Biopsych Test 3

Front 1

appetite control w/in the arcuate relies on two sets of arcuate neurons

Back 1

-(NPY/AgRP) neurons- each neuron expresses NPY (neuropeptide Y) and AgRP(agouti-related peptide)-these neurons stimulate appetite and reduce metabolism(leading to weight gain)
-other set of neurons are neurons containing (POMC (proopiomelanocortin) and CART (cocaine-and amphetamine related transcript))-these neurons inhibit appetite and increase metabolism-promoting weight loss

Front 2

both types of arcuate cells

Back 2

express leptin receptors and thus leptin influences the activity of both cell types
-leptin influences these cellular systems in opposite ways, it activates the appetite suppressing neurons (POMC/CART) and inhibits appetite increasing neurons (NPY/AgRP)-
-uses both systems to suppress hunger

Front 3

Ghrelin stimulates the NPY/AgRP cells to

Back 3

increase appetite

Front 4

primary regions w/in the hypothalamus that receive projections from these arcuate cells are called the

Back 4

second-order feeding neuclei-the two main regions are the LH and the paraventricular nucleus

Front 5

POMC/CART neurons project (primarily) to

Back 5

LH

Front 6

POM/CART neurons release

Back 6

alpha-MSH into the LH...which decreases LH activity
-since LH activity increases feeding...this results in a decrease in food intake

Front 7

The NPY/AgRP neurons also project to the

Back 7

LH
-these neurons release NPY into the LH and this increases feeding behavior

Front 8

infusion of mu-opioid receptor agonist DAMGO and GABA agonists

Back 8

increase feeding
so does infusion of AMPA receptor antagonists (and this glutamate effect requires activation of dopamine receptors)

Front 9

Endocannabinoids

Back 9

are very much involved in stimulating feeding

Front 10

24 hr molecular cycle driving the rhythmic activity of SCN cells (the process w/rproteins)

Back 10

1. clock and cycle bind together=dimer
2.dimer binds DNA enhancing transcription of Period (Per) and Cryptochrome (Cry)
3. Per and Cry bind with protein Tau
4. This protein complex inhibits the activity of the clock/cycle dimer slowing transcription of the per and cry genes and therefore slowing the production of the Per and Cry proteins
5. Per and cry proteins eventually break down, releasing clock/cycle from inhibition and allowing the cycle to start over again, this cycle takes 24 hrs to complete.

Front 11

tau mutations

Back 11

the period is shorter than normal

Front 12

single clock mutants

Back 12

period is longer than normal

Front 13

double clock mutants

Back 13

arrhythmic

Front 14

ultradian rhythms

Back 14

occur more than once per day (feeding, and hormone release)- bouts of activity

Front 15

an endogeneous cirannual clock

Back 15

runs at 365 days

Front 16

infradian rhythms

Back 16

occur less than once per day

Front 17

slow-wave sleep (SWS)

Back 17

divided into four stages characterized by slow-wave EEG activity

Front 18

Rapid-eye-movement sleep (REM)

Back 18

characterized by small amplitude, fast-EEG waves, no postural tension, and rapid eye movements. most often associated with dreaming

Front 19

waking

Back 19

desynchronized EEG beta activity, dominated by waves of fast frequency and low amplitude

Front 20

Alpha rhythm

Back 20

occurs in relaxation, a regular oscillation of 8 to 12 Hz

Front 21

Stage 1 sleep

Back 21

shows events of irregular frequency and smaller amplitude, as well as vertex spikes, or sharp waves
-heart rate slows, muscle tension reduces, eyes move about

Front 22

Stage 2 sleep

Back 22

defined by waves of 12 to 14 Hz that occur in bursts, called sleep spindles
-k-complexes appear- sharp negative EEG potentials

Front 23

Stage 3 sleep

Back 23

continued sleep spindles as in stage 2
-defined by the appearance of large-amplitude,very slow waves called delta waves, occur about once per second

Front 24

Stage 4 sleep

Back 24

-delta waves are present about half the time
-REM sleep follows active EEG with small-amplitude, high frequency waves, like an awake person
-muscles are flaccid-called paradoxical sleep

Front 25

Night terrors

Back 25

sudden arousals from stage 3 or 4 SWS, marked by fear and autonomic activity

Front 26

the forebrain and sleep

Back 26

the forebrain alone can generate SWS

Front 27

reticular formation is able to activate the cortex, which

Back 27

will wake up sleeping animals, lesions of this area will cause sustained sleep

Front 28

area of the pons is responsible for

Back 28

REM Sleep- lesions of a pontine region ventral to the locus coeruleus can affect REM sleep - small lesions abolish muslce atonia larger lesions abolish REM Sleep altogether

Front 29

cataplexy

Back 29

sudden loss of muscle tone, leading to collapse

Front 30

hypocretin-releasing neurons in the lateral hypothalamus control

Back 30

the transitions from wakefulness to SWS, and from SWS to REM sleep

Front 31

sleep paralysis

Back 31

brief inability to move just before falling asleep, or just after waking up

Front 32

somnambulism

Back 32

sleepwalking, occurs during stages 3 and 4 SWS, and may persist into adulthood.

Front 33

REM Behavior Disorder (RBD)

Back 33

characterized by organized behavior, from an asleep person
-usu. occurs after age 50 and may be followed by begining symptoms of Parkinson's disease.

Front 34

sleep state misperception

Back 34

occurs when people report insomnia even when they were asleep

Front 35

sleep-onset insomnia

Back 35

is a difficulty in falling asleep, and can be caused by situational factors, such as shift work or jet lag

Front 36

sleep-maintenance insomnia

Back 36

is a difficulty in staying asleep and may be caused by drugs or neurological factors.

Front 37

sleep apnea

Back 37

breathing may stop or slow down b/c muscles in the chest and diaphragm may relax too much or pacemaker respiratory neurons in the brain stem may not signal properly
-can lead to cardiovascular disorders

Front 38

Sudden Infant death syndrome (SIDS)

Back 38

is sleep apnea resulting from immature respiratory pacemaker systems or arousal mechanisms

Front 39

the extracellular compartment is subdivided into the

Back 39

interstitial fluid (fluid between cells and blood plasm (protein rich fluid that carried blood cells.

Front 40

osmotic pressure

Back 40

is when water moves down its concentration gradient

Front 41

osmolality

Back 41

concentration of a solute in a solution

Front 42

>0.9% hypertonic
<0.9% hypotonic

Back 42

physiological saline

Front 43

two different states can signal that more water is needed

Back 43

1) low extracellular volume (hypovolemic thirst)
2) hight extracellular solute concentration (osmotic thirst)

Front 44

blood pressure is detected by

Back 44

baroreceptors

Front 45

in reponse to decreased blood volume the kidneys release a hormone called

Back 45

renin into the circulation

Front 46

renin starts a hormonal cascade that (after several steps) leads to the production of

Back 46

angiotensin II

Front 47

Angiotensin II has several water conserving actions

Back 47

-constricts blood vessels
-causes release of vasopressin (which both constricts blood vessels and reduces the flow of water to the bladder
-causes the release of aldosterone (which stimulates kidneys to conserve Na+
-infusion of Angiotensin II into preoptic area increases drinking behavior

Front 48

Angiotensin II acts at several brain regions primarily in the

Back 48

circumventricular organs (regions near walls of ventricles)

Front 49

regions near ventricles have easier access to

Back 49

hormones (like a peptide in the blood stream)

Front 50

subfornical organ, (OVLT) and area postrema are important for

Back 50

monitoring blood osmolality

Front 51

there are osmosensory neurons in specific regions of the hypothalamus that can sense and can code the conc.

Back 51

Of salts and solutes in the water and can mediate osmotic thirst.

Front 52

preoptic area, supraoptic nucleus, paraventricular nucleus

Back 52

these hypothalamic regions then project to locomotor output nuclei that execute drinking behavior

Front 53

the basic unit of measuring food energy is the

Back 53

kilocalorie

Front 54

most of the energy in meal is used for

Back 54

digestion with only 12% utilized for behavioral processes

Front 55

Glucose

Back 55

is the principal sugar used by the body for energy
-converted to glycogen and stored in liver and skeletal muscle

Front 56

gylcogenesis

Back 56

glucose to glycogen (regulated by insulin- a pancreatic hormone)
-this process is mediated by a second pancreatic hormone called glucagon

Front 57

for longer-term energy storage, lipids (fats) are stored in

Back 57

adipose tissue

Front 58

first mechanism for insulin release is

Back 58

conditioned insulin, release is evoked by the sight and smell of food

Front 59

second mechanism for insulin release

Back 59

is food entering the stomach and intestine...this releases gut hormones that stimulates the pancreas to release insulin

Front 60

third mechanism is

Back 60

activation of glucodetectors in the liver (by elevated glucose) which also causes the pancreas to release insulin

Front 61

Liver and pancreas communicate via the nervous system using the

Back 61

vagus nerve which goes to the NTS (aka NST; nucleus of the solitary tract)
-information from NTS then travels to the hypothalamus

Front 62

satiety

Back 62

the feeling of being full or satisfied after eating enough food

Front 63

if high levels of insulin are injected

Back 63

animals eat more (because free glucose is converted to glycogen (glycogenesis) for storage

Front 64

hunger is coordinated by the

Back 64

hypothalamus

Front 65

early studies (1940) showed that lesions of the

Back 65

ventromedial hypothalamus caused obesity in rats

Front 66

lesions of the Lateral hypothalamus (LH)

Back 66

cause aphagia (refusal to eat)
also show adipsia (reduced drinking)

Front 67

Leptin is more important for

Back 67

long term regulation
-negative feedback system- signal comes from fat adipose tissue
-produced in fat cells, secreted into the bloodstream, goest to the brain and acts in a variety of places (focus on arcuate nucleus), then provides a signal to the brain that is a measure of the body's energy reserves in the form of fat)

Front 68

Ghrelin (and there are many others) are important for

Back 68

rapid changes in hunger
-acts on a faster time scale, comes from the gut
-released into the bloodstream by endocrine cells of the stomach
-powerful stimulator of appetite
ghrelin rise during fasting and drop after a meal is eaten
-give ghrelin- animals eat like crazy

Front 69

both leptin and ghrelin act in the

Back 69

arcuate nucleus to regulate hunger

Front 70

if LTP is already established and NMDA receptors are blocked

Back 70

there is no effect on the expression of LTP

Front 71

LTP is common at neurons that express both

Back 71

NMDA and AMPA receptors

Front 72

NMDA receptors are blocked by

Back 72

Mg2+ and this prevents Ca2+ entry

Front 73

AMPA activation partially polarized the membrane and removes

Back 73

the Mg2+ blockage, which means that NMDA receptors can then admit Ca2+ upon glutamate binding

Front 74

Large influx of Ca2+ at NMDA receptors activates

Back 74

protein kinases (enzymes that add phosphate groups to other porteins), among these proteins are protein kinase A, protein kinase C, tyrosine kinase, and calcium calmodulin (CaM kinase)
-blocking these protein kinases prevents LTP

Front 75

CaM kinase phosphorylates AMPA receptors already present in the membrane of the

Back 75

dendritic spine increaseing their conductance to Na+ and K+
-and , phosphorylation of AMPA receptors inside the cell promotes the movement of the receptor onto the membrane surface, which allows more receptors to be available to stimulate the spine

Front 76

the antibiotic anisomycin

Back 76

inhibits protein synthesis, and at low doses it does not have toxic effects

Front 77

in mice anisomycin has been used to show that protein synthesis is

Back 77

critical for long-term memory but not short term memory

Front 78

standard, impoverished and enriched conditions first demostrated that the brain can be altered by

Back 78

experience,showing that differences in environmental conditions cause changes in neurochemistry and neuroanatomy in rodent brain
-enriched animals have greater acetyl-cholinesterase in cortex, developed thicker and heavier occipital cortex, more dendritic spines and greater branching than rats in impovereshed conditions

Front 79

long-term habituation (as demonstrated by the slug) is due to a

Back 79

decrease in the number of synapses

Front 80

Long-term potentiation (LTP)

Back 80

is a stable and enduring increase in the effectiveness of synapses

Front 81

the magnitude of the EPSP is the measure of

Back 81

synaptic strength

Front 82

LTP resembles memory in the following ways

Back 82

-can be induced w/in seconds
-last for days or weeks
-has a fragile consolidation period that last for several minues after its intial induction

Front 83

LTD is

Back 83

when stimulation of the presynaptic neurons results in a weakening of the synapse

Front 84

the hippocampal formation consists of the

Back 84

hippocampus, the dentate gyrus, and the subiculum

Front 85

main inputs to the hippocampal formation come from the

Back 85

entorhinal cortex (via the perforant pathway through the subiculum)

Front 86

LTP occurs in several places in the hippocampal formation:

Back 86

-stimulate subiculum measure in dentate gyrus
-stimulate dentate gyrus measure in CA3
-stimulate CA3 measure in CA1

Front 87

if NMDA receptors are blocked prior to LTP induction

Back 87

the development of LTP is blocked

Front 88

basic attributes of memory

Back 88

space, time, sensory perception, and affect (emotion) and locomotor responding

Front 89

most robust effect on memory is seen with a lesion to these regions

Back 89

anterior entorhinal and perirhinal cortices

Front 90

rats with hippocampus lesions have trouble with this test

Back 90

radial arm maze study

Front 91

rats with caudate lesions have trouble when

Back 91

placed in a different spatially oriente chamber turning he same way as previously to find food

Front 92

delayed non-match to sample

Back 92

must choose btw. A and B (novel), when previously under A was food, only gets reward if it chooses B

Front 93

rats w/lesions of extra striate cortex have trouble w/

Back 93

delayed non-match to sample

Front 94

memory acquisition to retrieval

Back 94

memories begin by sensory transduction and the brain encodes the info. in a way that allows storage of short term memory
-some info. is then consolidated into long term memory storage
-in final stage of processing, info. that was stored is retrieved for use

Front 95

in a memory test if subjects are presented pictures while MRI'ed (which areas showing activation are associated with a higher likelyhood of remembering?)

Back 95

right prefrontal cortex and both parahippocampal areas were activated during this initial viewing
(also found to be important in the memory of words except only the left sides)

Front 96

changes that may indicate info. storage include

Back 96

greater release of neurotransmitter, increased number or sensitivity of receptors

Front 97

classic example of neural plasticity (Hebbian synapse)

Back 97

when one neuron alters the activity of another neuron, there are structural changes that allow for fire more easily
-these synapses grow stronger when the presynaptic terminal repeatedly causes the postsynaptic cell to fire
-not just firing of the presynaptic cell, but also its effectiveness at altering the activity of the postsynaptic cell

Front 98

episodic memory is

Back 98

autobiographical memory such as knowing when you learned a word

Front 99

deficits in episodic memory are associated w/

Back 99

cortical damage (for example frontal-parietal and parieto-occipital)
-there are increases in blood flow in these regions during episodic memory

Front 100

nonassociative learning involves a

Back 100

change in behavior after exposure to a single stimulus

Front 101

Habituation

Back 101

decrease in behavioral responding as the stimulus is repeated

Front 102

sensitization

Back 102

an increase in behavioral responding as the stimulus is repeated

Front 103

associative learning

Back 103

learning that involves relations btw. events

Front 104

primacy

Back 104

the first words of a list

Front 105

recency

Back 105

last words of a list

Front 106

if you wait and ask subjects about a list of words then

Back 106

recency effects go away because it's STM, but primacy effects stay b/c it's LTM

Front 107

the memory trace

Back 107

is the record laid down in memory

Front 108

blockade of D1, but not D2, dopamine receptors w/in the nucleus accumbens

Back 108

prevents this behavior early in training, but not if rats have been well trained

Front 109

in this case dopamine receptors blockade mimics extinction. This suggests that dopamine either provides a

Back 109

reinforcement signal or boosts motivated behavior

Front 110

cellular studies suggest that dopamine activation of D1 receptors provide

Back 110

a reinforcement signal via promoting LTP

Front 111

H.M. is a patient that suffered from severe epileptic seizures (what was the result?)

Back 111

-had anterior temporal lobes removed both sides including amygdala and hippocampus
-short term memory is ok
-IQ above average
forgets everything that happened 5 mins or so previously
-motor learning was ok

Front 112

declarative memory

Back 112

facts and info. aquired through learning (memories we are aware of accessing)

Front 113

non-declarative memory

Back 113

procedural memory- memory that is demonstrated by performance, rather than a conscious recollection

Front 114

patients w/damage to the dorsomedial thalamus show

Back 114

impairment in declarative memory

Front 115

patient N.A. had damage to one side of his thalamus and bilateral damage to mammilary bodies

Back 115

old memories remained intact, couldn't form new ones

Front 116

memory loss w/Korsakoff's is associated w/damage to

Back 116

dorsomedial thalamus and mammiliary bodies

Front 117

semantic memory is

Back 117

generalized memory, such as knowing the meaning of a word

Front 118

BLA then stimulates

Back 118

the central amygdala (CeA)

Front 119

BLA receives and integrates sensory info.

Back 119

BLA is the locus of sensory convergence and a cite for CS-US associations

Front 120

intra-amygdaloid circuit conveys the

Back 120

CS-US association to the central amygdala (CeA)

Front 121

CeA sends divergent projections to

Back 121

hypothalamus (LH and PVN) and brainstem (PAG and PB) to control autonomic, hormonal, and behavioral outputs.

Front 122

LTP is induced in the BLA by

Back 122

tetanic stimulation of the hippocampal formation

Front 123

high, but not low, frequency stimulation of the hippocampus

Back 123

increased EPSP (% of baseline) amplitude in the BLA

Front 124

electrode placed in the LA of awake rats and changes in neuron activity were measured following tone presentation. Pairing the tone wih an aversive foot shock_____

Back 124

potentiated the neuronal response

Front 125

unpaired presentations of the tone and shock did not result in

Back 125

any potentiation of the neural response

Front 126

data indicate that positive and negative motivation are both regulated

Back 126

w/in the the nucleus accumbens shell (in a rostrocaudal manner)

Front 127

rats will only self administer electrical stimulation if it results w/in

Back 127

the nucleus accumbens

Front 128

associative mechanisms become ______ while hedonic set points _______

Back 128

sensitized, are reduced such that drug cues more easily evoke negative affect resulting in persistent relapse and drug addiction

Front 129

rats with lesioned dopamine systems still are able to learn

Back 129

a conditioned taste aversion, therefore while dopamine signaling plays an important role, many other neurotransmitters are involved

Front 130

activation of mu-opioid receptors w/in the nuceus accumbens shell results in

Back 130

a robust increase in positive taste reactivity

Front 131

damgo is

Back 131

a mu-opioid receptor agonist,

Front 132

infushion of damgo into the nucleus accumbens shell

Back 132

increases hedonic taste reactivity, feeding behavior and feeding/positive hedonics if infused into the ventral pallidum

Front 133

GABA receptors and blockade of glutamate receptors both

Back 133

decrease neuronal activity w/in the nucleus accumbens, both manipulations increase positive hedonics

Front 134

this area is imporatant for the fear response

Back 134

amygdala

Front 135

information about conditioned stimulus enters this area of the amygdala

Back 135

lateral amygdala

Front 136

neurons in the lateral amygdala encode the

Back 136

association btw. cue and shock

Front 137

lateral amygdala stimulates the

Back 137

basolateral amygdala (BLA)

Front 138

physiological arousal

Back 138

expressions or displays of autonomic responses (i.e. increased heart rate)

Front 139

motivation

Back 139

behavior important for seeking pleasure and avoiding pain

Front 140

the more aversive taste reactivity that is shown,

Back 140

the more coaine the rates take (since taste cue is decreasing dopamine signaling, the increased cocaine seeking could be a compensation for that)

Front 141

what allows for relapse liability to persist longer than withdrawal symptoms?

Back 141

drug influence on learning and memory systems

Front 142

craving resulting from drug cues results from

Back 142

sensitized associative motivational systems

Front 143

learning and memory systems assessed by drug cues are both

Back 143

activated and pathologically strengthened by the associative processes and drug reinforcement

Front 144

neural restructuring is associated w/

Back 144

behavioral sensitization by amphetamine and cocaine

Front 145

by enhancing dopamine transmission, abused drugs

Back 145

engage brain mechanisms normally used for reinforcement driven learning

Front 146

Long term depression (LTD) is a

Back 146

reduction in EPSP amplitude following the training stimulation and can be caused by a reduced number of synapses or weakening of existing synapses

Front 147

at the level of the dopamine cells w/in the VTA...

Back 147

a single injection of cocaine strengthens glutamate synapses on the dopamine neurons that project to the nucleus accumbens

Front 148

hedonia

Back 148

component of happiness, positive effect

Front 149

positive taste reactivity

Back 149

increased dopamine signaling w/in the nucleus accumbens shell

Front 150

aversive taste reactivity is associated w/

Back 150

decreased dopamine signaling w/in the nucleus accumbens

Front 151

Saccharin evoked increases in dopamine signaling

Back 151

are greater in the shell compared to the core

Front 152

Quinine evoked decreases in dopamine signaling

Back 152

occur only w/in the shell...no decrease is observed w/in the core

Front 153

conditioned dopamine release caused by cue onset

Back 153

occurred w/in the core late in the training

Front 154

unconditioned dopamine release following cocaine infusion occurred specifically w/in

Back 154

the shell both early and late in training

Front 155

4 aspects of emotions

Back 155

feelings, actions, physiological arousal, motivation

Front 156

feelings

Back 156

subjective states that humans experience

Front 157

actions

Back 157

behaviors such as defensive or aggressive behaviors

Front 158

opiates can have both

Back 158

stimulant and depressant effects(stimulant effects at low doses...depressant effects at high doses)

Front 159

direct injection of opioid into the ventral tegmental area (VTA) causes

Back 159

a robust stimulant effect (these effects are masked at higher doeses that act to reduce behavioral activation)

Front 160

once drug leaves the system, the animal will experience

Back 160

withdrawal (these symptoms are opposite of acute effects)

Front 161

microdialysis used to

Back 161

sample the neurochemical environment of specific brain regions following drug infusions

Front 162

morphine injections cause greater increases in

Back 162

dopamine transmission w/in the nucleus accumbens shell compared to the nucleus accumbens core

Front 163

if a drug is reinforcing, it may facilitate a

Back 163

conditioned place preference

Front 164

aversive events, drugs, etc...can cause a

Back 164

conditioned place avoidance

Front 165

blocking D1 dopamine (but not D2 dopamine receptors) w/in the nuceus accumbens shell prior to morphine injections...prevents

Back 165

morphine induced conitioned place preference
-this effect is specific to the shell...since D1 blockade in the core has no effect

Front 166

all abused drugs not just opiates increase

Back 166

dopamine signaling w/in the nucleus accumbens

Front 167

cocaine also increases

Back 167

dopamine signaling preferentially w/in the nucleus accumbens shell

Front 168

diff. btw. microdialysis studies and fast-scan cyclic voltammetry

Back 168

fast scan cyclic voltammetry (uses micro electrodes made from a single strand of carbon fiber) measures dopamine 10 times per second, microdialysis studies measure dopamine once every 10 mins or so

Front 169

blockade of dopamine autoreceptors increases

Back 169

the frequency of dopamine release events

Front 170

cocaine slows

Back 170

dopamine uptake and increases the duration of dopamine release events (also increases the frequency of dopamine release events)(only w/in the nucleus accumbens shel...cocaine causes release events that resemble those evoked by autoreceptor blockade (via raclopride infusion)
-this effect is prevented by preventing activation of dopamine neurons w/in the VTA, thus cocaine increases activation of dopamine neurons

Front 171

exogenous administration of cortisol

Back 171

enhances memory for drug words

Front 172

beta adrenergic antagonists prevent

Back 172

enhanced memory by TSST and cortisol

Front 173

left frontal cortex is associated w/

Back 173

language production and syntax (grammar)

Front 174

left temporal lobe is associated w/

Back 174

language comprehension (semantics)

Front 175

Broca's(BA44/45) patients often had

Back 175

right hemiparesis (weakening of the right arm and leg)
-this aphasia is associated with damage in the frontal lobe, not due to damage to the motor strip

Front 176

Wernicke's patients had damage in the

Back 176

posterior region of the superior temporal gyrus
-this aphasia is often associated w/damage to the temporal lobe near Heschel's gyrus (primary auditory cortex)

Front 177

aphasia refers to a disorder of

Back 177

language apparent in speech, in writing (agraphia) or in reading (alexia) produced by injury to brain areas specialized for these functions

Front 178

anarthria

Back 178

paralysis or incoordination of the musculature of the mouth

Front 179

these deficits/damages are not considered aphasic disturbances

Back 179

-severe intellectual impairment
-loss of sensory input (vision or hearing)
-paralysis or incoordination of the musculature of the mouth (anarthria)
-hand paralysis

Front 180

primary aphasia

Back 180

due to problems with the language-processing mechanisms

Front 181

secondary aphasia

Back 181

due to memory impairments, attention disorders, or perceptual problems

Front 182

disorders of comprehension (2)

Back 182

-poor auditory comprehension
-poor visual comprehension

Front 183

disorders of production

Back 183

-poor articuation
-word-finding deficit (anomia)
-unintended words of phrases (paraphasia)
-loss of grammar or syntax
-inability to repeat aurally presented material
-low verbal fluency
-inability to write (agraphia)
-loss of tone in voice (aprosidia)

Front 184

three test parameters for the classification of aphasias

Back 184

1) spontaneous speech
2) auditory comprehension
3) verbal repetition

Front 185

nonfluent aphasias

Back 185

difficulties in articulating but relatively good auditory verbal comprehension (Broca's severe, Broca's mild)

Front 186

fluent aphasias

Back 186

fluent speech but difficulties either in auditory verbal comprehension or in the repetition of words, phrases, or sentences spoken by others (e.g., Wernicke's or sensory aphasia; Anomic)

Front 187

"Pure" aphasias

Back 187

there are selective impairments in reading, writing, or the recognition of words (e.g., agraphia, alexia without agraphia)

Front 188

PCP (phencyclidine)

Back 188

also known as angle dust
-NMDA antagonist (blocks the central calcium channel)

Front 189

give PCP for two weeks to monkeys and they show frontal cortex deficits similar to humans with schizophrenia leading some scientists to suggest that there is an

Back 189

under activation of glutamate receptors in schizophrenia

Front 190

patients with depression show increases in blood flow (which suggests increases in activation) of

Back 190

the frontal cortex and the amygdala

Front 191

with depression blood flow in amygdala can be normalized with

Back 191

anti depressants

Front 192

with depression blood flow is decreased in

Back 192

parietal and posterior temporal cortex and anterior cingulate...systems important for attention and language

Front 193

monoamine hypothesis

Back 193

drugs that increase monoamine signaling alleviate depressive symptoms

Front 194

the earliest anti depressants were

Back 194

monoamine oxidase (MAO) inhibitors- prevent the breakdown of monoamines and therefore increase their signaling (serotonin & norepinephrine)

Front 195

reserpine reduces

Back 195

norepinephrine and serotonin release in the brain
-this drug causes profound depression

Front 196

Electroconvulsive shock therapy (ECT) also alleviates symptoms of

Back 196

major depression and is still used in patients that are resistant to drug treatment
-believed to work by causing monoamine release

Front 197

serotonin is especially important for depression

Back 197

suicide victims have reduced serotonin metabolites in the brain

Front 198

hallusinations with schizophrenia are primarily

Back 198

auditory

Front 199

these drug users have symptoms similar to patients with schizophrenia

Back 199

chronic amphetamine users (amphetamine psychosis)- experience paranoia, auditory hallucinations, bizarre motor behavior-->led to idea that dopamine is important for schizophrenia

Front 200

dopamine hypothesis

Back 200

dopamine is important for schizophrenia -block dopamine receptors, you can block these symptoms
-drugs that block receptros at D2 are called neuroleptics or antipsychotics, therefore dopamine must be involved
the idea that schizophrenia results from either excessive levels of dopamine or highly sensitive dopamine receptors

Front 201

the dopamine receptor antagonist thorazine (chloropromazine)

Back 201

eliminates the symptoms of amphetamine psychosis
-also alleviates symptoms of schizophrenia
these drugs block postsynaptic D2 dopamine receptors

Front 202

if a schizophrenia medication acts by blocking D2 receptors it is called a

Back 202

typical neuroleptic

Front 203

boosting dopamine levels in parkinson's patients can induce

Back 203

symptoms of schizophrenia

Front 204

while dopamine receptors are blocked rapidly by drugs, dopamine can only be part of the schizophrenia story, because

Back 204

it takes weeks for symptoms to go away

Front 205

atypical neuroleptics are drugs

Back 205

that treat schizophrenia but do not primarily block D2 receptors (ex: clozapine blocks serotonin(5HT2A receptors)

Front 206

glutamate hypothesis

Back 206

derived from observing what people are like when they take PCP

Front 207

Psychotomimetic

Back 207

a state resembling schizophrenia

Front 208

if both twins have a train they are said to be _____ for this trait

Back 208

concordant

Front 209

in sets of twins that are discordant for schizophrenia they often differ in

Back 209

other traits (such as differences in motor coordination)

Front 210

patients with schizophrenia have greater difficulty making

Back 210

smooth-pursuit movements with their eyes than non-schizophrenics
-motor neuron will go to just a few muscle fibers in the eyes, whereas in the leg it wil lgo to thousands- innervation ratio important for being able to do these smooth pursuits

Front 211

Genes important for schizophrenia are located on at least

Back 211

15 or 23 chromosomes

Front 212

people with schizophrenia have

Back 212

-enlarged lateral ventricles
-ventricular enlargement is not related to length of illness
-patients with larger ventricles don't respond as well to medication

Front 213

twins that are discordant for schizophrenia show differences in their limbic systems

Back 213

-twins with schizophrenia have smaller limbic structures (hippocampus and amygdala)
-since these regions are near the ventricles...enlarged ventricular systems may be due to atrophy of limbic structures

Front 214

hippocampal pyramidal cells of chronic sufferers of schizophrenia exibit a

Back 214

characteristic diorganization
-the more impaired the person...the more disorganized the cellular structure of the hippocampus

Front 215

those with early onset schizophrenia have

Back 215

-a thicker corpus callosum
-significant loss of cortical gray matter during adolescence as well

Front 216

patients with schizophrenia show impairments in neuropsychological tests that indicate damage to

Back 216

frontal cortex
-display perseveration
-you also see a blunted level of activity in frontal cortex and this is decreased further or doesn't go up when they're doing the task

Front 217

hypofrontality hypothesis suggests that

Back 217

underactivation of the frontal lobes is important for schizophrenia
-display low blood flow in frontal cortex
-drugs that improve symptoms increase blood flow in frontal lobes

Front 218

prosody

Back 218

the intonation pattern, or sound envelope, of an utterace (interpreting whether the tone is friendly, sarcastic, condescending or excited)

Front 219

Narrative

Back 219

ability to construct or understand a story line

Front 220

inference

Back 220

ability to "fill in the blanks"

Front 221

Neurological approach and Wernicke-Geschwind model

Back 221

-frontal lobe damage (BA 44/45) is associated with deficits in language production
-superior temporal lobe damage is associated with language comprehension

Front 222

psychological perspective

Back 222

-frontal lobe damage (BA44/45) is associated with semantic deficits

Front 223

reading is accomplished through two routes

Back 223

-phonological route (sounding out)
-Direct route (words as pictures)

Front 224

right hemisphere contribution to language

Back 224

prosody, narrative, inference and lying

Front 225

positive (abnormal behavioral states that have been gained) symptoms of schizophrenia include

Back 225

delusions and hallucination

Front 226

negative symptoms of schizophrenia include

Back 226

emotional withdrawal and impoverished thought

Front 227

% of monozygotic twins that are concordant for schizophrenia

Back 227

50

Front 228

in PET studies, resting state of aphasics show

Back 228

hypometabilism in the temporoparietal region

Front 229

crossed aphasia

Back 229

aphasia arising from right hemisphere damage

Front 230

Wada technique uses this chemical

Back 230

sodium amobarbital

Front 231

three pieces of evidence that contradict a strict localizationist model of language

Back 231

1) effects of stimulation of the anterior and posterior speech zones on speech functions are remarkably similar
2) stimulation of the neocortex considerably beyond the classical areas of Broca and Wernicke disrupts speech functions
3) stimulation of speech zones affects more then just talking--produces deficits in voluntary motor control of facial musculature as well as short-term memory and reading

Front 232

it is more likely that the brain is organized in units devoted to phonology, syntax, and semantics rather than the classical model of

Back 232

speaking, repeating, and listening

Front 233

visual language processing - reading (2 routes)

Back 233

1) Phonological route to reading --see the word, sound it out -->understand the meaning (grapheme-to-phoneme)
2) Direct route- printed words are directly linked to menaing (useful to reading irregular words, such as "yacht" or "colonel")

Front 234

surface alexia (damage to direct route)

Back 234

-reading by sound
-can not recognize words but can understand them by using grapheme to phoneme relations
-words can be understood if they ae 'sounded' out
-regular words are read normally ("home" or "dome")
-irregular words are not read properly: yacht, debt, ache, or quay
-patients read 'lace' as 'lake'
-these patients can pronounce regular non-words (e.g., glimay)
-overgeneralization of rules

Front 235

Phonological alexia (damage to the phonological route)

Back 235

-patients do not have problem reading previously learned words (regular or irregular) as they are using the direct route
-patients extract meaning directly from the visual form of the word
-they have problems reading new words both regular or irregular
-intact direct route is not enough b/c they do not have the connection btw. the visual form of the word and meaning

Front 236

Deep alexia (related to phonological alexia)

Back 236

-key feature are semantic errors
-patients read semantically related words in place of the word they are trying to read (e.g., "merry" as "Christmas", "cow" as "horse")
-function words are very difficult for these patients
-concrete words better than abstract words
-unable to read nonwords

Front 237

the right hemispheres language abilitites include

Back 237

-being able to extract basic meaning, it cannot
-produce speech, use phone-to-grapheme correspondance or understnad syntax

Front 238

Allophones

Back 238

different representations of the same phoneme (e.g. /p/ in /pill/ vs. /spill/)

Front 239

individuals with Wernicke's aphasia produce the wrong phoneme--> phoneme substitution, whereas individuals with Broca's aphasia

Back 239

have difficulty producing the correct allophone of a phoneme (lack of fine control)--> mispronounciation of a phoneme

Front 240

syntax

Back 240

the admissible combinations of words or phrases and sentences (called grammar in popular usage)

Front 241

individuals with damage to anterior parts of the brain (e.g. Broca's aphasia) show difficulties with

Back 241

syntax

Front 242

patients with Broca's aphasia not only have a problem with production, but also with

Back 242

comprehending syntax

Front 243

semantics

Back 243

meaning of words and word combinations

Front 244

Broca's aphasic patients have relatively intact semantic processing --> problems arise when syntax is important, wheras Wernicke's aphasia is characterized by

Back 244

semantic deficits (understanding the meaning of words, whereas there understanding of syntax is intact)

Front 245

anterior regions (i.e., the frontal lobe) are important for

Back 245

speech production and syntax

Front 246

posterior regions (i.e., temporal and parietal lobe) are important for

Back 246

comprehension and semantic processing

Front 247

Diachisis

Back 247

damage in one part of the brain can create problems for another

Front 248

Broca's Aphasia (Non-Fluent Aphasia or expressive aphasia) deficits

Back 248

-nonfluent speech, short phrases, pauses, makes errors, repetitious errors in grammar, omits function words (verbs-Telegraphic speech)
-poor repetition
-somewhat good comprehension
-can be mild or severe

Front 249

Fluent aphasia (Wernicke's Aphasia) deficits

Back 249

-problems in comprehending speech input or reception of language
-fluent meaningles speech
-word salad
-paraphasias- errors in producing specific words
-semantic paraphasias-substituting words similar in meaning ("barn"-"house")
-phonemic paraphasias- substituting words similar in sound ("house" - "mouse")
-Neologisms- non words ("galump")
-deficit in categorization of sounds (e.g., "I" vs. "r")
-Poor repetition
-impairment in writing

Front 250

concept center

Back 250

place where meanings are stored

Front 251

transcortical motor aphasia

Back 251

comprehension and repetion are preserved, however the speech is non-fluent
-damage to the area connecting the concept center and Broca's area

Front 252

transcortical sensory aphasia

Back 252

repetition is preserved, speech is fluent but comprehension is impaired
-damage to area connecting Wernicke's area and the concept center

Front 253

Anomic Aphasia (a.k.a. fluent aphasia, amnesic aphasia)

Back 253

-comprehend speech
-fluent speech
-repetition OK
-cannot name objects
-naming problems tend to be the result of damage to the temporal cortex
-verb finding problems tend to be a result of left frontal damage

Front 254

Global Aphasia

Back 254

associated with extensive left hemisphere damage
-deficits in comprehension and production of language

Front 255

According to psycholinguists, language has three components

Back 255

phonology, syntax and semantics

Front 256

phonology

Back 256

sounds that compose language and the rules that govern their combination

Front 257

phoneme

Back 257

the smallest unit of sound that can siignal menaing

Front 258

SSRI

Back 258

selective serotonin reuptake inhibitors- prozac
-work better than MAO inhibitors and have fewer side effects
-in rats increase neurogenesis in the hippocampus
-blocking serotonin transporters increases serotonin levels rapidly but it takes weeks for depressive symptoms to be improved
-massive placebo effect 33%

Front 259

HPA axis

Back 259

hypothalamic pituitary adrenal axis

Front 260

Cushing's syndrome

Back 260

depression resulting from very high levels of circulating glucocorticoids (such as cortisol)
-in hypothalamus, CRH producing cells project to portal system and is released into portal veins that travel to anterior pituitary
-Anterior pituitary produces ACTH
-ACTH is released when stimulated by CRH
-ACTH travels to adrenal gland
-ACTH stimulation of adrenal gland causes glucocorticoid release into the blood stream
-this feeds back into the brain and decreases CRH release

Front 261

causes of Cushing's

Back 261

1) pituitary tumor that results in excessive ACTH production
2) tumor in the adrenal gland that results in hypersecretion of cortisol
3)cortisol replacement therapy
-the majority of patients with Cushing's get depression sooner than other symptoms (obesity)

Front 262

Dexamethasone is

Back 262

a potent synthetic glucocorticoid that suppresses the natural rise in cortisol levels first thing in the morning
-in depressed patients dexamethasone fails to suppress early morning rise in serum cortisol
after treatment, it starts to work normally
-this data suggest that depressed people have CRH neurons that are abnormally excited this causes ACTH to be released too easily or, depressed people may have impaired negative feedback regulation of the system (such as too few or insensitive brain glucocorticoid receptors)

Front 263

patients with panic attacks have

Back 263

temporal lobe abnormalities

Front 264

Benzodiazepines are

Back 264

used to treat anxiety-called anxiolytics (ex: Valium) these are GABA agonists

Front 265

intense trauma will activate brainstem systems that sensitize subject to future stimuli s

Back 265

fear conditioning, behavioral sensitization, and extinction
(Locus coeruleus-norepinephrine, Ventral tegmental area- dopamine, endogenous opiates, Corticotropin-releasing hormone, amygdala

Front 266

sich vergewissern

Back 266

to ascertain

Front 267

anschließend

Back 267

afterwards

Front 268

etw. eingeben

Back 268

to type sth. in

Front 269

etw. übertragen

Back 269

to carry sth. over

Front 270

die Eingewöhnung

Back 270

acclimatization, familiarization

Front 271

auf den Schulhof

Back 271

at school

Front 272

der Schulhof

Back 272

school ground, playground

Front 273

die Sprachkenntnisse

Back 273

command of language, linguistic proficiency

Front 274

etw. akk. benötigen

Back 274

to be in need of sth.

Front 275

auf etw. akk zurückgreifen

ex: Um auf deinen Rucksack zurückzugreifen

Back 275

to resort to sth.

Front 276

der Zugriff

Back 276

access

Front 277

das Männchen

Back 277

boar, little man

Front 278

fürs Erste

Back 278

for the time being, as a start