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1
Q

biological rhythms

A

regular fluctuations in any living process

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2
Q

circadian rhythms

A

the physical, mental, and behavioral changes an organism experiences over a 24-hour cycle

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3
Q

ultradian rhythms

A

biological rhythms shorter than a day

varys several minutes to hours long

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4
Q

infradian rhythms

A

biological rhythms that take more than a day because they repeat less than once per day

example: 28 day human menstrual cycle

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5
Q

human and many other primates are __

A

diurnal - active during the day

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6
Q

the free-running period

A

the time between two similar points of successive cycles

example: sunset to sunset

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7
Q

every animal has its own:

A

endogenous clock; periods vary from one individual to another

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8
Q

phase shift

A

the shift of activity produced by a synchronizing stimulus

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9
Q

zeitgeber

A

any cue that an animal uses to synchronize its activity with the enviornment

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10
Q

light acts as a powerful:

A

zeitgeber

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11
Q

large lesions of the hypothalamus interfered with:

A

circadian rhythms

specifically legions in SCN - suprachiasmatic nucleus

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12
Q

SCN contains an __

A

endogenous clock, and generates a circadian rhythm

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13
Q

tau mutation

A

mutation affecting the endogenous clock

within the SCN itself there must be a mechanisim that can drive a circadian rhythm in activity, this biological clock is affected by mutation of the gene tau

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14
Q

in mammals, light information from the eyes reaches the

A

SCN directly

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15
Q

retinal ganglion cells contain a special photopigment called

A

melanopsin, makes them sensitive to light

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16
Q

people who are blind often show

A

a free-running circadian rhythm, with difficulties getting to sleep at night and staying awake during the day

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17
Q

do people on western or eastern side go to bed later?

A

western side go to bed later, because the sun sets later on the western side of time zone compared to the east

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18
Q

students attending highschools that start after 8:30 am demonstrated:

A

improved academic preformance, less sleeping in class, reduced incidence of depression, 70% fewer car crashes

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19
Q

Clock and Cycle Proteins (the molecular clock process)

A

bind together to form a dimer

dimer binds to DNA, enhancing transcription of genes fore Period and Crytochrome

Per and Cry bind together as a complex that inhibits activity of the Clock Cycle dimer, slowing transcription of per and cry genes, and therefore slowing production of the per and cry proteins

the per and cry proteins break down, releasing clock/cycle from inhibition and allowing the cycle to start over again. The rate of gene transcription, protein complex formation, and protein degradation result in a cycle that takes about 24 hours to complete

retinal ganglion cells detect light with melanopsin, and their axons in the retinohypothalamic tract release glutamate onto neurons in the SCN, the glutamate stimulations leads to increase transcription of the per gene, synchronizing the molecular clock to the day-night cycle

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20
Q

two classes of sleep

A

Rem and non-rem

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21
Q

fully awake brain eeg activity

A

low amplitude waves and fast frequencies, 15-20 hz, this pattern is sometimes referred as beta activity or a desynchronized EEG

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22
Q

when relaxed and eyes closed eeg shows:

A

regular oscillation at a frequency of 8-12 hz, known as alpha rhythm

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23
Q

stage 1 sleep

A

drowsiness causes time spent in alpha rhythm decreases, and eeg shows waves of smaller amplitude and irregular frequency, as well as sharp waves called vertex spikes

this is the beginning on non-rem sleep and is accompanied by slower heart rate and relaxation, under the eyelids the eyes may roll about slowly. lasts about several minutes and gives way to stage 2

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24
Q

stage 2 sleep

A

12-14 hz waves, called sleep spindles that occur in periodic burst, by K complexes. If awakened during these first 2 stages of sleep, many people deny that they have been asleep

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25
Q

stage 3 sleep

A

large amplitude very slow waves called delta waves, gives the name Slow Wave Sleep (SWS)

as night progresses delta waves become more prominent.

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26
Q

rem sleep

A

after SWS stage with a brief return to stage 2, REM occurs. EEG displays small amplitude high frequency, similar patterns to someone awake, except the eyes are darting rapidly about under their lids.

other skeletal muscles show atonia during this cycle - flacid muscle state

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27
Q

another name for rem is

A

paradoxical sleep, as the muscles are unresponsive but our brain waves look awake

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28
Q

half of the time people are asleep they are in stage

A

2, rem sleep accounts for 20% of total sleep

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29
Q

human sleep shows repeating cycles

A

90-110 minutes long, recurring four or 5 times a night, reflecting a basic ultradian rest-activity cycle.

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30
Q

stage 3 is most prominent in the

A

early night, and then tapers off as the night goes on

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31
Q

rem sleep is more prominent in the

A

later cycles of sleep

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32
Q

the first REM period is the

A

shortest, which the last REM period before waking may be 40 minutes. Brief arousal occasionally occur after a rem period, and a sleeper may shift posture at this time

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33
Q

Properties of REM sleep

A

variable heat rate and respiration, brain temp increase, brain blood flow increased, muscles are not tense, eye movements rapid, vivid dreams, low growth hormone secretion, increased firing rates in cerebral cortex

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34
Q

non-rem sleep properties

A

decline heart rate and respiration, decreased brain temp, reduced blood flow in cerebral, reduced tension, normal reflexes, twitching reduced, slow eye movement, vague thoughts, high in SWS, many cells reduced in cerebral cortex activity

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35
Q

night terror

A

sudden arousal from stage 3 SWS marked by intense fear and autonomic activation

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36
Q

activation synthesis theory

A

experiences in REM sleep are the more or less random results of which neurons happen to get activated. the brain strings together these disparate activated elements into a more or less coherent story.

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37
Q

unilateral sleep

A

one hemisphere sleeping while other watches for predator - seen in birds and dolphins

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38
Q

human infants can move directly from

A

an awake state to rem sleeps, rem sleep of infants is quite active, suggests the state provides stimulation to essential maturation of the nervous system

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39
Q

by 90, stage 3 of sleep has

A

disappeared

may be related to diminished cognitive functioning

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40
Q

sustained sleep deprivation causes rats to

A

die, within an average of 19 days

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41
Q

fatal familial insomina

A

people with mad cow disease, will eventually stop sleeping, and die 7-24 months after insomnia begins

autopsy reveals degeneration of cerebral cortex and thalamus

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42
Q

biological function of sleep

A

energy conservation, niche adaption, body and brain restoration, memory consolidation

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43
Q

ecological niche

A

unique assortment of enviornmental opportunities and challenges to which each organism is adapted, these adaption causes species to become better at gathering food at either night or daytime

nocturnal mice, adapt at sneaking around in dark to avoid predators

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44
Q

forebrain generates

A

slow wave sleep SWS, the forebrain alone can generate this without contributions from the lower brain regions, appears to be generated by basal forebrain releasing gaba into tuberomammillary nucleus in hypothalamus

lesions of basal forebrain causes insomnia, where electrical stimulation caused sleepiness

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45
Q

four interacting neural systems that underlie sleep

A
  1. forebrain generates SWS
  2. brainstem activates sleeping forebrain into wakefulness
  3. pontine system triggers REM
  4. hypothalamic system coordinates other 3 brain regions to determine which state were in
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46
Q

narcolepsy

A

frequent intense attack of sleep that last 5-30 minutes
show rem immediately upon following asleep

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47
Q

cataplexy

A

people with narcolepsy also show, a sudden loss of muscle tone leading to the collapse of the body without the loss of consciousness

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48
Q

mutant gene responsible for narcoletpic mammals

A

gene for a neuropeptide called orexin, mice with orexin gene knocked out display narcolepsy

rats can be made narcoleptic if injected with toxin that destroys neurons possessing orexin receptors, the narcoletpic dogs start losing orexin neurons at the age when symptoms of narcolepsy appear

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49
Q

humans with narcolepsy have lost ___ of orexin neurons

A

90%

orexin prevents the transition from wakefulness directly into rem

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50
Q

orexin is found exclusively in

A

hypothalamus

axons go to basal forebrain, reticular formation and locus coreulus

neurons of orexin project also into hypothalamic tuberomammillary nucleus

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51
Q

treatment of narcolepsy

A

use of amphetamines in the daytime\drug GHB helps narcoleptics

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52
Q

one hypothesis of sleep paralysis

A

results when the pontine center continues to impose paralysis for a short while after a person awakes from a REM episode

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53
Q

sleep enuresis

A

bed wetting, associated with SWS

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54
Q

somnambulism

A

sleep walking, occur during stage 3 SWS, more common in first half of night

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55
Q

rem behaviour disorder

A

people appear to be acting out a dream, occurs after the age of 50, more common in men than women

RBD onset is followed by parkinsons disease and dementia

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56
Q

sleep onset insomnia

A

difficulty falling asleep

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57
Q

sleep maintenance insomnia

A

trouble remaining asleep

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58
Q

sleep state misperception

A

they are sleeping without knowing it

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59
Q

sleep apnea

A

progressive relaxation of muscles of the chest, diaphragm, and throat cavity, or from changes in the pacemaker respiratory neurons of the brainstem

relaxation of the throat obstructs the airway, a kind of self-choking

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60
Q

sudden infant death syndrome

A

arises from sleep apnea as a result of immature systems that normally control respiration

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61
Q

emotion

A

subjective mental state accompanied by distinctive cognition, behaviours and physiological changes

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62
Q

James-Lange theory

A

physical changes in the body happen first, which then leads to the experience of emotion

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63
Q

Cannon-Bard Theory

A

it is the brains job to decide which particular emotion is an appropriate response to the stimuli

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64
Q

program fear

A

the emotion of fear shifts our perception, attention, cognition and action to focus on avoiding danger and seeking safety

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65
Q

eight basic emotions grouped in four pairs of opposites

A

joy/sadness
affection/disgust
anger/fear
expectation/suprise

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66
Q

superficial facial muscles

A

attach only between different points of facial skin, so when they contract, they change the shape of the mouth, eyes or nose or maybe create a dimple

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67
Q

deep facial muscles

A

attach to bone and produce larger-scale movements, like chewing

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68
Q

facial muscles innervated by

A

facial nerve VII innervates facial expression

motor branch of trigeminal nerve V innervates muscles that move jaw

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69
Q

facial feedback hypothesis

A

sensory feedback from our facial expressions can affect our mood, consistent with the james-lange notion that sensations from our body inform us about our emotions

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70
Q

brain self stimulation

A

people recieving electrical stimulation in the septum feel a sense of pleasure or warmth, or sometimes sexual excitement

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71
Q

cerbral cortex normally

A

inhibits rage responses

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72
Q

release of dopamine into the nucleus accumbens responsible for

A

pleasurable feelings

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73
Q

kluver bucy syndrome

A

a rare neuropsychiatric disorder due to lesions affecting bilateral temporal lobes, especially the hippocampus and amygdala. It is characterized by hyperorality, hypermetamorphosis, hypersexuality, bulimia, placidity, visual agnosia, and amnesia.

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74
Q

alexithymia

A

impairments in emotional awareness associated with dysfunction of insula

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75
Q

activity in cingluate cortex is altered in

A

sadness, happiness, and anger

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76
Q

left somatosensory cortex is deactivated in

A

both anger and fear

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77
Q

intermale aggression

A

agression between males of same species

males are 5 times more likely to be charged with murder in US

75% of assault arrests were male, 90% of murder were male

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78
Q

hormone tesosterone causes

A

intermale aggression, androgens clearly seem to increase aggression

treating castrated males with testosterone restores fighting behaviour

treating adult volunteers with extra testosterone wont increase aggresion

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79
Q

aggressive behaviour is modulated by brain activity associated with

A

GABA, vasopresin, and serotonin

most aggressive monkeys had the lowest levels of serotonin being released in the brain

serotonin inhibits aggression

drugs enhance GABA generally reduce aggression, paradoxically, alcohol seems to provoke aggression even though it enhances GABA

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80
Q

medial amygdala

A

analyzes smell information, allowing rats to distinguish between male rivals and females to be courted, this information is relayed to ventromedial hypothalamus, which serves as a trigger to aggressive behaviour

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81
Q

activation of VMH neruons can cause

A

males to be mating with females to suddenly attack them, inhibiting VMH reduces the likelihood of attack

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82
Q

maternal aggression

A

controlled by circuits in VMH, as well as preoptic area and pre mammillary nucleus and a serotonergic projection originating from the midbrain

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83
Q

psychopaths have reductions in

A

size and activity of prefrontal cortex, which may impair their ability to control impulsive behaviours

treatment that enhance serotonin activity in the brain might be useful adjunct to psychotherapeutic intervention

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84
Q

stress immunization

A

little stress early in life seemed to make animals more resilient to later stress

this only benefits when pups are promptly comforted after each stressful event

rat pups who had good moms had less likely of developing mood disorder, and rat pups who had bad moms lead to development of mood disorder

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85
Q

epigenetic regulation

A

represents a change in the ecpresison of the gene, rather than a change in the encoding region of the gene - occurs due to environmental factors

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86
Q

effects of bullying were are strong as

A

those of physical or sexual abuse

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87
Q

positive symptoms schizophrenia

A

abnormal behavioural states that have been gained; hallucinations, delusions, etc

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88
Q

negative symptoms schizophrenia

A

loss of normal functions such as slow and impoverished thought and speech, emotional and social withdrawal or blunted affect

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89
Q

twin studies show schizophrenia has

A

both environmental and genetic origins
50% chance the other twin will develop schizophrenia

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90
Q

DISC1

A

gene in one large scottish family of which had several schizophrenic members, carried a mutant disabled version of DISC1

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91
Q

epigenetic schizophrenic risks

A

paternal age, children fathered by older men have a greater risk of developing schizophrenia

sperm of older men had more opportunity to accumulate mutations possibly

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92
Q

people living in a big city are more likely to

A

develop schizophrenia, 1 and a half times more likely, possibly due to the stress of many social interactions

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93
Q

paternal stress increases the

A

likelihood of the baby developing schizophrenia

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94
Q

adolescents with schizophrenia lose ____

A

gray matter over wide regions at a faster rate compared to control adolescents

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95
Q

schizophrenics have enlarged

A

cerebral ventricles

96
Q

when DISC1 was inserted into mice they saw

A

development of enlarged lateral ventricles

97
Q

hypofrontality hypothesis

A

frontal lobes are underactive in people with schizophrenia

98
Q

what replaced the lobotomy as a treatment of schizophrenia

A

chlorpromazine, reduces positive symptoms

99
Q

long term effects of antipsychotics

A

dyskinesia, tardive dyskinesia

basically elaborate uncontrollable movements

if discontinuation of drugs, hypersensitivity psychosis can occur, marking an increase in positive symptoms

100
Q

dopamine hypothesis

A

people with schizophrenia have an excess of either dopamine release or dopamine receptors

antipsychotics block D2 receptors

101
Q

amphetamine psychosis

A

high doeses of amphetamine can cause excess dopamine to accumulate in synapses, resulting in amphetamine psychosis which is reversed by anti schizophrenic medication

102
Q

first-generation antipsychotics

A

d2 receptor antagonists

haloperidol has a greater affinity for d2 receptors than chlorpromazine and is more widely used now

103
Q

second generation antipsychotics

A

have only moderate affinity for D2 receptors

they have their highest affinity for blocking serotonin receptors

104
Q

why are second generation antipsychotics effective?

A

clozapine can increase dopamine release in frontal cortex, good for relieving negative symptoms in addition to positive symptoms relieved by first generation antipsychotics

several studies show that giving people 2 types of drugs shows no difference

105
Q

glutamate hypothesis

A

schizophrenia results in underactivation of glutamate receptors, which might account for reduced activity in frontal cortex

106
Q

depressive disorders are

A

highly heritable, concordance rate for identical twins is 40%

107
Q

depressed peoples brains show

A

increased amygdala activation, increased frontal lobe activity, decreased activity in parietal and posterior temporal cortex and anterior cingulate cortex

also have thinner cortex across large areas of the right hemisphere, also difficulties regulating stress hormone release

many studies show hippocampal volume reduction, and reduced activation of this region during memory tasks

108
Q

treatments

A

ECT, rTMS, MAO, SSRIs, tricyclics, CBT

CBT and SSRI together are more effective in combating depression than either one is alone

109
Q

why do more females than males develop depression

A

help-seeking behaviour is greater in women, could be because of differences in endocrine physiology

110
Q

people with depression and sleep

A

depressed people have irregular sleep patterns, and shown to enter REM much sooner after sleep onset, reduction in stage 3 sleep and an increase in stage 1 and 2

111
Q

People with BPD exhibit enlarged

A

ventricles, as seen in schizophrenia, more manic episodes the person has experienced, the greater the ventricular enlargment, suggesting worsening of brain loss overtime

112
Q

BPD has more in common with:

A

schizophrenia than depression

113
Q

BPD individuals benefit from taking

A

lithium

114
Q

people who experience recurrent panic attacks have

A

temporal lobe abnormalities, specifically in left hemisphere, also changes in the amygdala

115
Q

anxiolytic benzodiazepines

A

things like xanax and valium, combat anxiety, and are termed anxiolytics

anxiolytic benzodiazepines interact with binding sites of GABA receptors, where they act as noncompetitive agonists, causing a boost in GABA mediated postsynaptic inhibition and reduces the excitability of postsynaptic neurons

116
Q

Buspirone

A

agonist of Serotonin receptors that provides relief of anxiety

117
Q

PTSD memory disturbances are because of

A

smaller volume of right hippocampus, could also be due to inflammatories contributing to neural degeneration

118
Q

fear conditioning

A

sensitization and extinction work

119
Q

ptsd exhibits a paradoxical

A

long term reduction in cortisol levels, due to persistent increases in sensitivity to cortisol

120
Q

OCD shows best response to

A

CBT, and SSRI’s

121
Q

people with Tourettes also exhibit

A

ADHD or OCD

122
Q

Tourettes has a greater density of

A

D2 receptors in caudate nucleus of basal ganglia

123
Q

treatment of tourettes

A

haloperiodol, a d2 receptor antagonist, a first generation antipsychotic reducing tic frequency, but it has unpleasant side effects compared to second-generation antipsychotics that also show good response

DBS also benefits people with tourettes

124
Q

amnesia

A

severe impairment of memory, usually as a result of accident or disease

125
Q

retrograde amnesia

A

loss of memories that formed prior to an event, such as surgery or trauma

126
Q

anterograde amnesia

A

inability to form new memories after an event (surgery or trauma)

127
Q

memory deficit seems to be caused y

A

loss of medial temporal love including hippocampus

128
Q

declarative memory

A

facts and information acquired through learning

type of memory we use to answer “what” questions

things you know that you can tell others

129
Q

nondeclarative learning

A

shown by performance rather than conscious recollection, such as riding a bike

type of memory we use for “how” problems and is often nonverbal

things you know that you can show by doing

130
Q

delayed non-matching-to-sample task

A

a test of object recognition that requires monkeys to declare what they remember by identifying which two objects was NOT seen previously. Monkeys with damage to medial lobe are severely impaired on this task

131
Q

which brain structures are important for declarative memory

A

damage to both the hippocampus and nearby cortex

132
Q

damage to _______ can also cause amnesia

A

medial diencephalon, a limbic structure that has connections with dorsomedial thalamus and mammillary bodies

133
Q

Korsakoffs syndrome

A

degenerative disease in which damage is found to mammillary bodies and dorsomedial thalamus

people with this fail to recognize or sense any familiarity with some items, yet frequently deny anything is wrong. They often confabulate, that is, to fill a gap in memory with falsification that they seem to accept is true.

Damage to frontal cortex is also found in this disease, probably causes the denial and confabulation

main cause is lack of vitamin thiamine, alcoholics suffer this deficiency, treating them with thiamine will prevent further deterioration of memory but not reverse dmaage already done

134
Q

Hippocampus, mammillary bodies and dorsomedial thalamus is needed to __-

A

form new declarative memories

135
Q

episodic memory

A

a declarative memory that you show episodic memory when you recall a specific episode in your life or relate an event to a particular time and place

136
Q

semantic memory

A

a generalized declarative memory, such as knowing the meaning of a word without knowing where or when you learned the word

137
Q

The inability to recall autobiographical details of life may be due to

A

injuries to the frontal and parietal cortex.

138
Q

skill learning

A

learning how to preform a task by doing it over and over

139
Q

all three types of skill learning

A

sensorimotor, perceptual and cognitive skills all are impaired with damage to basal ganglia, cerebellum and motor cortex

140
Q

priming

A

is a change in the way you process a stimulus

priming does not require declarative memory, and is not impaired by damage to basal ganglia

141
Q

perceptual priming

A

this priming is related to reduced activity in bilateral occipitotemporal cortex

142
Q

conceptual priming

A

associated with reduced activation of left frontal cortex

143
Q

associative learning

A

learning that involves relations between two events

best studied form is classical conditioning

144
Q

Bell in pavlov is

A

conditioned stimulus

145
Q

salivation is the

A

unconditioned response

146
Q

the learned response to the conditioned stimulus (bell alone) is

A

conditioned response

147
Q

instrumental conditioning

A

association is formed between animals behaviour and the consequences of the behaviour

example - skinner box, animals learned by pressing bar they would get reward

148
Q

place cells

A

rat hippocampus contains these neurons that selectively encode spatial location

place cell activity indicates that the hippocampus remaps to new locations

149
Q

natural selection favours enlargement of

A

hippocampus to enhance spatial learning

150
Q

sensory buffers

A

briefest memories

151
Q

working memory

A

refers to the ability to actively manipulate information in your short term memory, perhaps retrieving information from long term memory to solve a problem or make us of information

considered subset of short term memory where info can be analyzed and manipulated

152
Q

memory system and the three processes

A

encoding of raw information from sensory channels into STM

consolidation of the STM into more durable LTM

retrieval of the stored information from LTM to use in working memory

153
Q

some strategies to prevent PTSD formation

A

block the effects of epinephrine in the amygdala by treating victims with antiadrenergic drugs shortly after trauma

154
Q

medial lobe and STM and LTM

A

medial love is not needed to encode sensory information into STM, or to retrieve information from STM BUT it is crucial to moving memories to STM to LTM

155
Q

environmental enrichment in rats shows

A

EC animals have heavier thicker cortex in the somatosensory and visual cortical areas, enhanced cholinergic activity, more dendritic branches, larger cortical synpases, more neurons in hippocampus, enhanced brain recovery from brain damage

156
Q

habituation

A

nonassociative learning, a decreased response to a stimulus as its being repeated

157
Q

long term habituation

A

reduction in number of synapses between sensory cell and the motor neuron

158
Q

cerebellar circuit is necessary for

A

eyeblink conditioning, and simple conditioning in humans

159
Q

hebbian synapses

A

when pre and postsynaptic neuron are repeatedly activated together, the synaptic connection between them would become stronger and more stable

“cells that fire together wire together”

these hebbian synapses could act together to store memory traces

160
Q

tetanus

A

brief high frequency burst of electrical stimuli

161
Q

long term potentiation

A

long-lasting enhancement of synaptic transmision, synapses become stronger and more effective

162
Q

NDMA receptor and LTP

A

drugs that block this receptor completely prevents new LTP, but does not effect synaptic changes that have already been established

163
Q

EPSP is mediated by

A

AMPA receptors by release of glutamate at the synapse

164
Q

retrograde transmitter

A

a diffusible gas that travels back across the synapse to alter the functioning of presynaptic neuron

induces the presynaptic terminal to release more glutamate than previously, thereby strengthening the synpase

LTP involved active changes on both sides of synpase

165
Q

mice engineered to overexpress NMDA receptors in hippocampus have

A

enhanced LTP and better than normal long term memory

166
Q

vigilance

A

global level of alertness of the indivudal

167
Q

overt attention

A

direct our eyes and attention to the same target

168
Q

cocktail party effect

A

how attention acts to focus cognitive processing resources on a particular target, if your attention drifts to another stimulus -for example if you start to listen to another conversation-it becomes almost impossible to simultaneously follow what your friend is saying

169
Q

dichotic presentation

A

different streams of speech simultaneously to peoples left and right ears via headphones, participants were able to report what they heard in the attended ear, but reported very little about what they heard on nonattended ear - this is referred to SHADOWING

170
Q

attentional spotlight

A

shifting around the enviornment, highlighting stimuli for enhanced processing

171
Q

perceptual load

A

immediate processing demands presented by a stimulus

when we focus on a complex stimulus, the load on our perceptual processing resources is so great that there is nothing left over

when we focus on easy stimuli, we may have enough perceptual resources left over to process additional stimuli

we only have enough of it to do one complex task at a time, or a few very simple ones

172
Q

people use cues to predict

A

stimulus location, shifting attention without shifting gaze

173
Q

Reactions times and brain process

A

neural processing required between input and output require V1, to PFC, then through premotor and primary motor cortex down to the spinal motor neurons and out the finger muscles

174
Q

reflective attention

A

involuntary reorientation towards a sudden or important event, like when a glass breaks in a restaurant

bottom-up process, because attention is being seized by sensory inputs from lower levels of the nervous system, rather than being directed by voluntary, top-down processes of the forebrain

175
Q

visual search

A

systematically scanning the world to locate a specific object among many

176
Q

conjunction search

A

searching for an item on the basis of a combination of two or more features, such as size and colour

can become difficult, if for example, you are looking for your friend in a large crowd, the bigger the crowd is the harder the task becomes

177
Q

temporal resolution

A

ability to track changes in the brain that occur quickly

178
Q

spatial resolution

A

ability to observe the detailed structure

179
Q

where waldo is an example of

A

conjunction searches

180
Q

ERP

A

event related protential tracks regional changes in brain activity much faster than fMRI does, and is great in studying moment-to-moment consequences of attention in the brain

181
Q

auditory N1 effect

A

selective attention enhances processing of a particular sound

182
Q

P3 effect

A

sensitive to higher-order cognitive processing of the stimulus qualities like the underlying meaning of the stimulus, identifying the speaker, and so on, which the P3 effect provides an example of late-selection effect on attention

183
Q

visual P1 affect

A

thought to reflect the initial sensory and attentional processing of a stimulus by specific areas of the cerebral cortex.

184
Q

enhancement in the cortical fusiform face are is seen

A

during attention to faces, or in the subcortical superior colliculus and lateral geniculate during attention to spatial arrays

185
Q

superior colliculus

A

controlling the movement of the eyes toward objects of attention, especially in overt forms of attention

lesions here show reduced inhibition of return for visual stimuli

superior colliculus helps direct our gaze to attended objects

186
Q

pulvinar

A

heavily involved in visual processing

important in orienting and shifting attention, important for filtering out to ignore distracting stimuli while engaged in covert attention tasks

tasks with large numbers of distracted induce greater activation of pulvinar

187
Q

dorsal frontoparietal and right temporoparietal

A

work together to continually select and shift between objects of interest

188
Q

lateral intraparietal area

A

crucial for voluntary attention

189
Q

Frontal eye field

A

damage to this region causes struggle to prevent their gaze from being drawn away toward peripheral distracted while they’re preforming a voluntary attention task

neurons of the FEF are crucial for ensuring our gaze is directed among stimuli according to cognitive goals rather than eye catching characteristics of the stimuli

190
Q

temporoparietal junction

A

involved in reflexive steering of attention toward novel or unexpected stimuli

acts as alerting signal

191
Q

dorsal stream of processing

A

responsible for voluntary attention, enhancing neural processing of stimuli and interacting with the pulvinar and superior colliculus to steer attentional spotlight around

192
Q

Hemispartial neglect

A

attention syndrome in which the person tends to completely disregard the left side of the world, disorder of attention itself, not spatial relationships

193
Q

balint syndrome

A

biparietal damage, oculomotor apraxia, optic ataxia, and shows profound restriction of attention (simultagnosia)

194
Q

simultagnosia

A

extreme narrowing of attentional spotlight, to the point that it cant encompass more than one object at a time

195
Q

claustrum

A

slender sheet of neurons buried within white matter of forebrain lateral to basal ganglia which plays a role in generating the experience of being conscious

196
Q

scientists call unconscious brain functions

A

cognitively impenetrable

197
Q

easy problem of consciousness

A

understanding how particular patterns of neural activity specific conscious experiences

198
Q

hard problem of consciousness

A

The problem of explaining the connection between the phenomena of subjective reality and brain processes

199
Q

qualia

A

subjective experiences of perceptions

200
Q

prefrontal cortex is main source of

A

goal-driven behaviours

201
Q

executive function involves

A

task switching, updating of cognitive plan based on new information, inhibition of responses that would compromise the plan

202
Q

hierarchial cognitive control

A

ability to direct short term actions while simultaneously keeping longer term goals in mind

203
Q

dorsolateral prefrontal cortex

A

associated with executive control and crucial for working memory and task switching

204
Q

obitofrontal cortex

A

crucial for goal directed behaviours

205
Q

ventromedial prefrontal cortex

A

valuation system, that ranks choices on the basis of their perceived worth. and potential reward

206
Q

choice system

A

dorsolateral prefrontal cortex, dorsal anterior cingulate cortex, and parietal regions - sifts through evaluated alternatives and produces the conscious decision

207
Q

when people are uncertain

A

prefrontal cortex becomes active, and dorsal cingulate cortex may imrpove decisions by delaying action until full procesing

208
Q

activity of the amygdala increases when

A

people have made wrong, costly choice, also increases in obitofrontal aspect of prefrontal cortex, probably reflecting the perception of diminished reward and increasing aversion to loss

209
Q

tachistoscope test

A

pit the two hemispheres against eachother using a device that presents visual stumli to the left or right half of the visual field

if stimulus exposure lasts less than 150 ms, input is restricted on one hemisphere because there is not enough time for the eyes to shift their direction

in humans, processing may involve transmission of information through corpus callosum to other hemisphere

210
Q

comunication involves

A

left hemisphere specilazation

211
Q

perception of music is shown in

A

right hemisphere, but in advanced musiciansm it appears to strongly rely on left hemisphere and enhanced connectivity between left and right planum temporal

212
Q

prosody

A

perception of emotional tone of voice, and is seen as a right hemisphere specialization

213
Q

Phonemes

A

basic speech sounds

214
Q

Morphemes

A

simple units of meaning, assembled into words with meaning → semantics

un-, fathom, and -able all adds up to one meaning: unfathomable

215
Q

aphasia

A

impairment in language ability, to varying degrees, caused by brain injury, especially to the left hemisphere

Patients with aphasia also exhibit:

Agraphia → impairment in writing
Alexia → impairment in reading
Apraxia → motor impairment; difficult in making sequences of movements

216
Q

paraphasia

A

substitution of a word by a sound, incorrect word, or unintended word

217
Q

Broca’s area

A

region of the left inferior frontal region involved in speech production

Anterior lesions that include Broca’s area produce nonfluent (or Broca’s) aphasia – Difficulty in producing speech, but not in comprehension

Many people with nonfluent aphasia also have hemiplegia → paralysis of one side of the body, usually the right side

218
Q

Wernicke’s area

A

Damage to the left posterior speech zone causes fluent (or Wernicke’s) aphasia

region of the left posterior temporoparietal cortex involved in perception and production of speech

Wernicke’s aphasia:
Fluent, meaningless speech accompanied by many paraphasias and minimal language comprehension
Impaired ability to repeat words or phrases

cant comprehend language but fluent in speech

May also include anomia, word deafness, and/or word blindness

219
Q

global aphasia

A

total loss of the ability to understand or produce language

Results from widespread left-hemisphere lesions, affecting all speech zones

The prognosis for language recovery is poor, and this aphasia is often accompanied by other neurological impairments

220
Q

The connectionist model of aphasia

A

Also known as the Wernicke-Geschwind model says deficits result from disconnection between brain regions in the language network

Wernicke’s area decode sounds and transmits information to Broca’s area via the arcuate fasciculus

Broca’s area sends a speech plan to adjacent motor cortex to produce speech

Lesions that disrupt connections produce conduction aphasia → an impairment in the repetition of words and sentences

221
Q

The motor theory of language

A

Proposes that anterior and posterior left-hemisphere language zones originally evolved as specializations for programming and executing complex movements

The systems are involved in both production and perception of complex motions that produce speech

Users of sign language employ the same neural mechanisms speakers do, and following comparable brain injury, they exhibit the comparable aphasias

222
Q

PET scans reveal different brain region activation patterns for each level of processing words:

A

Passively viewing → posterior area within the left hemisphere

Passively hearing → temporal lobes

Repeating word → motor and supplementary motor cortex, some of the cerebellum

Generating associated word → language related regions of the left hemisphere, including Broca’s areas

223
Q

Language development depends on exposure during a

A

sensitive period (critical period)

After this period, langage can be learned, but more effort is required and different brain regions are used

224
Q

FOXP2 gene

A

important for the normal acquisition for human language

225
Q

Non-primate species display vocalizations to:

A

Signal danger
Readiness to mate
Emotional state, etc.

226
Q

Mice with FOXP2 mutations have impaired

A

ultrasonic vocalizations

227
Q

Bird vocalizations range from simple sounds to

A

complex songs

Complex vocalizations are critical for reproductive behaviours

228
Q

Subsong

A

Human babbling

229
Q

Plastic song

A

Species specific notes and song elements, but not yet fully formed song production

230
Q

Crystalized song

A

A fully developed species-specific song that it similar to a tutor (demonstrator)

231
Q

Parallels between birds and humans:

A

Specialized neural system for vocal behaviour

Distinct phases of song production including critical period for learning songs

Requires exposure form parents or tutors to develop properly

Blocked FOXP2 expression produces errors, as in humans

Different dialects of birdsong exist even within the same species
Birdsong changes over time

232
Q

williams syndrome

A

caused by deletion of 28 genes from chromosome 7, causes various intellectual deficits but excellent verbal skills

possession of extra copies rather deletions produces syndrome of very poor expressive language

233
Q

deep dyslexia

A

errors related to meanings od words

234
Q

aquired dyslexia

A

result of injury usually to left hemisphere

235
Q

surface dyslexia

A

have difficulties restricted to the details and sounds of letters

doesn’t occur in native speakers of languages that are perfectly phonetic (Italian, where every letter is pronounced)

236
Q

people with hemispatial neglect following right parietal lobe damage

A

disregard the left halves of the words they see despite having normal vision

PSYCH 2220 FINAL (1 decks)

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