Psycho Bio Exam 4

Front 1

Delusions

Back 1

False beliefs held in spite of contrary evidence

—have been noted for centuries
--About one-third of the U.S. population reports symptoms of a psychiatric disorder
-Higher chance in Women, and age 18-25

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Schizophrenia

Back 2

A disordered state with unusual symptoms:
• Hearing voices
• Feeling intensely frightened
• Sensing persecution from enemies • Acting strangely

“first-rank symptoms” include auditory hallucinations, personalized delusions, and changes in affect (emotion)

Front 3

Positive symptoms of Schizophrenia

Back 3

Abnormal behaviors that are gained:

• Hallucinations
• Delusions
• Excited motor behavior

Front 4

Negative symptoms of Schizophrenia

Back 4

the result of lost functions:

• Slow thought and speech
• Emotional and social withdrawal
• Blunted affect or emotional expression

Front 5

Monozygotic Twins

Back 5

(identical)
-share identical genes

• If one identical twin suffers from schizophrenia, the other twin has a 50% chance of developing it
• Since some identical twins are unaffected, genes alone do not fully explain schizophrenia

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Dizygotic

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(fraternal)
- have half of their genes in common

• In dyzygotic twins the concordance rate drops to 17%

Front 7

Eye tracking with Schizophrenia

Back 7

People with schizophrenia display rapid, jerky eye movements, confirming motor abnormalities

The affected twin may also have subtle neurological signs, such as impaired motor coordination

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Genes that influence schizophrenia

Paternal age

Back 8

are scattered across many chromosomes

Some are known to participate in synaptic plasticity, one mutant is DISC1—disrupted in schizophrenia

Paternal age is an epigenetic factor involved—older men are more likely than young men to have children with schizophrenia

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Integrative model of schizophrenia

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says the cause is the interaction of genetic factors and stress

Front 10

Stressors that may cause schizophrenia include:

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• Transition from childhood to adulthood
• Prenatal stress, maternal illnesses
• City living—possibly due to pollutants, exposure to other diseases, crowded conditions, tense social interactions

Front 11

Brain changes in patients with schizophrenia:

Back 11

•Enlarged cerebral ventricles

Cortical abnormalities:
-a thicker corpus callosum
- abnormal prenatal neuronal migration in frontal cortex
- a loss of gray matter (shown at right)

•Functional maps show less metabolic activity in frontal lobes

Front 12

The hypofrontality hypothesis

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frontal lobes are underactive in people with schizophrenia

Front 13

Lobotomy

Back 13

the surgical separation of the frontal lobes from the rest of the brain
-Class example: Walter Freeman, “The Lobotomist”

Front 14

The dopamine hypothesis

Back 14

states that schizophrenia is caused by an excess of either dopamine release or dopamine receptors

Front 15

Evidence For The dopamine hypothesis

Back 15

-Effects of Neuroleptic drugs - all antipsychotic or neuroleptic drugs block postsynaptic dopamine D2 receptors

-Amphetamine Psychosis - increase in DA

-Parkinson’s Disease - L-Dopa

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Evidence Against The dopamine hypothesis

Back 16

-DA levels at autopsy

-Atypical neruoleptics block Serotonin

-PCP & other NMDA receptor antagonists

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All antipsychotic or neuroleptic drugs

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-block postsynaptic dopamine D2 receptors

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Typical neuroleptic drugs

Back 18

all antagonists at dopamine D2 receptors, and the dose can be predicted by a drug’s affinity for the D2 receptor

Ex: Haloperidol:
has greater affinity than chlorpromazine and is more widely used

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Problems with the dopamine hypothesis:

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• Drugs block D2 receptors much faster than symptoms are reduced
• Some patients don’t respond to the drugs
• A new class of drugs that successfully treat schizophrenia also does not support the dopamine hypothesis

Front 20

Amphetamine psychosis

Back 20

Heavy users of amphetamines may develop this

-causes schizophrenia-like symptoms

Amphetamines promote dopamine release and block its reuptake

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Antipsychotic drugs

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• Dyskinesia—impaired motor symptoms

• Tardive dyskinesia—characterized by repetitive involuntary movements, perhaps due to dopamine receptor supersensitivity

• Supersensitivity psychosis: and increased positive symptoms of schizophrenia may occur after stopping antipsychotic drugs

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Atypical neuroleptics

Back 22

Block serotonin receptors as well as D2 receptors

A new class of drugs that successfully treat schizophrenia also does not support the dopamine hypothesis
• Some atypical neuroleptics actually increase dopamine levels in the frontal cortex

Front 23

The glutamate hypothesis

Back 23

Says that schizophrenia is caused by underactivation of all glutamate receptors

Front 24

Phencyclidine (PCP)

Back 24

produces both positive and negative symptoms of schizophrenia
• PCP acts as an NMDA receptor antagonist, and prevents glutamate from acting normally

Other NMDA antagonists, like ketamine, have similar effects

Front 25

Tourette’s syndrome

Back 25

a neurological disorder involving repetitive behaviors due to disruptions of dopamine in the basal ganglia

diagnosed early, at 6–7 years—children may also exhibit ADHD or OCD

Patients may fling their arms, or kick, or make violent shoulder movements

Front 26

Tourette’s syndrome Twins studies

Back 26

an affected twin has more dopamine D2 receptors in the caudate nucleus of the basal ganglia than the unaffected twin

Front 27

Treatments for Tourette’s syndrome include:

Back 27

haloperidol, a D2 receptor antagonist, atypical antipsychotics, behavior modification, and deep brain stimulation

Front 28

Depression

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most prevalent mood disorder, characterized by:
• Unhappy mood
• Loss of interest and energy
• Changes in appetite and sleep patterns • Difficulty in concentration
• Restless agitation or torpor
• Pessimism and thoughts of death

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Unipolar depression

Back 29

depression that alternates with normal emotional states

Recurrent episodes of dysphoria andnegative thinking

Front 30

Bipolar disorder

Back 30

(formerly manic-depressive illness)
is characterized by depressive periods alternating with expansive mood, or mania

Front 31

Brain changes with depression:

Back 31

• Increased blood flow to the frontal cortex and amygdala, which mediates fear

• Decreased blood flow to areas implicated in attention

• Cortex of the right hemisphere is thinner

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Plastma Cortisol Levels in Depressed patients

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People who are depressed also have difficulties regulating stress hormone release

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Treatments for depression:

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• Electroconvulsive shock therapy (ECT)

• Transcranial magnetic stimulation (TMS)

• Monoamine oxidase (MAO)

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Electroconvulsive shock therapy (ECT)

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causes a seizure—an electrical current is passed through the brain

Front 35

Transcranial magnetic stimulation (TMS)

Back 35

also alters cortical electrical activity

Front 36

Monoamine oxidase (MAO)

Back 36

an enzyme that normally inactivates the monoamines: norepinephrine, dopamine, and serotonin

o Treatment with MAO inhibitors raises the level of monoamines at the synapse
o MAO inhibitors were the first antidepressants—their use led to the monoamine hypothesis
o Tricyclics, another generation of antidepressants, inhibit reuptake of monoamines

Front 37

Selective serotonin reuptake inhibitors (SSRIs)

Back 37

antidepressants that block the reuptake of serotonin at synapses

Ex: Prozac, Zoloft, Serzone, Lexapro, Cymbalta,

Front 38

Problems with idea of serotonin reduction as a cause of depression:

Back 38

• Long lag-time (often weeks) between treatment and reduction of symptoms

• Not everyone is helped, and there is also a large placebo effect

• SSRIs increase risk of suicide in children and adolescents

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Other treatments being researched for depression

Back 39

• Ketamine and leptin
• Vagal nerve stimulation
• Deep brain stimulation (DBS)—through a surgically implanted electrode

Front 40

Cognitive behavioral therapy (CBT)

Back 40

can be as effective as SSRIs, and when used together are more effective than either alone

Front 41

Men vs Women in depression

Back 41

More women than men suffer from depression
• May reflect patterns of help- seeking
• Gender differences in endocrine physiology, related to the reproductive cycle

Front 42

Postpartum depression

Back 42

immediately precedes or follows childbirth

Front 43

Sleep and Depression

Back 43

•Stage 3 of slow-wave sleep is reduced

•Patients enter REM sleep very quickly, with an increase of REM sleep in the first half of the night

Seasonal affective disorder (SAD) affects seasonal rhythms

Front 44

Animal Models:
Some signs of depression

Back 44

observable behaviors
• learned helplessness: an animal is exposed to a repetitive stressful stimulus. It is linked to a decrease in serotonin function
• Animals without olfactory bulbs show irritability, alcohol preference, and elevated stress hormones
• Certain rats show reduced activity and body weight, increased REM sleep, learning difficulties, and stress responses

Front 45

Bipolar disorder

Back 45

characterized by depressive periods alternating with periods of expansive mood, or mania

The rate of alternation between moods varies:
• Rapid-cycling consists of four or more cycles per year (though some have as many as several per day)

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Facts about Bipolar disorder

Back 46

-Men and women are equally affected
-Is heritable

Brain changes are similar to those seen in schizophrenia—enlarged ventricles and reduced gray matter

The element lithium is an effective treatment, but its use must be monitored for side effects

Front 47

Anxiety Disorders

Back 47

Phobic disorders, panic disorder, and generalized anziety disorder

Front 48

Phobic disorders

Back 48

intense irrational fears centered on an
object, activity, or situation that a person avoids

Front 49

Panic disorder

Back 49

recurrent attacks of intense fearfulness

Front 50

Generalized anxiety disorder

Back 50

persistent, excessive anxiety and worry

Front 51

Anxiolytics

Back 51

GABA receptors are widely distributed in the cortex, hippocampus, and amygdala

Ex: Benzodiazepines are used to treat anxiety
• They bind to GABA receptors and enhance GABA’s inhibitory actions

Serotonin agonists and SSRIs can also treat anxiety

Front 52

Posttraumatic stress disorder (PTSD)

Back 52

unpleasant memories repeatedly plague the victim

• Memory changes, such as amnesia
• Flashbacks
• Deficits in short-term memory

Decreased volume in the right hippocampus—may be a risk factor rather than a consequence

Front 53

Fear conditioning

Back 53

learning in which fear is associated with a previously neutral stimulus

Front 54

Obsessive-compulsive disorder (OCD)

Back 54

marked by recurring, repetitive acts
• Recurrent thoughts become obsessions

• Routine acts become compulsions

Serotonin dysfunction in the orbitofrontal prefrontal cortex plays a major role in OCD
heritable? OCD may be triggered by infections that cause a damaging immune response

Front 55

Treatments for OCD in addition to drugs include:

Back 55

• Psychosurgery—uses brain lesions to modify severe psychiatric disorders
-Cingulotomy—lesions of the cingulate cortex

Front 56

OCD and Tourette's syndrome

Back 56

often co-morbid

-they can occur together, and both involve disorders of the basal ganglia

Front 57

Learning

Back 57

the process of acquiring new information

Front 58

Memory

Back 58

• The ability to store and retrieve information

• The specific information stored in the brain

Front 59

distinction between learning and memory

Back 59

is arbitrary, as you can’t learn something without remembering it, and you can’t remember something without learning it.

Front 60

Declarative memory

Back 60

facts and information acquired through learning that can be stated or described to answer “what” questions

Things you know you can tell others

-2 types: Episodic(remembering first day of school) & Semantic(know the capital of france)

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Nondeclarative (procedural) memory

Back 61

shown by performance rather than recollection, to answer “how” questions

-3types: Skill learning)knowing how to ride bike),
Priming(being more likely to use a word you heard recently,
& Conditioning(Salivating when you see favorite food)

Front 62

Amnesia (2 types)

Back 62

severe memory impairment

•Retrograde amnesia - the loss of memories formed before onset of amnesia

•Anterograde amnesia - the inability to form memories after onset of a disorder

Front 63

Patient H.M.

Back 63

Henry Molaison
Suffered from severe epilepsy
•Bilateral temporal lobe excision: removed the amygdala, the hippocampus, and some cortex

After surgery seizures stopped, cold not retain any new long term memories

Suffered from: Severe Anterograde amnesia & mild retrograde amnesia
(only about 1-3 years before surgery)

Memory deficit caused by loss of hippocampus

Impaired in declarative memories, but intact nondeclarative (procedural) memories

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Delayed non-matching-to-sample task

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a test of object recognition memory that requires monkeys to declare what they remember

Monkeys must identify what was not seen previously, over a range of delay times

Medial temporal lobe damage, similar to Henry’s, causes impairment on this task

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Hippocampus

Back 65

is critical for declarative memories

is NOT involved in the storage of memory.

Front 66

Clive Wearing

Back 66

developed severe memory problems after a viral infection that damaged his temporal cortex.

•The patient suffered from memory loss (amnesia). •More precisely from severe anterograde amnesia •Also from mild retrograde amnesia

Front 67

Patient N.A.

Back 67

has amnesia due to accidental damage to the dorsomedial thalamus and mammillary bodies

Like H.M., he has short-term memory but cannot form declarative long-term memories

Front 68

Korsakoff’s syndrome

Back 68

a memory deficiency caused by lack of thiamine—seen in chronic alcoholism

–Brain damage occurs in mammillary bodies and dorsomedial thalamus, but not hippocampus

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Korsakoff’s syndrome Symptoms

Back 69

–Patients often fail to recognize or sense any familiarity with some items, even when presented repeated.

–Patients often confabulate—fill in a gap in memory with a falsification

Front 70

What is needed to form new declarative memories?

Back 70

studies make it clear that it is a brain circuit
Includes:

the hippocampus, mammillary bodies, and the dorsomedial thalamus

But are not the sites of storage

Front 71

Skill learning

Back 71

Nondeclarative (procedural)
learning to perform a challenging task through repetition
•All kinds of skill learning—sensorimotor, perceptual and cognitive—are impaired with damage to the basal ganglia

Front 72

Priming

Back 72

Nondeclarative (procedural)

a change in stimulus processing due to prior exposure to the stimulus
•Priming appears to be a function of the cortex—different types of priming are related to reduced activity in different cortical areas

Front 73

Associative learning

Back 73

Nondeclarative (procedural
the association between two stimuli, or between a stimulus and a response

• Classical conditioning (Pavlovian conditioning)—a neutral stimulus, when paired with another stimulus that elicits a response, is able to elicit that same response when presented alone

Eye-blink conditioning is critically dependent on an intact cerebellum

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Pavlovian (Classical) Conditioning

Back 74

• Meat powder—the
unconditioned stimulus (US) that evokes an unconditioned response (UR), salivation
• Bell sound—the
conditioned stimulus (CS) and the learned response to the CS alone, salivation, is the conditioned response (CR)

Front 75

instrumental conditioning—or operant conditioning

& Example

Back 75

an association is made between:
-Behavior (the instrumental response)
-The consequences of the behavior (the reward)

Ex:Skinner Box
•Lever press = food pellet
•Probability of future lever presses increases (reinforcer)
•Lever press = loud noise •Probability of future lever presses
decreases (punishment)

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Positive reinforcement

Back 76

introduction of an event or activity that increases the frequency of the behavior.

Front 77

Negative reinforcement

Back 77

removal of an event or activity that increases the frequency of the behavior.

Front 78

object recognition task

Back 78

Measures sensory perception and declarative recognition memory
• Rats must identify which stimulus in a pair is novel
• Cortical lesions produced impairments on this task

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Semantic memory

Back 79

subtype of declarative memory:

-generalized declarative memory
-knowing capital

Front 80

Episodic memory

Back 80

subtype of declarative memory:

-detailed autobiographical memory
-remembering first day of school

Front 81

cognitive map

Back 81

a mental representation of a spatial relationship

The hippocampus is important in spatial learning

It contains place cells that become active when in, or
moving toward, a particular location

Front 82

eight-arm radial maze

Back 82

tests spatial location memory

• Rats must recognize and enter an arm that they have
entered recently, to receive a reward
• Only lesions of the hippocampus produce a deficit in this predominantly spatial task

Front 83

Type of memory
Iconic memories

Back 83

are the briefest and store sensory impressions

Front 84

Type of memory
Short-term memories (STMs)

Back 84

usually last only for seconds, or throughout rehearsal

also known as working memory

Front 85

Type of memory
Long-term memories (LTMs)

Back 85

last for days to years
•Memories that can be retained without rehearsing them for hours or days without constant rehearsal.

EX•Where did you park this morning. •Your next dentists appointment •Where you next lunch meeting is

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Encoding

Back 86

sensory information is encoded into short- term memory

Front 87

Consolidation

Back 87

information may be consolidated into long-term storage

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Retrieval

Back 88

stored information is retrieved

Front 89

Neuroplasticity

Back 89

(or neural plasticity)
- the ability of the nervous system to change in response to experience or environment

Front 90

Neural Mechanisms Of memory

Back 90

-Molecular, synaptic, and cellular events store information in the nervous system
-New learning and memory formation involves changes in the strength of synapses in response to biochemical signals
-Memories can also require formation of new synapses or birth of new neurons

Front 91

Synaptic Changes

Back 91

• Increased neurotransmitter release
• Inactivation of the transmitter is
decreased
• A greater effect due to changes in receptors
• Influence by other neurons

Front 92

Long-term memories may bring about structural changes:

Back 92

• New synapses can form or old ones die back
• Training can bring about reorganization

Front 93

Three housing conditions: for lab animals and neuroplasticity

Back 93

• Standard condition (SC)
• Impoverished (or isolated) condition (IC)
• Enriched condition (or complex environment) (EC)
-in complex environment: enhanced &

• Experience/Learning produces many structural/functional changes

Front 94

Habituation

Back 94

– a decrease in response to a stimulus as it is repeated
-a form on non-associative learning (learning that involves only one stimulus)

Front 95

short-term habituation

Back 95

less transmitter released by sensory neuron produces the short term habituation

Front 96

long-term habituation

Back 96

results from fewer synapses

Front 97

habituation is NOT a result of:

Back 97

• failure of the sensory system to detect the stimulus
• failure of the motor system to respond

Front 98

Hebbian synapses

Back 98

cells that fire together wire together.
• could act together to store memory traces
Support of hebbian synapses were initially found in the hippocampus

Front 99

perforant path

Back 99

Electrodes are placed within the perforant path so that researchers can stimulate a group of presynaptic axons and then immediately record the electrical response of a group of postsynaptic neurons (dentate gyrus).

Front 100

Long Term Potentiation

Back 100

??

Front 101

LTP occurs:

Back 101

-in 3 different pathways within hippocampus
-occurs at synapses that use the transmitter glutamate
-depends on NMDA receptors (block them and you get no LTP) along with AMPA receptors

At low level activity, glutamate release at a synapse first activates only AMPA receptors
NMDA receptors at rest have a magnesium ion (Mg2+) block on their calcium (Ca2+) channels

Front 102

What happens with an influx of Ca2+ in LTP?

Back 102

activates intracellular enzymes, causing changes in AMPA receptors:
• Existingreceptorsmovetothe active synapse (increased conductance of ions)
• Activateretrogradesignalto increase neurotransmitter release

Front 103

Alzheimer’s Disease (AD)

& 3 stages

Back 103

a type of dementia characterized by progressive neurological degeneration and profound deterioration of mental functioning.

-NOT JUST A MEMORY PROBLEM,
-3 stages: 1.Forgetful/Apathetic/normal comprehension
2. Forgets Recent events/restless/comprehension reduced
3. Recent events fade fast/unresponsive/mute

Front 104

Prevalence of Alzheimer’s Disease

Back 104

• Affects about 4.5 million people in the US, but that figure is expected to rise to 14.3 million by 2050.
• Worldwide it affects 35.6 million people (2009) and 115.4 million people by 2050

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Age of onset for Alzheimer’s Disease

Back 105

• More common in elderly (65+)

and risk increases with age***

Front 106

Bio of AD

(Plaques)

Back 106

Accumulation of plaques (beta amyloid protein) that cluster among axon terminals (outside cell) above normal levels
• Interferes with neural communication
• Associated with cell death

Front 107

beta amyloid protein

Back 107

part of a larger molecule (amyloid precursor protein -APP) that is present in the cell membrane, but enzymes break up APP to make beta-amyloid protein.

binds to receptor on Acetylcholine neurons and initiates cell death.
Cell death correlated with cognitive impairment.

Front 108

Two forms of beta amyloid

Back 108

β secretase is the enzyme that cuts and determines how long the beta- amyloid protein is.
• Either 40 (short) or 42 (long) amino acids.

In normal brains, 90-95% of beta- amyloid proteins are the short form.
In AD brains, the long form rises to as much as 40%

Front 109

Problem with long forms of beta amyloid

Back 109

• Long form is more likely to fold themselves over and cause plaques
• When there are only few long strands (5-10%) the brain gets rid of them

Front 110

Pittsburgh Compound B (PIB) PET scan

Back 110

recognizes beta amyloid protein

Front 111

neurofribrillary tangles

Back 111

(Tau protein)
Tau protein is part of the microtubule system in axons.

Front 112

Areas affected in AD

Back 112

In addition to plaques and tangles, loss of synapses is a pathological hallmark of AD
• There is overall shrinkage of the brain as AD progresses

Regions in which damage occurs:
•Hippocampus
•Entorhinal cortex •Neocortex •Locus coeruleus •Raphe nuclei

Front 113

Risks factors for AD

Back 113

Most cases are sporadic,
but AD has been linked to:
• Traumatic Brain Injury
• Diabetes
• Stroke
• HeartDisease
• Women’shealth
 Women have greater risk
 Loss of ovarian hormones (estrogen and progesterone ) during
menopause is thought to be related)
• Smoking
 Heavy smoking (more than 2 packs a day). Nicotine binds to acetylcholine receptors
• Mitochondrial dysfunction

Front 114

most effective treatments for AD

Back 114

acetylcholinesterase inhibitors (Cholinesterase is the enzyme that metabolizes acetylcholine)
• Donepezil (Aricept)
• Rivastigmine (Exelon)
• Galantamine (Razadyne)
• Tacrine (Cognex)

NMDA antagonist are also used (glutamate binds to NMDA receptor)
• Memantine (Namenda)

Front 115

Novel treatments for AD

Back 115

Behavioral interventions:
Exercise
Environmental enrichment
Antioxidant-rich diet