Mcb 314 Exam 4

Front 1

4 features of emotions

Back 1

1. Inwardly experienced subjective "feelings" - happy, sad, angry, disgusted, surprised, scared

2. Outwardly observable behavioral responses - smile, shake, laugh, cry

3. Communication of internal state to others - body language, facial expressions

4. Physiological changes (autonomic involvement) - tears, heart rate, blood pressure

Front 2

2 theories of emotion

Back 2

James-Lange theory and Cannon-Bard theory

Front 3

James-Lange theory (1880s)

Back 3

physiological expression (heart rate, sweating, dry mouth) leads to conscious emotional experience

Front 4

Cannon-Bard theory (1920s)

Back 4

conscious emotional experience leads to physiological expression

Front 5

Current view on emotion

Back 5

emotional responses involve a two way interaction between expression and experience; a mixture of both theories

Front 6

Cannon and Bard cat experiments

Back 6

catswith cortex removed, but with the posterior hypothalamus intact (connected to spinal cord),exhibited shamrage, anundirected outburst resembling fear and aggression; -posteriorhypothalamus is important for expression of anger and aggression, and this response is normallyinhibited by cortical brain centers

cerebral cortex regulates emotional expression via connections to hypothalamus

Front 7

What is the limbic areas?

Back 7

a group of brain areas important in emotional processing

Front 8

What does limbus mean?

Back 8

border or belt

Front 9

Limbic structures form the inner border of the _________

Back 9

cortex

Front 10

Limbic system is misleading term because:

Back 10

these areas interact with many other brain areas

Front 11

What constitutes the limbic areas?

Back 11

cingulate gyrus, hippocampus, amygdala, anterior thalamic nucleihypothalamus

Front 12

How does the rabies virus affect the limbic areas?

Back 12

Rabies virus causes inflammation in limbic areas of the brain.Animals may become restless and aggressive. They might try to bite other animals or objects. In other cases, infected animals may become shy and try to hide. These behaviors reflect disruption of emotional processing circuits.

Front 13

What is the papez circuit?

Back 13

a major limbic pathway that is hypothesized to link emotional experience (cingulate cortex) and emotional expression (hypothalamus)

Front 14

What does the cingulate cortex do?

Back 14

cingulate cortex mediates emotional experience

Front 15

What does the hypothalamus do?

Back 15

hypothalamus mediates emotional expression

Front 16

What does the hippocampus do?

Back 16

hippocampus mediates episodic memory (autobiographical)

Front 17

Are emotional facial expressions voluntary or involuntary?

Back 17

involuntary

Front 18

What are emotional facial expressions controlled by?

Back 18

controlled by hypothalamus and medial forebrain areas

Front 19

How does fake smile occur?

Back 19

voluntary pathways from motor cortex can mimic emotional expressions, but imperfectly; able to voluntarily control of upward turn of mouth/lips, but unable to voluntarily activate orbicularis oculi muscles around the eyes

Front 20

What is a Duchenne smile

Back 20

smile involving both eye muscles and mouth muscles

Front 21

What is a mirror neuron?

Back 21

A mirror neuron is a neuron that fires both when an animalacts and when the animal observes the same action performed by another.

Front 22

What does human infant data say about mirror neurons?

Back 22

Human infant data suggest that the mirror neuron systemdevelops before 12 months of age, and may help infants understand other people's actions.

Front 23

What evidence is there for mirror neurons being related to empathy?

Back 23

Experiments using fMRI, EEG, and MEG have shown that certain brain regions (the anterior insula, anterior cingulate cortex, and inferior frontal cortex) are active when people experience an emotion (disgust, happiness, pain, etc.) and when they see another person experiencing an emotion.

Front 24

What does Ramachandran think about mirror neurons?

Back 24

thinks mirror neurons and the human capacity for empathy are the basis for the emergence of civilization.

Front 25

How is the amygdala related to fear?

Back 25

Learned fear (as opposed to innate fear), the amygdala is involved in forming memories and associations related to aversive events, forms negative associations with initially neutral stimuli

Front 26

What animal studies have been made to relate the amygdala to fear?

Back 26

bilateral amygdalectomy reduces fear and aggression in animals (Klüver-Bucy syndrome);

electrical stimulation of amygdala -> increased vigilance or attention

Front 27

What human studies have been made to relate the amygdala to fear?

Back 27

fearful faces produce greater amygdala activity than happy/neutral faces (functional brain imaging),

case study: woman with bilateral destruction of amygdala unable to recognize fear in facial expressions

Front 28

What are 5 features of predatory aggression?

Back 28

attack prey for food, few vocalizations, no amygdala involvement, activation of lateral hypothalamus (feeding center), low levels of sympathetic activity

Front 29

What are 4 features of affective aggression?

Back 29

used for show, not to obtain foodvocalizations, threatening posturecat hissing and arching its backactivation of amygdala, high levels of sympathetic activity(fight or flight response)

Front 30

How is serotonin connected to the limbic system?

Back 30

serotonergic neurons from the Raphe nuclei project to the hypothalamus and limbic structures

Front 31

What does serotonin do for aggression?

Back 31

serotonin helps keep aggression in check, low serotonin levels could unleash disproportionately violent reactions to mild threats

Front 32

What is the ultimatum game?

Back 32

Ultimatum game: Player A is allotted a sum of money, but must make a proposal for a split with a second player B. If player B accepts the offer, both get the money according to the proposal. If player B refuses, neither gets any money. Serotonin-depleted individuals are more likely to refuse low offers and are more likely to get angry at Player A for making a low offer. Administering SSRIs makes test subjects more ‘agreeable’ to accepting low offers.

Front 33

What does circa - dian mean?

Back 33

Approximately, a day;

Front 34

Will circadian rhythms continue in the dark?

Back 34

normally synchronized to daily cycles of light and dark (entrainment)if light stimuli and other cues are removed, circadian rhythms will continue in the dark (free running)

Front 35

Where is the SCN (suprachiasmatic nucleus)?

Back 35

The hypothalamus houses a circadian clock called the suprachiasmatic nucleus (SCN); SCN neurons contains a molecular clock; lesions to the SCN disrupt circadian rhythms of behavior and hormone secretion; master circadian clock

Front 36

Where does SCN neurons get retinal input?

Back 36

SCN neurons gets retinal input from specialized photoreceptive ganglion cells; these ganglion cells contain their own special photopigment, melanopsin - melanopsin is slowly excited by light (over several seconds); not dependent on rods or cones for detecting light - transgenic mice that lack retinal photoreceptors will still entrain their activity patterns to light if melanopsin- containing ganglion cells are present

Front 37

What is sleep??

Back 37

a readily reversible state of reduced responsiveness to the environment;one-third of our lives spent in sleep state; long-term sleep deprivation is devastating, potentially fatal

Front 38

What are the stages of sleep?

Back 38

stage 1, 2, 3/4, rem

Front 39

What is stage 1 sleep?

Back 39

initial stage of non-REM sleep between sleep and wakefulness; characterized by theta activity (3.5-7.5 Hz) EEG waves; muscles are active but reduced muscle tension

Front 40

What is stage 2 sleep?

Back 40

non-REM sleep that is defined by bursts of regular 14- to 18- hertz EEG waves called sleep spindles

Front 41

What is stage 3/4 sleep?

Back 41

slow-wave sleep that is defined by the presence of large amplitude, slow delta waves

Front 42

What is REM sleep?

Back 42

rapid eye movement (REM) phase, muscles are paralyzed (sleep paralysis), brain is highly active, EEG similar to awake state; dreaming

Front 43

How do dolphins sleep?

Back 43

need to breathe air every minute or so, sleep cycle lasts for 12 hours, left hemisphere sleeps, both sides awake, right hemisphere sleeps

Front 44

What is the EEG and what's it used for?

Back 44

Noninvasive measurement of cortical activity from scalp, Used to diagnose neurological conditions such as epilepsy, sleep disorders

Front 45

What is the EEG measuring?

Back 45

EEG records very small electrical fields generated by synaptic currents from thousands of neurons; EEG amplitude reflects NUMBER OF NEURONS and SYNCHRONY

Front 46

4 categories of EEG rhythms based on frequency

Back 46

Beta, alpha, theta, delta

Front 47

What's beta EEG

Back 47

Beta: 14-40 Hzalert, conscious activity (high frequency, low amplitude)

Front 48

Whats alpha EEG

Back 48

Alpha: 8-13 Hz quiet, awake state (relaxed, meditative)

Front 49

What is theta EEG

Back 49

Theta: 4-7 Hz light sleep states

Front 50

What is delta EEG

Back 50

Delta: < 4 Hzdeep sleep (slow frequency, high amplitude EEG)

Front 51

How do thallamic oscillations display themsleves on EEGs?

Back 51

contribute to synchronized, large amplitude EEG waves, involves both intrinsic membrane properties and extrinsic feedback circuit properties

Front 52

What is an epiletic seizure?

Back 52

pathological form of synchronous brain activity

Front 53

What are the effects of epiletic seizure?

Back 53

arising from tumor, trauma, infection, vascular disease, cause often unknown, results from a disruption of normal balance of excitation/inhibition, often involving GABAergic circuits; outward effects can include uncontrolled body movements (tonic-clonic seizure), loss of consciousness, or brief loss of awareness (absence seizure)

Front 54

What is orexin and an alternate name for it?

Back 54

Orexin, also called hypocretin, is a peptide neurotransmitter that regulates arousal and wakefulness.

Front 55

How is orexin produced?

Back 55

produced by neurons in the hypothalamus, targets include Raphe nuclei (serotonin) and locus coerelus (NE)

Front 56

How is orexin and narcolepsy related?

Back 56

The most common form of narcolepsy (excessive sleepiness and sleep attacks) is caused by a lack of orexin in the brain due to destruction of the cells that produce it.

Front 57

What is adenosine?

Back 57

adenosine is a putative endogenous somnogen, actions are generally inhibitory, reduces neural activity, acts as a sedative, adenosine accumulates in the brain during prolonged wakefulness and may constitute the physiological signal for homeostatic sleep need

Front 58

What does putative endogenous somnogen mean?

Back 58

putative: supposed

somnogenic = sleep promoting, elevated adenosine levels cause drowsiness

Front 59

What does caffeine do to adenosine receptors?

Back 59

caffeine blocks adenosine receptors; caffeine readily crosses the blood-brain barrier; caffeine is structurally similar to adenosine, and is capable of binding to adenosine receptors on the surface of cells without activating them, thereby acting as a competitive inhibitor; blocks the drowsiness signal

Front 60

How does REM sleep prevent people from acting in their dreams?

Back 60

characterized by reduced somatic sensation and complete muscle paralysisprevents individuals from acting out their dreams; sleep paralysis is the sensation of temporarily being unable to move that sometimes occurs when awakening from REM sleep; GABA acting on dorsal column nuclei is responsible for reduced somatic sensationGlycine acting on alpha motor neurons in the ventral horn is responsible for muscle paralysis

Front 61

What is Broca's area?

Back 61

Paul Broca, 1864left hemisphere (typically)inferior frontal lobelanguage production

Front 62

What is Wernicke's area

Back 62

Carl Wernicke, 1874left hemisphere (typically)superior temporal lobelanguage understanding

Front 63

What constitutes Broca's aphasia? (expressive aphasia)

Back 63

difficulty speaking, non-fluent, halting, difficult to initiate, labored, can understand language that is heard or read, anomia - problem “finding” words

Front 64

What is Wernicke's aphasia? (receptive aphasia)

Back 64

fluent speech, but random, nonsensical, off-topic, …poor comprehension, can’t follow instructionscan “read” words, without understanding what they mean

Front 65

What is conduction aphasia (associative aphasia)?

Back 65

lesion of arcuate fasiculus (fiber tract) connecting Wernicke’s area and Broca’s area

Front 66

What happens in conduction aphasia?

Back 66

good speech comprehension, fluent speech production, poor speech repetition, paraphasiaunintended substitution of words/phonemes

Front 67

How does aphasia manifest bilingually?

Back 67

second language typically suffers more than first-learned, but not always; languages learned simultaneously suffer equally

Front 68

How does aphasia manifest in sign language users?

Back 68

analogous to speech aphasias - in one subject with both verbal and sign-language abilities, both modalities recovered together following left hemispheric stroke (suggests shared brain regions for both verbal and sign language)

Front 69

What is the Wada procedure?

Back 69

determine hemispheric dominance for speech, often performed before brain surgery for epilepsy, anesthetize half the brain by injecting anaesthesia into carotid artery; in most cases, anaesthesia of the left hemisphere disrupts speech

Front 70

Split-brain subject with left hemispheric language dominance will exhibit:

Back 70

can name words/objects presented to the right visual fieldunable to name words/objects presented to the left visual field, but is able to draw them

Front 71

Language abilities of the right (non-dominant) hemisphere

Back 71

can read and understand numbers, letters, and short words, but response must be nonverbal; right hemisphere better at drawingcomplex puzzles3D perspectivesound nuances

Front 72

What is attention?

Back 72

the brain selectively processes subsets of information from the incoming sensory data stream, ability to “focus” on a particular object or task, ignore distractions, improves performance on behavioral tasks

Front 73

Attention enhances _____ detection

Back 73

visual

Front 74

Attention reduces _________

Back 74

Visual reactoin times; visual transduction - unchanged, visual processing - faster, motor coding - unchanged, muscle activation - unchanged

Front 75

What is hemispatial neglect syndrome?

Back 75

a disorder involving attentional blindness to an entire half-space; most commonly involves neglect of the left half-space and is associated with lesions of right posterior parietal cortex; The disparity may reflect the fact that the right hemisphere is specialized for spatial processing of both L and R visual fields.; L side of brain: processes and can direct attention to objects in R visual fieldR side of brain: processes and can direct attention to either L or R visual fields

Front 76

What do neuroblasts give rise to?

Back 76

neurons and glia

Front 77

What does the dorsal telencephalon make?

Back 77

origin of pyramidal neurons and cortical astrocytes

Front 78

How do cells migrate along the dorsal telencephalon?

Back 78

cells migrate vertically from ventricular zone along thin radial glial fibers

Front 79

What does the ventral telencephalon make?

Back 79

origin of inhibitory interneurons (GABAergic) and oligodendrocytes

Front 80

How do cells migrate along the ventral telencephalon?

Back 80

cells migrate laterally over a relatively long distance to arrive at their final location in cortex

Front 81

What are the three phases in forming long-range connections?

Back 81

find/follow appropriate pathway, find appropriate target structure, find specific target cell type and formsynapse

Front 82

What is a growth cone?

Back 82

dynamic, actin-supported extension of a developing axon seeking its synaptic target

Front 83

What is fasciculation?

Back 83

bundling of axons held together by cell adhesion molecules (CAMs)

Front 84

NCAM

Back 84

neural cell adhesion molecule, axon fasciculation

Front 85

Laminin

Back 85

proteins of the basal lamina of extracellular matrix (ECM)

Front 86

Integrins

Back 86

CAMs that mediate attachment to ECM

Front 87

Three steps in formation of CNS synapse

Back 87

dendritic filopodium contacts axon, synaptic vesicles and active zone proteins recruited to presynaptic membrane,neurotransmitter receptors accumulate on postsynaptic membrane

Front 88

What is nonassociative learning

Back 88

Change in behavioral response over time in response to a single type of stimulus

Front 89

What are the two parts of nonassociative learning

Back 89

habituation: decreased behavioral response over time to repeated stimulation; sensitization: increased behavioral response over time to repeated stimulation

Front 90

What is associatve learning?

Back 90

Change in behavioral response over time to repeated pairing of two different stimuli

Front 91

What does classical conditioning do?

Back 91

repeated pairing of CS and US (with CS slightly preceding US); after conditioning: presentation of CS alone will elicit CR

Front 92

4 Experimental advantages of invertebrate nervous systems

Back 92

small nervous systems, large neurons, identifiable neurons, identifiable circuits

Front 93

LTP and LTD can be viewed as two aspects of a

Back 93

Hebbian synaptic modification rule

Front 94

What's a Hebbian synaptic modification rule?

Back 94

1. neurons that fire together, wire together

2. neurons that are out of sync, lose their link

3. mechanism involves different types of glutamate receptors (AMPA, NMDA, metabotropic)

Front 95

What is BCM (Bienenstock, Cooper, Munro) theory

Back 95

theoretical model for bidirectional changesin synaptic strength(increases and decreases)

Front 96

What is the BCM hypothesis?

Back 96

when the postsynaptic cell is weakly depolarized, active synapses undergo LTD, when the postsynaptic cell is strongly depolarized, active synapses undergo LTP;

Front 97

What is amnesia?

Back 97

abnormal forgetting; loss of long-term, declarative memories that should have been retained and/or inability to store new memories

Front 98

What is retrograde amnesia?

Back 98

forgetting things that had occurred prior to the time of the trauma

Front 99

What is anterograde amnesia?

Back 99

inability to form new memories following the time of trauma

Front 100

What is transient global amnesia?

Back 100

brief episode (hours-days), usually involving both anterograde and retrograde symptoms

Front 101

What is the hypothesis for Hebb and the cell assembly?

Back 101

Hypothesis: external events are represented by reciprocally interconnected groups of cortical neurons (cell assembly)

Front 102

What's the cell assembly concept?

Back 102

1. formed via Hebb rule: cells that fire together, wire together

2. memories are distributed among all the linked cells in the assembly

3. memory completion: partial activation of the assembly can trigger activation of the entire assembly

Front 103

What was Patient H.M.?

Back 103

to control severe epilepsy, Henry Molaison underwent surgery to bilaterally remove large portions of the medial temporal lobes including most of hippocampus and amygdala; surgery at age 27, in 1953

Front 104

What were the side effects of patient H.M.'s surgery?

Back 104

severe anterograde amnesia and partial retrograde amnesia; had little effect on perception, intelligence, personality and short term memory; Procedural memories and procedural learning

Front 105

What happened to Clive Wearing?

Back 105

musician, suffered extensive damage to temporal lobes and hippocampus at age 46 (viral encephalitis); severe anterograde amnesia, unable to store new memories, working memory ~10-30 sec

Front 106

The hippocampus and related medial temporal lobe structures play an important role in memory consolidation

Back 106

initially, the medial temporal lobe (MTL) links together various attributes of an event originating in diverse cortical areas, during consolidation, the links are moved from MTL to the original cortical areas, before consolidation is complete, the hippocampus and related structures are required to access and retrieve the stored memories

Front 107

What is DNMS?

Back 107

Delayed non-match to sample task

Front 108

What happens during DNMS?

Back 108

compare presented objects with a previously presented object after a delay, select the ‘novel’ non-matching object to obtain a reward, a form of RECOGNITION MEMORY, medial temporal lobe structures are important for memories longer than about 10-30 seconds

Front 109

What is the Radial arm maze?

Back 109

Normal rats learn which arms have food, and go down each arm only once, Rats with hippocampal lesions learn which arms have food, but visit those arms multiple times (i.e., return again after having already collected the food)

Front 110

What is the Morris water maze?

Back 110

rat must learn to find the location of a submerged platform, visual cues are placed around the pool, requires intact hippocampus; hippocampal ‘place cells’ fire when animal is in a specific location; place cells ‘rotate’ with external visual cues

Front 111

What part of the brain activates during the human PET imaging study during spatial navigation of a virtual town

Back 111

hippocampus

Front 112

What part of the brain is involved in habit learning?

Back 112

Striatum

Front 113

What does the striatum do?

Back 113

procedural memory task, slow learning over many repeated trials, automatic, unconscious response, T-maze task, low/high frequency tone indicates whether rat should turn left/right to receive a reward, neural responses in striatum change during learning

Front 114

What part of the brain is working memory involved?

Back 114

prefrontal cortex (PFC); PFC neurons are active during ‘delay’ period in delayed-response tasks

Front 115

Wisconsin card-sorting task

Back 115

sort cards by one of: color, shape, number; subjects are told right-or-wrong on each trial, sorting categories change periodically; patients with pre-frontal lesions have difficulty whenever the sorting category is changed

Front 116

What part of the brain is involved in working memory for eye movements?

Back 116

Lateral Intraparietal Cortex; area LIP neurons involved in guiding eye movements, active during ‘delay’ of delayed-saccade task

Front 117

Neurology

Back 117

branch of medicine concerned with the diagnosis and treatment of nervous system disorders, some representative neurological disorders; Alzheimer’s disease, Parkinson’s disease, stroke, multiple sclerosis, epilepsy

Front 118

Psychiatry

Back 118

branch of medicine concerned with the diagnosis and treatment of psychological disorders, representative psychiatric disorders (mental illness), anxiety disorders, affective (mood) disorders, depression, schizophrenia, psychosis

Front 119

Fear/stress

Back 119

an appropriate, adaptive response to threatening situations

Front 120

Anxiety disorders

Back 120

an inappropriate expression of fear / stress; panic disorder, generalized anxiety disorder, post-traumatic stress disorder (PTSD), phobias, obsessive-compulsive disorder

Front 121

What is compulsion?

Back 121

compulsion, repeated behaviors/rituals like hand-washing; not being able to perform the ritual causes great anxiety

Front 122

What is OCD hypothesis?

Back 122

hyperactivity in a positive feedback loop (self-reinforcing) :orbitofrontal cortex (decision-making, risk/reward, worry) cingulate gyrus (emotional coloring, Papez circuit, anxiety) basal ganglia (caudate/globus pallidus, action selection) thalamus orbital frontal cortex; severe OCD cases are sometimes treated by neurosurgical procedures that interrupt this loop; SSRIs are effective in treating many cases, serotonin may be involved in modulating circuit function

Front 123

What is a panic disorder?

Back 123

recurring, severe panic attacks; dysregulation (hypersensitivity) of HPA axis

hypothalamus, corticotropin-releasing hormone (CRH) pituitary gland, adrenocorticotropic hormone (ACTH) adrenal gland, cortisol

Front 124

what is a panic attack?

Back 124

inappropriate/exaggerated stress response; fight-or-flight symptoms: palpitations, sweating, trembling, shortness of breath, chest pain, nausea, dizziness, tingling sensations, …

Front 125

what are the treatment approaches for panic disorders?

Back 125

psychotherapy: stimulus-response relationship can be modified by experience, anxiolytic drugs: benzodiazepines (enhance GABA transmission)ativan (lorazepam), valium (diazepam), xanax (alprazolam)

Front 126

How is HPA regulated?

Back 126

HPA axis is regulated by the amygdala and hippocampus

Front 127

How do the amygdala and hippocampus both regulate the HPA axis?

Back 127

Both structures regulate CRH-releasing neurons of the hypothalamus

Front 128

How does the amygdala activate the HPA axis?

Back 128

enhances CRH release

Front 129

How does hippocampus deactivates the HPA axis?

Back 129

suppresses CRH release, glucocorticoid (cortisol) receptors in hippocampus - respond to cortisol released by the adrenal gland, forms a negative feedback loop

Front 130

What are two types of Anxiolytics

Back 130

Benzodiazapines (e.g. Valium, Xanax), SSRIs (e.g. Prozac, Celexa)

Front 131

What do benzodiazapines do?

Back 131

enhance GABA neurotransmission, suppression of circuits that trigger stress response?, can have other effects in addition to anxiolytic properties (dose dependent) - sedative, hypnotic, anticonvulsant, muscle relaxant, therapeutic effects are immediate

Front 132

What do SSRIs (e.g. Prozac, Celexa) do?

Back 132

selective-serotonin reuptake inhibitors, particularly effective for OCD, also act as antidepressants, therapeutic effect take several weeks to develop

Front 133

What are three types of Affective Disorders?

Back 133

“mood” disorders, depression, bipolar disorder (manic-depressive disorder)

Front 134

Two types of depression

Back 134

1.major depressive disorder (clinical depression, unipolar) - prolonged periods of sad, hopeless, worthless, pessimistic feelings; disrupted eating and sleeping patterns; fatigue; loss of interest or pleasure in activities; dysthymia - milder, more enduring form of depression

2. bipolar disorder (manic depressive disorder): repeated episodes of mania and depression; mania

Front 135

What is mania

Back 135

increased energy and activity, decreased need for sleep, pressured speech, racing thoughts, short attention span, distractible, irritable

Front 136

Two Biological bases of affective disorders

Back 136

Monoamine hypothesis, Diathesis-stress hypothesis

Front 137

What is the monoamine hypothesis?

Back 137

problems with diffuse modulatory systems - norepinephrine and serotonin; monoamine-related antidepressants must be taken for several weeks to become effective - chronic alteration of monoamine pathways may trigger longer-term ‘reconfiguration’ of modulated brain circuits

Front 138

What is Diathesis-stress hypothesis?

Back 138

diathesis = predisposition (genetic factors); focus is on HPA axis - blood levels of cortisol and CSF-levels of CRH are elevated in depressed individuals, influenced by both genetic and environmental factors

Front 139

What is Serotonin transporter polymorphism

Back 139

Two alleles of 5-HT transporter gene (long & short), evidence for gene x environment influences, supports diathesis-stress hypothesis

Front 140

What loss of contact with reality in schniaizophreia

Back 140

delusions (often persecutory), auditory hallucinations (hearing voices), jumbled, incoherent speech (word salad), emotional impairment

Front 141

Sscnisaghpherinia is a combination of ______

Back 141

combination of genetic and environmental influences

Front 142

What are the anatomical correlates (highly variable) of schizophrenia?

Back 142

enlarged ventricles, reduced hippocampal volume, changes in basal ganglia, frontal cortex

Front 143

What are teh pharmacological correlates of schiznophrenia?

Back 143

dopamine and glutamate effects

Front 144

Dopamine hyper-activity hypothesis of schizophrenia

Back 144

drug effectiveness of dopamine antagonists in treating schizophrenia is correlated with D2 receptor binding affinity, amphetamines enhance dopamine neurotransmission, “amphetamine psychosis” from chronic overuse has symptoms similar to schizophrenia

Front 145

Glutamate hypo-activity hypothesis of schizophrenia

Back 145

abnormally low levels of glutamate receptors found in the postmortem brains of those diagnosed with schizophrenia, PCP (phencyclidine), an NMDA receptor blocker, induces schizophrenia-like symptoms