areas surrounding the thalamus

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52
Q

is there localization of emotions in the brain?

A

no

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53
Q

behavioral activation system (BAS)
which hemisphere?
level of arousal?
can characterize __ & __

A

left hemisphere
low to moderate arousal – tendency to approach
happiness or anger

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54
Q

behavioral inhibition system (BIS)
which hemisphere?
level of arousal?
inhibits __
stimulates emotions like __ & __

A

right hemisphere
increased arousal/attention
inhibits action
fear & disgust

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55
Q

describe fear

A

response to immediate danger

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56
Q

describe anxiety

A

response to future danger

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57
Q

describe the behavioral tests for fear and anxiety

A

if you pair a stimulus with shock, the animals will associate the stimulus with the shock, increasing the startle response. if you pair a stimulus in the absence of danger (pleasure), the stimulus becomes a safety signal and decreases the startle reflex

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58
Q

amygdala
important for?
damage?

A

important for the startle reflex
damage leads to impaired ability to recognize fear & anxiety
(sensory info –> central amygdala –> pons –> startle reflex)

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59
Q

(following BIS and BAS theories…)
people with more activity in the left hemisphere are __
while people with more activity in the right hemisphere are more __

A

happier
withdrawn (experience more unpleasant emotions?)
(key: you want a more active left hemisphere!)

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60
Q

the amygdala responds most strongly to

A

facial expressions that are hard to interpret

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61
Q

amygdala
input from..
output controls..

A

input from pain fibers, vision, hearing
output controls autonomic fear responses

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62
Q

describe monkeys with damage to the amygdala

A

they’re tamer, display less fear to predators/threats
also have impaired social behaviors

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63
Q

urbach-weithe disease

A

fearlessness (damage to amygdala due to accumulation of calcium)

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64
Q

attack behaviors are controlled by which part of the amygdala?

A

corticomedial amygdala

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65
Q

describe anger
& does it lead to aggression?

A

an emotional response
only sometimes leads to aggression

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66
Q

describe aggression and label the 2 types

A

action or behavior, results in an attack
proactive & reactive

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67
Q

describe proactive aggression

A

predatory, related to social gain (like asserting dominance), and not always a result of anger

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68
Q

describe reactive aggression

A

unplanned, from retaliatory intent

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69
Q

predictors of violence (3)

A

past violent behavior, grew up in violent environment, exposure to lead

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70
Q

serotonin inhibits __

A

impulsive behavior

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71
Q

cortisol inhibits __

A

aggression

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72
Q

anxiety __ cortisol

A

increases

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73
Q

anger __ cortisol

A

decreases

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74
Q

aggression occurs from __ serotonin release (turnover)

A

low
(however, this is a weak correlation)

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75
Q

serotonin turnover

A

the amount of serotonin that neurons released, absorbed, and replaced

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76
Q

aggressive behavior depends on the ratio of __:__

A

testosterone to cortisol

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77
Q

aggression occurs from a __ of testosterone

A

burst
(not baseline!)

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78
Q

enzyme MAOa responsible for

A

preventing accumulation of dopamine, serotonin, and norepinephrine
low activity here is linked to aggression

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79
Q

adrenal glands release

A

norepinephrine, cortisol, and aldosterone

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80
Q

link between hippocampus and PTSD

A

smaller hippocampus could predispose people to PTSD

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81
Q

what does norepinephrine do (in relation to stress)

A

stimulates the sympathetic nervous system

82
Q

what does cortisol do (in relation to stress)

A

increases blood glucose = extra energy

83
Q

what does aldosterone do (in relation to stress)

A

maintains blood/salt volume; suppresses the less urgent bodily activities

84
Q

describe one’s tendency to anxiety

A

it remains fairly consistent over time
(aka, you don’t suddenly become a highly anxious person)

85
Q

panic disorder/attacks are linked to abnormalities in which part of the brain

A

hypothalamus

86
Q

people with panic disorders/attacks have decreased __ and increased __

A

decreased GABA
increased orexin

87
Q

the most commonly used anti-anxiety drugs
and what do they do

A

benzodiazepines
they bind to GABA receptors and facilitate the effects

88
Q

alcohol has similar effects in regards to

A

benzodiazepines (anti-anxiety)

89
Q

what 2 bodily systems does stress activate

A
  1. sympathetic nervous system
  2. the HPA axis
90
Q

what’s in the HPA axis (3)?

A

hypothalamus, pituitary gland, adrenal cortex

91
Q

describe HPA axis path

A

activation of hypothalamus –> anterior pituitary secretes ACTH –> ACTH stimulates adrenal cortex –> adrenal cortex secretes cortisol –> cortisol enhances metabolic activity, elevates blood sugar levels, increases alertness

92
Q

results of the HPA axis path (3)

A

enhanced metabolic activity
elevated blood sugar levels
increased alertness

93
Q

what is the dominant response to prolonged stressors

A

HPA axis

94
Q

what is the sympathetic nervous system for

A

fight or flight, brief emergency responses

95
Q

the immune system uses what kind of cells?

A

leukocytes

96
Q

what are leukocytes?

A

white blood cells

97
Q

B-cells
mature where?
secrete what?
2 types?

A

mature in bone marrow
secrete antibodies
2 types: antibodies & antigens

98
Q

antibodies

A

y-shaped proteins that attach to particular kinds of antigens

99
Q

antigens

A

surface proteins that are antibody-generator molecules

100
Q

T-cells (2)

A

attack intruders directly
help other T/B cells to multiply

101
Q

natural killer cells
attack what?(2)

A

attack tumor cells & cells infected w viruses

102
Q

3 kinds of leukocytes

A

B-cells
T-cells
natural killer cells

103
Q

what happens during a bacterial infection?

A

leukocytes/others produce cytokines
cytokines release prostaglandins

104
Q

stressful situations cause the production of __ cytokines and prostaglandins

A

MORE

105
Q

prolonged stress leads to a __ immune system

A

weakened

106
Q

prolonged stress damages which part of the brain?
(at least this one lol)

A

hippocampus

107
Q

depression has a huge sex difference when it comes to the changes in immune response
true or false

A

true

108
Q

describe classical conditioning

A

like Pavlov’s dogs
involves..
conditioned stimulus (sound)
unconditioned stimulus (meat)
unconditioned response (salivate)
conditioned response (salivate)
sometimes the CR resembles the UCR, sometimes it doesn’t

109
Q

describe operant/instrumental conditioning

A

response leads to either reinforcer or punishment

110
Q

what’s an engram

A

a physical representation of what had been learned

111
Q

describe the engram studies with lashley

A

performed several knife cuts in rat cortices that were trained in a variety of mazes
none of the cuts actually impaired rats’ performance

112
Q

lashley’s principles after engram studies (2)

A

equipotentially: all parts of cortex contribute to things equally
mass action: cortex works as a whole (more cortex=better)

113
Q

Thompson’s engram studies (modern)

A

suggested that the engram could be located in cerebellum
results: showed cells in LIP were consistently activated

114
Q

red nucleus receives input from __

A

the LIP and cerebellum

115
Q

what happens, in regards to learning, if you suppress the red nucleus?

A

motor response is suppressed
but not the learning

116
Q

what happens, in regards to learning, if you suppress the LIP?

A

no learning occurs

117
Q

short memory

A

memory of events that have just occurred
(Hebb)

118
Q

long memory

A

memory of events from times further back
(Hebb)

119
Q

working memory

A

involves the retention of information for a period of time sufficient for a cognitive process to occur
(delayed response task shows this type of memory)

120
Q

can you always turn short memory to long?

A

no

121
Q

is there variation in the time needed to consolidate memories?

A

yes

122
Q

memories can consolidate quickly if they are __

A

emotionally significant
(flashbulb memories)

123
Q

why are emotional experiences remembered more easily?

A

they arouse the locus coerleus and eventually increase epinephrine & cortisol, which activates the amygdala and hippocampus

124
Q

which part of the brain stores working memory?

A

prefrontal cortex

125
Q

episodic memory

A

personal events

126
Q

explicit memory

A

declarative

127
Q

implicit memory

A

learned habits, etc.

128
Q

semantic memory

A

factual information

129
Q

procedural memory

A

development of motor skills and habits

130
Q

which part of the brain consolidates declarative memory?

A

hippocampus

131
Q

what happens with a bilateral lesion in the hippocampus?
(patient HM)

A

moderate retrograde amnesia & severe anterograde amnesia
most specifically impairs explicit/declarative memory
*impaired storage of long-term
*severe impairment of episodic
*working memory in-tact, unless distracted
overall, has better implicit memory

132
Q

3 cells important for spatial memory

A

place cells
time cells
grid cells

133
Q

place cells

A

tuned to particular spatial locations
(some are also time cells)

134
Q

time cells

A

respond at a particular point in a sequence of time

135
Q

grid cells

A

hexagonal grid of neurons, respond to different sets of locations
give input to place cells

136
Q

striatum consists of (2)
and is part of the

A

caudate nucleus and putamen
part of the basal ganglia

137
Q

striatum important for

A

learned habits or learning what will likely happen (concluding/making a decision informedly)

138
Q

hippocampus: __ memory
striatum: __ memory

A

h: explicit
s: implicit

139
Q

hippocampus
speed of learning?
type of behavior?
based on what type of feedback?

A

can learn in a single trial
flexible responses
sometimes connects info over a delay

140
Q

striatum
speed of learning?
type of behavior?
based on what type of feedback?

A

learns gradually over many trials
habits
generally require prompt feedback

141
Q

cortisol leads to overstimulation of

A

the adrenal glands
(which leads to extra testosterone)

142
Q

habituation
describe
what’s the change at the synapse

A

decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli
decreased release of neurotransmitters at the synapse
potassium gates are blocked in the sensory neuron

143
Q

sensitization
describe
what’s the change at the synapse

A

increased response of a mild stimuli after exposure to more intense stimuli
serotonin from the “facilitating neuron” blocks K+ channels in the presynaptic neuron, which then causes a prolonged released of transmitters, leading to prolonged sensitization

144
Q

briefly described long-term potentiation

A

more responsive to new input of the same type

145
Q

3 properties of long-term potentiation

A
  1. specificity: only highly active synapses become strengthened
  2. cooperativity: (simultaneous) 2 or more axons produce LTP stronger than just 1
  3. associativity: pairing weak input with strong input enhances later responses to weak input
146
Q

memories stored:
made and recalled in:

A

stored in cerebral cortex
made/recalled in hippocampus

147
Q

as a synapse strengthens, another is weakened
true or false

A

true

148
Q

LTP goes hand-in-hand with LT..

A

D! Depression

149
Q

the 2 glutamate receptors linked to LTP

A

AMPA and NMDA

150
Q

what kinds of receptors are AMPA and NMDA

A

ionotropic

151
Q

which glutamate receptor depends on the degree of potentiation

A

NMDA

152
Q

describe process of LTP with the AMPA and NMDA receptors

A
  1. sodium enters thru AMPA as glutamate is attaching, magnesium is blocking NMDA
  2. AMPA gets depolarized, activating NMDA receptor which throws off the magnesium
  3. glutamate enters thru both AMPA and NMDA, but CALCIUM now also enters but only thru NMDA
153
Q

__ is key to LTP

A

calcium

154
Q

after calcium enters NMDA, then more __ are created (+ dendritic branching), leading to future responsiveness

A

more AMPA

155
Q

__ synapses are absolute after LTP establishment

A

NMDA

156
Q

extensive stimulation of post-synaptic neuron causes the release of

A

retrograde transmitters

157
Q

what happens after the retrograde transmitters reach the presynaptic neuron?(4)

A
  1. decrease in AP threshold
  2. increase in neurotransmitter release
  3. expansion of axons
  4. transmitter release from more sites
158
Q

retrograde amnesia

A

memory loss of the past

159
Q

anterograde amnesia

A

memory loss in the present

160
Q

Korsakoff’s syndrome

A

associated with alcoholism
vitamine B1 (thiamine) deficiency
impairs brain metabolizing glucose
loss-shrinkage of neurons
involves confabulation: guessing to fill in memory gaps

161
Q

alzheimer’s disease

A

gradually progressive
primarily associated with old age
early onset most likely due to genes
associated proteins: (1)amyloid beta & (2)tau
(1) creates plaques & widespread atrophy
(2) creates tangles

162
Q

today’s belief of the mind-brain relationship

A

monism

163
Q

categories of monism

A

materialism
mentalism
identity position

164
Q

describe the threshold of consciousness

A

you’re either conscious of something or you’re not (no in-between)

165
Q

binocular rivalry

A

slow and gradual shifts of the eye sweeping from one side to the other

166
Q

stimulus must be identified as __ before you become conscious of it

A

meaningful

167
Q

phi phenomenon

A

construction of a conscious experience after the event (change in perception)
we are capable of becoming conscious of something after it’s gone

168
Q

decreased spread of brain activity leads to loss of

A

consciousness

169
Q

top-down attention

A

intentional

170
Q

bottom-up attention

A

something grabbing your attention

171
Q

broca’s aphasia

A

confluent aphasia
impairment of language production, speech is meaningful but sparse

172
Q

wernicke’s aphasia

A

fluent aphasia
impairment of language comprehension, appears to speak smoothly but is actually speaking nonsense

173
Q

dyslexia

A

several genes are linked, everyone experiences it differently

174
Q

decisions based on values made in: (2)

A

basal ganglia
ventromedial prefrontal cortex

175
Q

what kind of learning does the basal ganglia do

A

slower learning

176
Q

what kind of learning does the ventromedial prefrontal cortex do

A

faster learning

177
Q

which part of the brain monitors confidence in decisions

A

VMPC (ventromedial prefrontal cortex)

178
Q

decision info is relayed the

A

orbitofrontal cortex

179
Q

what does the orbitofrontal cortex do

A

it compares expected rewards

180
Q

how psychological diseases are classified

A

DSM 5
ICD 10

181
Q

antagonist

A

drug that blocks neurotransmitter

182
Q

agonist

A

drug that mimics or increases a neurotransmitters’ effects

183
Q

affinity for a receptor

A

measure of drug’s tendency to bind to receptor

184
Q

efficacy of receptor

A

a drug’s effectiveness
and side effects

185
Q

what is the ALDH2 gene linked to

A

addiction

186
Q

nucleus accumbens

A

where addictive drugs release dopamine or norepinephrine

187
Q

name all antidepressants (that we care about in this class)

A

tricyclics
SSRIs
SNRIs
MAOIs
atypical/miscellaneous

188
Q

tricyclics

A

blocks reabsorption of happy neurotransmitters – encourages the use of these transmitters rather than the cell just giving up
side effects: drowsiness, dry mouth, difficulty urinating, heavy irregularities

189
Q

SSRIs

A

selective serotonin reuptake inhibitors
examples: Zoloft, prozac

190
Q

SNRIs

A

serotonin norepinephrine reuptake inhibitors
ALSO improve certain aspects of memory
examples: Cymbalta, effexor

191
Q

MAOIs

A

monamine oxidase inhibitors
usually only prescribed if SSRIs and tricyclics don’t work

192
Q

bipolar I

A

full blown episodes of mania

193
Q

bipolar II

A

milder manic phases, called hypomania

194
Q

schizophrenia diagnosed after how long

A

6 months

195
Q

antipsychotic drugs

A

first gen
second gen aka atypical

196
Q

first gen antipsychotic drugs

A

phenothiazines
butyrophenones
both block dopamine synapses

197
Q

second gen antipsychotic drugs

A

(atypical)
they are anti-serotonin
side effects: weight gain, bad immune system

198
Q

2 major dopamine pathways

A

mesolimbocortical system
mesostriatal system

199
Q

glutamate hypothesis for schizophrenia

A

increased dopamine, leading to decreased glutamate (same effects)

200
Q

PCP inhibits

A

NMDA glutamate receptors
supports glutamate hypothesis for schizophrenia

201
Q

schizophrenia is typically diagnosed __ in life

A

later

Biopsychology (3 decks)

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