Bio 334 (Part 4)

Front 1

where in the brain is language primarily

Back 1

left cerebral cortex

Front 2

which hemisphere is capable of speech

Back 2

left hemisphere

Front 3

does right brain have some understanding of language

Back 3

YES

Front 4

major language regions in the left brain

Back 4

broca's area, motor cotex, angular gyrus, wernicke's area, auditory cortex

Front 5

what is aphasia

Back 5

loss of ability to produce and/or to comprehend language

Front 6

what is wernicke's aphasia

Back 6

fluent aphasia=patients easily generate words, but the statements have little meaning

Front 7

what are paraphasic errors

Back 7

when patients substitute incorrect sounds or words.

Front 8

what is broca's aphasia

Back 8

motor or nonfluent aphasia= patients have difficulty generating words

Front 9

what is aggramatism

Back 9

patients don't use function words (articles, pronouns, conjuctions)

Front 10

what is the first stage of language processing

Back 10

frequency and temporal analysis carried out bilaterally in auditory cortex followed by phonological processing (extracting phonemes)

Front 11

two streams in language processing

Back 11

1. ventral stream
2. dorsal stream

Front 12

ventral stream

Back 12

maps sensory information onto "lexical conceptual representations"

Front 13

dorsal stream

Back 13

maps sensory information onto "articulatory motor representations"

Front 14

what is one problem associated with learning to speak a language

Back 14

spoken language doesn't reliably indicate breaks between words with a pause

Front 15

which properties of syllables do humans identify and use

Back 15

statistical properties

Front 16

what is attention

Back 16

a neural process by which you enhance your perception of certain stimuli relative to other stimuli in the environment

Front 17

what is bottom-up attention

Back 17

when the object “grabs” your attention without conscious knowledge of the stimulus. The stimulus is more salient than the background.

Front 18

what is top-down attention

Back 18

you consciously look for a specific object

Front 19

steps in change blindness

Back 19

1. visual transients produced by changes in color, shape,orientation that draw your attention to the location of the change
2. visual memory of what was at the site of the change so that you can identify what changed

Front 20

what does attention enhance

Back 20

detection of stimuli at site of attention

Front 21

what does attention reduce

Back 21

detection of stimuli away from site of attention

Front 22

what might the parietal lobe be involved in

Back 22

disengaging visual attention

Front 23

4 steps of shifting attention

Back 23

1. disengage from present location
2. move your attention to the new location
3. engage your attention at the new location
4. inhibit the previous site of attention

Front 24

neglect syndrome

Back 24

damage to the right parietal lobe disrupts visual attention to the left side of the visual space

Front 25

what does the parietal lobe participate in

Back 25

visual attention, in particular shifting visual attention

Front 26

Darwin's analysis regarding emotion

Back 26

1. cross-species similarities in the expression of emotion
2. there were a limited set of fundamental emotions

Front 27

james lange's theory of emotion

Back 27

ANS changes precede and produce emotions. We experience emotion as a consequence of autonomic activity

Front 28

cannon-bard theory of emotion

Back 28

the stimulus activates the thalamus which distributed the inputs to the cortex to create emotion and autonomic changes simultaneously. the autonomic changes are independent of emotion.

Front 29

problems with james-lange theory

Back 29

-emotions can be experienced even if no sense of physiological response is present
-fearful & angry states have similar autonomic responses, how do different emotions arise from similar physiological states?

Front 30

problems with canon-bard theory

Back 30

-emotions are less intense with the brain disconnected from the viscera
-artificial manipulations of autonomic activity can induce emotions

Front 31

zajonc theory of emotion and facial efference

Back 31

changes in venous blood flow created by patterns of facial muscle contractions produces small changes in brain temperature that alters mood

Front 32

describe the two stream circuit of emotion starting with the "thought stream" thalamus

Back 32

->sensory cortex ->cingulate gyrus produced perception, thought, and memory

Front 33

describe the two stream circuit of emotion starting with the "feeling stream" thalamus

Back 33

->mammillary bodies (hypothalamus)-> anterior thalamus -> cingulate cortex evoked the body's physiological response.

Front 34

what do emotions result from

Back 34

cingulate cortex activity

Front 35

what can emotions be evoked from

Back 35

sensory stimuli (thought stream) or physiological responses (feeling stream)

Front 36

what neural system did MacLean outline

Back 36

the limbic system= emotion arises by integrating external sensations with information from the body.

Front 37

what parts of brain play important roles in emotion

Back 37

-ventromedial prefrontal cortex/orbital frontal
-amygdala
-anterior cingulate cortex
-nucleus acumbens
-vental pallidum (basal ganglia)
-hypothalamus/basal forebrain

Front 38

what did Domasio and colleagues hypothesize

Back 38

that PFC creates "somatic markers" that link ANS activity to emotionally significant previous events, the somatic marker hypothesis

Front 39

what cant PFC lesion patients do

Back 39

identify long-term negative or positive consequences

Front 40

effect of frontal lobotomies

Back 40

disconnect the frontal and cingulate cortex in individuals with severe psychosis, blocking "too much" emotion

Front 41

amygdala

Back 41

"almond shaped" nucleus in the anterior end of the temporal lobe with several subdivisions- involved in fear

Front 42

evidence required to show that amygdala is involved in fear conditioning

Back 42

1. lesion of the amygdala b4 learning should prevent acquisition of fear conditioning
2. blocking cellular changes in the amygdala necessary to convert short-term to a long term memories should prevent long-term conditioned fear
3. the amygdala should alter its activity with fear conditioning

Front 43

does memory for emotional stimuli differ between sexes

Back 43

YES

Front 44

explain women's superior memory for emotional pictures

Back 44

better integration of brain processes associated with emotional experience into memory

Front 45

what is the insula

Back 45

neural center for disgust

Front 46

what receives emotional info for further evaluation

Back 46

1. rostral anterior cingulate cortex
2. dorsal anterior cingulate cortex
3. dorsomedial prefrontal cortex
4. ventromedial prefrontal cortex

Front 47

what do raCC and vmPFC do

Back 47

-gate info flow into conscious awareness
-provide excitatory and inhibitory feedback to core limbic structures

Front 48

what is arousal a measure of

Back 48

excitement level

Front 49

what is valence a measure of

Back 49

positivity

Front 50

part of brain associated with positive arousal

Back 50

nucleus accumbens

Front 51

part of brain associated with negative arousal

Back 51

amygdala

Front 52

where does nucleus accumbens receive dopamine input from

Back 52

ventral tegmental area (VTA)

Front 53

in who does activation of nucleus accumbens occur

Back 53

ppl who report experiencing pleasure

Front 54

what do humorous stimuli inc

Back 54

blood flow in many brain regions including nucleus accumbens

Front 55

what does amphetamine cause

Back 55

release of dopamine from dopamine terminals

Front 56

what is nucleus accumbens

Back 56

rostral striatum region in humans where the caudate and putamen and not divided by the internal capsule

Front 57

how much do the primary sensory and primary motor area account for

Back 57

20% of the neocortex

Front 58

association cortex

Back 58

remaining 80% of neocortex which is involved in further perceptual processing of sensory info, in motor planning, and in cognition

Front 59

cognition

Back 59

collective term for the complex functions of the brain having to do with language, thought, and the construction perceptions

Front 60

what does the neurochemical basis of mental illness typically involve

Back 60

norepinephrine, dopamine, serotonin

Front 61

cartesian dualism

Back 61

body and mind were considered separate entities- disorders of the body has a physical cause and were province of medicine but disorders of the mind had a spiritual or moral basis and were the province of religion

Front 62

Freud's influence on mental illness views

Back 62

mental illness arose from conflict between conscious and unconscious aspects of the psyche (mind)

Front 63

Freud's treatment for mental illness

Back 63

helping patients uncover incidents, usually from childhood that were suppressed from consciousness and hidden in the unconscious mind.

Front 64

how did psychopharmacology treatment of mental illness start

Back 64

with the chance discovery of antipsychotic action of chloropromazine (1952)

Front 65

what does biological psychiatry attempt to do

Back 65

establish the underlying neurochemical basis for mental illness

Front 66

anxiety disorders

Back 66

inappropriate expression of fear that is disabling

Front 67

stressor

Back 67

threatening stimulus

Front 68

what is the stress response characterized by

Back 68

-avoidance behaviors
-elevated arousal and vigilance
-activation of sympathetic division of the ANS
-release of cortisol (a glucocorticoid hormone) from the adrenal glands

Front 69

normal response to stress

Back 69

hypothalamic-pituitary-adrenal (HPA) axis:
-release of cortisol from adrenal glands is triggered by ACTH
-ACTH is released by the anterior pituitary gland under control of parvocellular neurosecretory neurons located in the paraventricular nucleus of the hypothalamus
-parvocellular hypothalamic neurons release CRH into the blood of the portal circulation

Front 70

what causes CRH (corticotropin releasing hormone) release

Back 70

neocortex & thalamus send sensory info that increases activity in the amygdala, which in turn activates the hypothalamus and stimulates CRH release

Front 71

where has inappropriate activation of the amygdala by non-threatening stimuli been implicated

Back 71

anxiety disorders

Front 72

effect of cortisol binding to glucocorticoid receptors on hippocampal neurons

Back 72

enhances their activity, inhibits CRH release from hypothalamic neurosecretory neurons. (hypothalamus provides neg feedback regulation of HPA)

Front 73

effect of continuous exposure of hippocampus to cortisol during chronic stress

Back 73

-reduces the number of dendrites of hippocampal neurons
-neuronal death in hippocampus
-loss of inhibitory control of HPA axis by the hippocampus, inducing a vicious cycle of runaway activation

Front 74

what have anxiety disorders been linked to

Back 74

-hyperactivity of the amygdala
-reduced activity in the hippocampus

Front 75

describe the regulation of HPA axis by the hippocampus

Back 75

prolonged elevation of cortisol -> loss of neurons in the hippocampus -> dec. inhibition of HPA axis by the hippocampus
-> enhanced release of cortisol from adrenal glands ->cycle restarts

Front 76

treatments for anxiety disorders

Back 76

-psychotherapy
-anxiolytic drugs

Front 77

psychotherapy mechanism

Back 77

may use the ability of the brain to alter synaptic efficacy based on experience to reduce the ability of non-threatening stimuli to activate the stress response

Front 78

anxiolytic drugs

Back 78

-benzodiazepines
-selective serotonin reuptake inhibitors
-serotonin norepinephrine reuptake inhibitors

Front 79

benzodiazepine action

Back 79

bind to GABA_A receptors and make them more responsive to GABA.
(presumably they act to suppress activity of stress circuits)

Front 80

ethanol affect on GABA

Back 80

facilitates GABA actions

Front 81

where are neurons that release serotonin found, where do they project to

Back 81

in the raphe nuclei of the brain stem and project diffusely through the brain and spinal cord

Front 82

how does serotonin act

Back 82

via G-protein coupled receptors to modulate neuronal activity in many brain regions

Front 83

what is serotonin's action terminated by

Back 83

reuptake via serotonin transporters

Front 84

what is SSRIs therapeutic effect caused by

Back 84

some unknown adaptive changes in the brain to chronically elevated external serotonin

Front 85

one adaptive effect of SSRIs

Back 85

increase the number of glucocorticoid receptors in the hippocampus- this might enhance the feedback inhibition of the HPA axis by the hippocampus

Front 86

norepinephrine

Back 86

diffuse modulatory system that targets many brain regions

Front 87

where are the neurons that release norepinephrine found

Back 87

in the locus coeruleus in the brain stem

Front 88

what is norepinephrine's action terminated by

Back 88

reuptake via norepinephrine transporters

Front 89

effect of SNRIs

Back 89

inhibit both serotonin and norepinephrine transporters, prolonging the action of both neurotransmitters

Front 90

affective disorders

Back 90

disorders of emotional state or mood (affect)

Front 91

major depression

Back 91

severe depression lasting >2 weeks, often without obvious external cause and often accompanied by the feeling of losing control of one's emotional state

Front 92

major depression symptoms

Back 92

-lowered mood & dec interest
-loss of appetite
-insomnia
-fatigue
-feelings of worthlessness & guilt
-diminished concentration
-recurrent thoughts of death

Front 93

dysthymia

Back 93

milder form of depression but is chronic

Front 94

what is bipolar disorder characterized by

Back 94

repeated bouts of mania or hypomania, sometimes alternating with depression

Front 95

manic phase

Back 95

-abnormally elevated, expansive, or irritable mood (DIGFAST)
Distractibility
Indiscretion
Grandiosity
Flight of ideas
Activity increase
Sleep deficit
Talkativeness

Front 96

hypomania

Back 96

similar to mania but doesn't severely impair social interactions or work performance (in fact creativity & performance can be greatly enhanced)

Front 97

monoamine hypothesis

Back 97

depression and mania are disruptions of one or both of these diffuse modulatory systems (catecholamine & serotonin)

Front 98

clues that led to monoamine hypothesis

Back 98

1. treatment of high bp with reserpine, which blocks loading of serotonin & catecholamines into synaptic vesicles, caused depression in 30% of patients
2. a drug for treating tuberculosis that inhibited MAO (enzyme that degrades catecholamines & serotonin) produced mood elevation
3. the antidepressant drug, imipramine, was found to block the reuptake of serotonin and norepinephrine

Front 99

what is the diathesis-stress hypothesis of affective disorders

Back 99

predisposing factors interact with stress to produce depression

Front 100

evidence supporting diathesis-stress hypothesis

Back 100

-anxiety & depression coexist in patients, and anxiety is related to HPA axis
-in depression, pituitary & adrenal gland are enlarged
-in depression, # CRH neurons in hypothalamus and expression of CRH inc.
-blood cortisol & CRH concentration in CSF are elevated in depressed patients
-elevated CRH is reduced by treatments that alleviate depression
-delivery of CRH to the brain in animals produces behavioral effects similar to depression in humans
-rats that receive lots of maternal care as pups have inc glucocorticoid receptors in hippocampus, reduced reduced CRH in hypothalamus, less anxiety
-inc in glucocorticoid receptors in hippocampus is mediated by serotonin release
-effect of experience on adult anxiety is restricted to postnatal critical period
-in humans, childhood abuse & neglect increase risk for developing affective & anxiety disorders
-dec. feedback inhibition of HPA axis may make brain more susceptible to depression & anxiety

Front 101

treatments for affective disorders

Back 101

-electroconvulsive therapy
-tricyclic antidepressant drugs (block reuptake of NE & serotonin)
-selective serotonin reuptake inhibitors
-MAO inhibitors (block enzyme degradation of serotonin & norepinephrine)
-lithium (treats bipolar disorder)

Front 102

psychosis

Back 102

loss of contact with reality

Front 103

schizophrenia

Back 103

disruption of perception, thought, mood, movement, and loss of contact with reality

Front 104

percent of population schizophrenia affects

Back 104

1% of population

Front 105

what are positive symptoms

Back 105

occurence of abnormal thoughts and behaviors

Front 106

examples of positive symptoms of schizophrenia

Back 106

delusions, hallucinations, disorganized speech, catatonic behavior

Front 107

what are negative symptoms

Back 107

absence of normal responses

Front 108

examples of negative symptoms of schizophrenia

Back 108

reduced expression of emotion, poverty of speech, difficulty initiating goal-directed behavior, memory impairment

Front 109

describe familial nature of schizophrenia

Back 109

variations in a number of genes have been linked to increased susceptibility to schizophrenia

Front 110

can genetic background enhance vulernability to developmental/enrionmental factors that lead to schizo?

Back 110

YES

Front 111

gross changes in schizophrenic brains

Back 111

1. ventricles are enlarged in the brain of schizo identical twin-> consistent with a loss of brain tissue in schizo
2. reduced metabolic activity in frontal lobes of schizo. patient-> consistent with reduced activity or loss of neurons in the frontal lobes of schizo.

Front 112

what do amphetamine addicts sometimes experience

Back 112

amphetamine psychosis, with symptoms similar to schizo.

Front 113

what does amphetamine cause

Back 113

massive dopamine release

Front 114

what are drugs that improve positive symptoms of schizo. called?

Back 114

neuroleptic drugs-> blockers of dopamine D2 receptors

Front 115

what might be involved in schizo.?

Back 115

dopamine projections from VTA to the frontal lobes

Front 116

effect of "typical" neuroleptics targeting D2 receptors in the striatum and the cortex

Back 116

common motor problems (extrapyramidal symptoms) in patients taking these neuroleptic drugs->distinct gait that resembles Parkinson's

Front 117

what is dyskinesia

Back 117

another common side effect of neuroleptic drugs

Front 118

what naturally occurring compounds alter perception & cognition, and can induce hallucinations

Back 118

-psilocybin, found in psilocybin mushrooms
-mescaline, in peyote cactus

Front 119

what does the similarity of hallucinogens and serotonin suggest

Back 119

that the diffuse serotonin neuromodulatory system might be involved in some of the symptoms of schizophrenia

Front 120

what have "Atypical" neuroleptics been found to be more potent blockers of

Back 120

serotonin receptors

Front 121

what symptoms do atypical neuroleptics reduce

Back 121

negative symptoms

Front 122

what do atypical neuroleptics affect

Back 122

other neurotransmitter systems like norepinephrine, histamine, and ACh

Front 123

what is phencylidine

Back 123

non-competitive antagonist of NMDA receptors, and it blocks by occupying a site within the open pore

Front 124

what other NMDA receptor blockers that occupy same site on open pore as phencylidine

Back 124

ketamine and MK-801

Front 125

what do NMDA hypomorphs exhibit

Back 125

schizophrenia-like symptoms, such as repetitive movements and altered social interactions

Front 126

glutamate hypothesis of schizophrenia

Back 126

reduced NMDA receptor activity plays a role in schizophrenia

Front 127

what are deficits in cognition caused by brain damage

Back 127

-agnosias
-apraxias

Front 128

global cognitive loss

Back 128

alzheimer's disease

Front 129

what does damage in perisylvian fissure in dominant hemisphere lead to

Back 129

severe aphasias

Front 130

right hemisphere damage

Back 130

subtle deficits of language, humor or irony

Front 131

agnosia

Back 131

inability to identify objects based on sensory info, even though the primary sensory cortical areas are intact

Front 132

what do specific types of agnosia typically result from

Back 132

lesions in parietal or temporal lobe, in areas near the primary sensory cortex for the major sense

Front 133

what is tactile agnosia where patient has normal sense of touch in hands but cant identify object in hands

Back 133

astereognosis

Front 134

what's alexia

Back 134

-visual agnosia, which results from lesions of angular gyrus
-patients can can't recognize written words

Front 135

prosopagnosia

Back 135

visual agnosia where patients are unable to recognize familiar faces

Front 136

apraxia

Back 136

difficulty in programming complex series of movements, without paralysis, sensory deficits, or problems performing simple tasks

Front 137

where are lesions responsible for apraxia

Back 137

in parietal and temporal areas

Front 138

different forms of apraxia

Back 138

-ideational apraxia
-ideomotor apraxia
-limb-kinetic apraxia
-orofacial apraxia
-verbal or speech apraxia

Front 139

what do lesions in supramarginal gyrus produce

Back 139

conduction aphasia and a form of apraxia in which patients cant follow verbal commands to carry out motor actions (similar to ideomotor apraxia)

Front 140

dementia

Back 140

loss of cognitive abilities

Front 141

alzheimers disease

Back 141

most prevalent form of serious age-related dementia, produced by progressive death of neurons in a wide variety of brain regions including neocortex

Front 142

gross brain changes in alzheimers brain

Back 142

-shrinkage of gyri
-sulci expanded
-cortex shrinks
-no hippocampus

Front 143

what do PET scans of alzheimers patients show

Back 143

severely depressed metabolic activity cuz of no neurons

Front 144

why do neurons die in alzheimers disease

Back 144

two types of abnormal structures accumulate in areas where neurons are dying: neuritic plaques and neurofibrillary tangles

Front 145

what are neuritic plaques

Back 145

extracellular accumulations of protein, consisting largely of beta-amyloid protein (A-beta)

Front 146

what are neurofibrillary tangles

Back 146

abnormal intracellular aggregates of a microtubule-associated protein called tau

Front 147

what is tau

Back 147

normal component of microtubules that helps stabilize the polymers of tubulin molecules

Front 148

what does dephosphorylated tau do

Back 148

binds to tubulin and stabilizes microtubules

Front 149

what does phosphorylated tau do

Back 149

dissociates from tubulin, destabilizing microtubules

Front 150

what molecule myperphosphorylates tau in alzheimers disease

Back 150

cyclin-dependent kinase 5 (cdk5)

Front 151

what occurs as a result of hyperphosphorylated tau

Back 151

chronic disruption of microtubules, which may kill neurons

Front 152

how is A-beta produced

Back 152

selective proteolytic of a protein called amyloid precursor protein (APP) which is a normal component of neuronal membranes

Front 153

what is A-beta like normally

Back 153

soluble, and doesnt accumulate in the extracellular space of the brain. it is cleared into CSF

Front 154

A-beta in alzheimers disease

Back 154

insoluble, accumulate into plaques

Front 155

what are secretases

Back 155

proteases that release A-beta

Front 156

what does beta-secretase do

Back 156

cuts off most of the extracellular part of APP

Front 157

what does gamma-secretase do

Back 157

cuts within the membrane to release A-beta

Front 158

two forms of A-beta produced, which is more toxic and why

Back 158

40 amino acids or 42 amino acids, the latter is toxic because its more hydrophobic

Front 159

what has been shown to produce familial alzheimers disease (early onset that progresses rapidly)

Back 159

variety of mutations in APP

Front 160

where are mutations for alzheimers

Back 160

-within A-beta portion of APP or at other sites that inc production of A-beta
-mutations in presenilin, component of gamma-secretase complex responsible for cleavage of A-gamma

Front 161

when is synthetic Alpha-beta toxic

Back 161

when applied to cortical and hippocampal neurons in culture or in vivo

Front 162

why is A-beta toxic

Back 162

-inflammation
-excitotoxicity
-synaptotoxicity
-decreased spontaneous action potential activity

Front 163

inflammation of A-beta

Back 163

local inflammation which may damage surrounding neurons

Front 164

excitotoxicity of A-beta

Back 164

neuronal death induced exogenous A-beta can be lessened by NMDA receptor blockers. thus, A-beta may cause depolarization which allows Ca in through NMDA receptors

Front 165

synaptotoxicity of A-beta

Back 165

exogenous A-beta causes reduced numbers of dendritic spines in hippocampal neurons and loss of excitatory synapses

Front 166

treatments of alzheimer's disease

Back 166

-anti inflammatory drugs
-reducing production of beta and gamma-secretase inhibitors; promoting alpha-secretase
-reducing oligomerization of A-beta (prevents formation of dimers)
-up-regulate enzymes that degrade extracellular A-beta
-neuroprotective compounds; try to prevent neuronal death causes by excitotoxicity or prevent loss of synapses