Exam 4 Questions

8/12/2019 Exam 4 Questions

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What is a stressor?

Anything that throws body out of allostatic

balance

What is allostasis?

Allostasisis the process of achieving stability, orhomeostasis,through physiological or

behavioral change

What are the 3 stages of a stress response?

1. Alarm: SNS activation

2. Resistance: decreased SNS activity; increased HPAactivity cortisol& other hormones for maintaining

prolonged alertness & increased immune function (to

fight infections & to heal wounds)

3. Exhaustion: NS and Immune system are spentperson

is tired, inactive, and vulnerable to illness

What is the role of the sympathetic NS in the stress response?

sympathetic nervous system(SNS) is one of the three parts of theautonomic nervous

system,along with theentericandparasympatheticsystems. Its general action is to

mobilize the body's nervous systemfight-or-flight response.It is, however, constantly

active at a basal level to maintainhomeostasis.[1]

What is the HPA and what is its rolein the stress response?

Hypothalamus, pituitary gland, adrenal cortex Hypothalamus makes CRH Pituitary makes ACTH

adrenal secretes cortisol increase in blood sugar &

metabolism

Activated w/ prolonged stressors
http://en.wikipedia.org/wiki/Homeostasishttp://en.wikipedia.org/wiki/Homeostasishttp://en.wikipedia.org/wiki/Homeostasishttp://en.wikipedia.org/wiki/Autonomic_nervous_systemhttp://en.wikipedia.org/wiki/Autonomic_nervous_systemhttp://en.wikipedia.org/wiki/Autonomic_nervous_systemhttp://en.wikipedia.org/wiki/Autonomic_nervous_systemhttp://en.wikipedia.org/wiki/Enteric_nervous_systemhttp://en.wikipedia.org/wiki/Enteric_nervous_systemhttp://en.wikipedia.org/wiki/Enteric_nervous_systemhttp://en.wikipedia.org/wiki/Parasympathetic_nervous_systemhttp://en.wikipedia.org/wiki/Parasympathetic_nervous_systemhttp://en.wikipedia.org/wiki/Parasympathetic_nervous_systemhttp://en.wikipedia.org/wiki/Fight-or-flight_responsehttp://en.wikipedia.org/wiki/Fight-or-flight_responsehttp://en.wikipedia.org/wiki/Fight-or-flight_responsehttp://en.wikipedia.org/wiki/Homeostasishttp://en.wikipedia.org/wiki/Homeostasishttp://en.wikipedia.org/wiki/Sympathetic_nervous_systemhttp://en.wikipedia.org/wiki/Sympathetic_nervous_systemhttp://en.wikipedia.org/wiki/Sympathetic_nervous_systemhttp://en.wikipedia.org/wiki/Sympathetic_nervous_systemhttp://en.wikipedia.org/wiki/Homeostasishttp://en.wikipedia.org/wiki/Fight-or-flight_responsehttp://en.wikipedia.org/wiki/Parasympathetic_nervous_systemhttp://en.wikipedia.org/wiki/Enteric_nervous_systemhttp://en.wikipedia.org/wiki/Autonomic_nervous_systemhttp://en.wikipedia.org/wiki/Autonomic_nervous_systemhttp://en.wikipedia.org/wiki/Homeostasis


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Beneficial in the short-term; detrimental in the long-

term

Negative consequences of stress (like effects on

learning and memory) can be induces by stressitself, or by an injection of cortisol!

Why do you feel terrible during finals week?

Acute activation boosts the immune system,

even improves memory Useful for escaping a predator

*but*Powerful, inescapable, temporary stress body

reacts like illness, w/ increased immune activity Like exam week!

body increases production of natural killer cells (a type of

white blood cell for fighting infections) and cytokines.

Cytokines help fight infections, but they are also the bodys

way of telling the brain you are sick, so you have sickness

syndrome (fever, exhaustion, decreased appetite)

What are some factors that affect the stress response?

Individuals perception of their own ability to cope

with stress

Intensity of the stressor (novel environment vs. life-

threatening situation)

Individuals control over the stressor Duration of stressor

Personality traits (individuals with high anxiety) are

more likely to show impaired memory after stressor)


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Gender (males more affected than (young)

femalessome measures improvein females!)

Age (older more vulnerable to deleterious effects

of stress than younger; early stress might notshow cognitive effect until later in life)

What are some effects of long-term stress?

Hippocampal damage (b/c increased cortisol makes

hippo. neurons more vulnerable) Chronic infant stress leads to deceased hippo

plasticity & impaired spatial memory in adulthood

(rats)

Explicit memories (consolidated by hippocampus)

are esp. vulnerable to stress; implicit memories are

not (sometimes opposite effect!)interesting b/c

amygdala increases branches and other brain

regions that do implicit learning (like cerebellum)

are not as affected by stress. Reproductive effects:

Decreased libido in women

Can inhibit menstrual cycle, ovulation in women

Decreased sexual performance in men

Decreased immune function, Prolonged sickness

syndrome?? Prolonged increase in cortisol decreases protein

synthesis, including proteins for the immune

systemso lots of eitherfeelingsick or beingsick.

Increased blood sugar (b/c stress (cortisol?) causes

pancreas to release glucagon)is this bad if happens

for too long??


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Maybe people w/ low cortisol are ill-equipped

to handle extreme stress

Vietnam vets w/ brain damage & PTSD: those w/

damage to amygdala NEVER had PTSD!

What is an engram, and what were Lashleys critical mistakes in looking for the

engram?

A physical representation of a memory

Lashley: trained rats, then cut* or lesioned^ certain areas of

cortex *no significant effect on performance; the bigger the

lesion, the greater the impairment (location didnt matter) 2 false assumptions:

(1) memory is in cortex

(2) all memories are physiologically the same

What are implicit memory and explicit memory? What brain regions are important for

each?


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What are some differences b/t short-term memory (working memory) and long-term

memory? What brain region is important for working memory?

Short Term Memory

Small capacity CYZUAUF

Fades quickly unless rehearsed

Once forgotten, it is gone Working memory is alternate way of thinking of

STM: lasts hours to days w/o rehearsal: where car

is parked, when/where lunch date is


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Time needed for consolidation varies,

especially depending on familiarity of topic &

emotional content

Long Term Memory Infinite capacity

Lasts indefinitely

Could be forgotten and then later remembered w/

appropriate cues. Phone # vs. names of grade school teachers

Working memoryDelayed response task

Dorsolateral prefrontal cortex

What were some of HMs impairments; what could he still do?

HM: anterograde amnesia Lost declarative (explicit)

memory & spatial memory

Intact procedural memory

(a type of implicit) and

working memory

With regard to memory, what are some functions of the hippocampus?

Active during formation of memories & during

recall

Consolidation (STM LTM)


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Declarative/explicit memory

Spatial memory Increased activity in hippocampus

when doing spatial task (ex:imagining best route; fMRI)

Damage impairment of spatial

tasks

London taxi drivers: hippo active

during spatial tasks; larger posterior hippo

& positive correlation to time being a taxi

driver Birds that live at high altitude and bury seeds

= larger hippocampus

Place neurons

What other brain regions are important in learning and memory, and what type of

learning do they subserve?

Cerebellum: for learning a conditioned response Also for motor learning (skills) & cognitive

stuff too.

Parietal lobe: if damage, dont spontaneously

elaborate on memories

Temporal lobe (ant./inf.): damage causes

semantic dementia SD: loss of factual knowledge

Probably b/c this region is a hub for retrieving

info; not the location of storage.


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Prefrontal cortex: learning reward and

punishment Also working memory of course

What is a Hebbian synapse?

Hebbian synapse: a synapse that

increases in effectiveness b/c of

simulataneous activity in pre- and

postsynaptic neurons What is LTP? What receptors are necessary?

Long Term Potentiation: a burst of stimulation

from axons, e.g., 100 excitations per second for

1-4 seconds onto dendrites, results in

potentiated (strengthened) synapses for minutes,days or weeks

Necessitates glutamate receptors: AMPA and

NMDA receptors

What are some presynaptic changes that occur in LTP? What are some postsynaptic

changes that happen in LTP?

Presynapticchanges during LTP

Retrograde transmitter from dendrite to

axon terminal, usually nitric oxide (NO)


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Decreased threshold for producing APs

Increased release of neurotransmitter

Expansion of axon (seen in prev. slide along

w/ increase in spine number Release of NT from more sites along axon

What is evidence that there is a functional connection between LTP and actual

learning?

Neurons change early in training, a

preliminary step before behavioral change

Research with mice abnormal NMDA receptors impair learning

drugs that block LTP block retention of

learned material

drugs that facilitate LTP facilitate learning

LTP increases certain proteins, & blocking

those proteins weakens memories

LTP increases GAP-43& over

production of GAP-43 enhances

learning and problem solving

following training, LTP seen in hippocampus

quickly and in cerebral cortex 90-180 minutes

later (this might have been in rats)

What are some cognitive and non-cognitive symptoms of dementia? What are the 4

As of demenita?

The diseases of aging

Different causes; similar presentations


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Impairment in memory & cognition, accompanied by

decreased ability to relate/function at home/work/social

settings

Noncognitive symptoms: delusions, suspicions,hallucinations, agitation, depression

Up to 2/3 of AD patients develop delusions & hallucinations

Depression & dementia are often comorbidhave to distinguish b/t

the two

Also have to distinguish b/t dementia and psychosis

Amnesia Loss of memory (working memory goes first)

Agnosia Loss of ability to recognize objects

ApraxiaLoss of knowledge about how to do

things

AphasiaLoss of speech

What are some symptoms of Alzheimers Disease (AD)?

Deficits in explicit and implicit memory Better procedural than declarative memory

First symptoms can be mild anterograde amnesia

Gradual progression to more serious memory loss and Language problems (loss of vocabulary)

Confusion

Depression

Restlessness


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Hallucinations

Delusions

Sleeplessness

Loss of appetite

Sundowning

End stage is usually coma; death usually caused by an

infectionVery early cognitive symptoms (difficulty committing new things to

memory) can be noticed up to 8 yrs before symptoms progress enough

to meet criteria for AD.

In early stages of Alzheimer's disease, there is a steady decline.Symptoms include: loss of recent memory, language skills and motor

skills. The person may become hostile and agitated due to the losses

that are occurring. Visual-spatial skills are impaired. There is an inability

to orient in an unfamiliar environment. Depression may also be present.

What is the difference b/t early-onset and late-onset AD? Which one has a stronger

genetic contribution?

Early onset People


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People w/ Downs Syndrome get AD if theysurvive to middle age. So looked on chromosome

21found gene linked to many cases of early

onset AD

Late onset: Over 60 yr old

5% of people b/t 65-74 yr old

50% of people over 85 yr old

Some genes that increase risk, but only account for small

percentage of cases

Half of patients have no known relative with A.D. Yoruba people (Nigeria): lots of A.D. genes; very little

A.D.

What do the neurons and the brain of an AD patient look like?

Brain atrophy Loss of neurons

Loss of spines & synapses Loss of connections between neurons

Proteins fold abnormally, clump, and interfere w/

neuronal activity

Plaques and tangles: Where are they (inside or outside of cells) and what forms them?

Amyloid precursor protein Normally important in neuron growth,

survival and post-injury repair (?)

cleaved to A40

in AD, cleaved to A42


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A42 accumulates (usually prior to behavioral symptoms)

widespread atrophy of cortex, hippocampus, etc amyloid

plaques (formed from degenerating axons & dendrites, in

the places b/t neurons) Tau

Normally part of intracellular support structure of neurons;

involved in transporting things w/in the cell

Abnormal form in AD (hyperphorphorylated; aggregates w/

other strands of tau)

Produces tangles, from degenerating structures w/in

neuronal cell bodies

What are some treatment options for Alzheimers Disease?

Drugs to stimulate Acetylcholine receptors or prolong Ach release Ach system is first to go Aricept One area damaged (basal forebrain) is important in Ach system & for

arousal NMDA receptor antagonists to block excitotoxicity Anti-inflammatory drugs (inflammation may be caused by plaques and lead to

neuronal dysfunction) Drugs to stimulate cannabinoid receptors Limits overstimulation by glutamate Looks good in rat model of AD

Antioxidants to block -amyloid Aged mice: curcumin (in yellow dye and tumeric) reduces amyloid and

plaques Immunization

to produce antibodies against -amyloid Researched in mice & humans (a few life-threatening side effect in

humans though, so research stopped)

Worth mentioning: Memory books, respite for caregivers

Know causes, symptoms, and (when applicable) treatment options of Korsakoffs

Syndrome, Parkinsons Disease, Huntingtons disease and CJD.

Korsakoffs Syndrome


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Aka. Wernicke-Korsakoff Syndrome

Brain damage caused by prolonged thiamine (vitamin B1)

deficiency Usually in alcoholics: poor diet: lots of carbs; no vitamins

Thiamine needed to metabolize glucose (fuel for the brain)

Shrinkage of neurons, esp. in mammillary bodies & dorsomedial

nucleus of thalamus, which sends axons to prefrontal cortex

Damage of axons & myelin

Can also involve other brain areas

Symptoms of Korsakoffs

Syndrome

Like damage to prefrontal ctx

Apathy

Confusion

Retrograde & anterograde amnesia

Better implicit than explicit memory

Difficulty reasoning thru memories (ex. what event happened

first?) Confabulation: person takes a guess to fill in blanks of memory

Learning becomes difficult b/c confabulate answers and then

remember the confabulation instead of the correct answer

Eye abnormalities (nystagmus, oculomotor paralysis, paralysis of

conjugate gaze)

Ataxiaof stance and gait

Parkinsons Disease

Loss of dopaminergic cells in

substantia nigra that project to

striatum less excitation of cortex


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Rigidity, muscle tremors, slow

movement, difficulty initiating movement (or cognitive

activity)

Dementia can be similar to AD, but movement problems are

first and predominant sign in PD Depression

Deficits in memory and reason

Mix of causes Genetics? Yes for early-onset

Toxins? MPTP MPP, which is toxic to SN neurons

Exposure to MPTP or similar chemical in

pesticides and herbicides

Drugs: cigarettes & coffee decrease vulnerability;marijuana increases vulnerability

Virus? PD symptomS

Huntingtons Disease

Loss of cells in caudate & putamen

Arm jerks & facial twitches, later tremors and

writhing Cognitive changes and psychiatric symptoms, which often

develop prior to movement disorders Depression & anxiety

sleep disorders

memory impairment

Hallucinations & delusions

Poor judgement

Alcoholism & drug abuse Sexual disorders

Genetic (autosomal dominant) 95% penetrance

Chromosome 4

Trinucleotide repeate (C-A-G)

Normal gene makes protein huntingtin


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More repeats get it earlier

Earlier it begins quicker it progresses

Abnormal huntingtin harms neurons by:increasing NT release,

decrease BDNF release, impairs mitochondria

Creutzfeldt-Jakob Disease Familial (Inherited) or sporadic (spontaneous)

New variant CJD (nvCJD): these are known as transmissible

spongiform encephalopathies BSE or Mad cow disease

nvCJD resulting from contaminated instruments or transplants

For PD, HD and Korsakoffs, what brain regions are involved?

What are prions? Prions (protein-based infectious agent);

Misfolded proteins that promote refolding of native

proteins into diseased states There is a normal prion protein which is a membrane-

bound protein that is implicated in LTP and long-term

memory. This is what becomes abnormal and affects

other prion proteins.

Infectious (acquired), spontaneous (sporadic) orinherited (familial)

Pruisner won Nobel Prize in 1997

Symptoms: rapidly progressing dementia, confusion, blurred vision,

hallucinations, incoordination, changes in gait, muscle twitching and

stiffness, seizures, personality changes, nervousness, speech

impairment, sleepiness

What kind of language do other species have? What do we learn from studying how

other species communicate or from their potential for language?


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Chimps: attempted to teach chimps ASL or other visualsystems.

Chimps didnt use symbols in new original combinations

Used symbols to request, not describe Produced requests more then they understood

Bonobos: very human-like; what Kanzi learned: 250 human words; language of 2-2 yr old

Understand more than they can produce

Use symbols to name/describe

Request items they dont see

Use symbols to describe past

events Original, creative requests

Why so much better than chimps? More language potential?

Started younger?

Method of training (observation/

imitation)

Elephants imitate the sounds they hear,

including vocalizations of other elephants

Dolphins learn to respond to

gestures and sounds

Alex, the African gray parrot Learned to give spoken answers to

spoken questions (What color is

the key? What object is gray? Howmany blue keys are there?)

What do we learn from this? How to teach language to people

who do not easily learn it


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Our concept of language is

ambiguous

What are the hypothesis on how humans evolved language?

How did humans evolve language?

Hypothesis 1: a by-product of overall brain

development:

But some people w/ normal sized brain dont have normal

language; language requires specialization, not justexpansion

Family w/ normal intelligence and normal activity in

language centers but poor language skills (dominant gene)

Another problem: Williams syndrome: Deletion of many genes on chromosome 7; decreased gray

matter

mental retardation, but skillful use of language

How did humans evolve language?

Hypothesis 2: an extra brain module, aka, a

new specialization

Language acquisition device Built-in mechanism (instinct) for acquiring language

that is uniquely human Can be explained by evolution

Steven Pinkers The Language Instinct (also Noam

Chomsky)

Ease w/ which children learn language


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Even if no one teaches them, they invent their own

Applies to deaf and hearing children

Certain brain areas necessary for language, but

language isnt their only job Probably not a totally separate brain module

Is there a critical period for learning language? If so, when is it? Is there a critical

period for learning a second language?

The younger the betterprobably a critical

period but no sharp cut-off age No exposure to any language in infancy and

young childhood never develop much skill at

any language

Learn foreign language before puberty to speak

w/o an accent

Where is language? Generally (L hemisphere, with a role for the right as well) and

specifically? Are a persons first and second languages inthe same location?

Left hemisphere 95% of strongly right handed people have

language on L side

60% of left-handed and ambidextrous

have language on L

Child w/ L hemispherectomy before puberty can acquire

language on R

R hemisphere is important for some aspects of language,

like prosody.


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If acquire 2nd

language later, 2 separate areas,

1 for each

If acquire early, more overlap w/ aphasia, can lose 1 language and preserve

other

Emotionality can make 2nd

language tougher

What is aphasia? What causes it and who does it affect?

Impairment of language Due to brain injury

Can be very mild to very severe

Can affect any symbol system (language, music, math)

Around 1 million people in US

Can happen to anyone

Can be transient

What are Brocas aphasia and Wernikes aphasia? What are the symptoms of each

and what brain regions are involved?

BROCAS APHASIA

Non-fluent aphasia

Caused by damage to Brocas area & surrounding area Part of frontal lobe of L cortex near motor cortex

Difficulty with motor production of words speak slowly and inarticulately

Omit prepositions and conjunctions, and have difficulty

understanding them Trouble saying no ifs ands or buts

Trouble reading to be or not to be but can read two bee oar

knot two bee


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So problem w/ language, not just vocal muscles

Trouble with writing and gestures

Comprehension deficits w/ complicated sentence structure

WENIKES APHASIA

Fluent aphasia Impaired ability to remember names of objects Impaired language comprehension Articulate speech (speak smoothly) but

nonsense Difficulty finding the right word Are Brocas area and Wernikes area the only brain areas important for

language?

Need connection b/t Wernikes area and motor

cortex/Brocas area for understanding and forming

words. Lose connection b/t WA and BA conduction aphasia: speak

like WA but good comprehension

Get activation of motor cortex w/ any action word

(kick activates foot part of motor cortex)

Alexia w/o agraphia: damage to particular part of

parietal lobe

What are mood disorders?

Affective disorders


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Illnesses that effect the emotional

coloring with which we see the world

What are some common myths about suicide? What should you do if you fear

someone you know is contemplating suicide?

Thoughts of suicide are considered a medical

emergency

Myths: people who talk about it never do it

you can precipitate someone into doing it by askingthem about it.

If you think someone might be depressed and

considering suicide: Discuss your concern with simple straightforward

questions

Encourage person to seek medical treatment

Keep weapons away from depressed person

All attempts should be taken seriously, even if theyappear to be an obvious cry for help

especially worrisome in adolescents who might

not understand how easy it is to actually

complete the task

Risk is especially high for people who have expressed

suicidal thoughts or have attempted suicide in the past

Be able to recognize the symptoms of major depression, atypical depression,

dysthymia and bipolar disorder. Be able to recognize the symptoms of mania.

Atypical depression


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Responds to positive and negative experiences, but

especially sensitive to negative experiences

Often have many partners, frequent break-ups

Weight gain, hypersomnia, increased appetite

Respond best to SSRIs with psychotherapy

Dysthymia Mild and persistant (chronically miserable)

Tend toward the emotional and cognitive

symptoms

Sometimes worsen into major depression double depression

Can be brought on by specific life events

Bipolar Disorder

Used to be called manic-depressive disorder

Can cycle over different periods of time Rapid cycler b/t extremes in days or hours

Symptoms of mania

Restless activity (goal-directed or psychomotor

agitation)

Decreased need for sleepenormous surge of

energy

Excitement (elevated, expansive or irritable

mood)

Laughter Self-confidence (inflated self-esteem or

grandiosity)

Rambling speech


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Flight of ideas or subjective experience that

thoughts are racing

Loss of inhibitions (excessive

involvement in pleasurable activities

that have high potential for painful

consequences)

Distractibility

Impairments in verbal memory Is there a role for hormones in depression? What is the evidence?

Stress can elevate cortisol weak immune system,

impairment of sleep stage set for depression

Females vs. males Equal in boys and girls

More common in women than men (in all cultures,

not due to who seeks treatment)

Sex hormones: Emotional distress after giving birth

Baby blues

Postpartum depression

Drug-induced drop in estrogen and progesterone

cause depression in women who already sufferedfrom PPD

Estrogen relieves depression during menopause

Prolonged cortisol: weakens immune system, impairs sleep, therefore

sets stage for depression


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Females vs males: equally uncommon in boys and girls, more common

in girls/women then boys/men after puberty (for all cultures for which

data exist and not due to women being more likely to seek treatment)

What is the difference b/t bipolar I and bipolar II?

Bipolar I: full manic episodes Lifetime prevalence ~2%

Equally common in men & women, found

in all cultures

Bipolar II: mild manic episodes, mostlyw/ agitation or anxiety

What do adoption studies and twin studies tell us about the heritability of mood

disorders?

Identical twins: 50% chance

Fraternal twins, siblings, children: 5-10%chance of developing it

Adoptive children w/ bipolar disorder likely

to have biological relative with mood

disorder

Several genes more common in people w/

bipolar, but these only increase risk. Having a relative with a mood

disorder increases your likelihood of


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developing a mood disorder (but not

necessarily the same one)

Identical twins: 65% chance Fraternal twins: 14% chance Most genes that may be involved are

related to dopamine or serotonin

transmission (particularly, their

receptors)

What neurotransmitter systems are most genes involved in mood disorders related to?

Most genes that may be involved are

related to dopamine or serotonin

transmission (particularly, their

receptors)

Understand the graph on slide 6 (really you should always understand all of the graphs

and figures from lectures!).


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What are treatment options for depression? Compare/contrast SSRIs, MAOIs, atypicalantidepressants.

Psychotherapy produces metabolic changes similar to drugs

and person is less likely to relapse after treatment

67% improve with drugs or psychotherapy or both, 33%

improve with no treatment

Sleep deprivation works for certain patients

depressed people enter REM sleep early, have

trouble staying asleep and awaken early

one night of total sleep deprivation or rescheduling

sleep pattern relieves depression

like drugs, reduces REM

Tricyclics block the reuptake of dopamine,

norepinephrine, or serotonin. SSRIs specifically

block the reuptake of serotonin. MAOIs block

the enzyme MAO, which converts dopamine,

norepinephrine, or serotonin into inactive


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chemicals. Atypical antidepressants have

varying effects.

Be able to recognize the symptoms of schizophrenia. Understand what those

symptoms are.

Split or fragmented mind

A disorder characterized by deteriorating

ability to function in everyday life and bysome combination of hallucinations,

delusions, thought disorder, movement

disorder, and inappropriate emotional

expressions Symptoms vary between people (H and D for

some; TDs predominate for others)

Some have brain damage, others dont

Acute: quick onset, high likelihood of

recovery

Chronic: gradual onset, long-term course

What does it mean that some symptoms are positive symptoms and others are

negative symptoms?


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Positive Behavioral

Symptoms Behaviors that are present that shouldnt be

Psychotic: Delusions: unfounded beliefs

Hallucinations: abnormal sensory experiences

Increased activity in thalamus, hippocampus, cortex

Disorganized: Inappropriate emotional displays

Bizarre behavior

Incoherent speech

Thought disorder: difficulty understanding and using

abstract concepts

Negative Behavioral Symptoms

Negative: behaviors that are absent that should be

present, including weak: Social interactions

Emotional expressions

Speech

Working memory

Stable and hard to treat

What do twin studies and adoption studies tell us about the heritability of schizophrenia?

Twin studies:


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MZ > DZ> siblings

MZ still have just 48% concordancewhy? Maybe a gene is activated in one and suppressed in another.

Also, note DZ>siblings.

Share same amt of DNAso whats going on? Maybe moresimilar prenatal/neonatal environment for DZ twins than

siblings.

Adoptions studies: More resemblance to biological parents than adoptive

parents One study showed that home (adoptive) environment must be

somehow dysfunctional for effect from biological parents to

manifest Especially increased if bio mom is schizophreniccould

represent poor prenatal environment

What are some prenatal and neonatal risk factors for schizophrenia?

Poor nutrition of mom during pregnancy

Extreme stress early in pregnancyPremature birth

Low birth weight

Complications during delivery

Head injuries in childhood (cause or

effect?)Rh-incompatibility


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Season-of-birth effectmaybe due to

virus

Other infections in mom too: rubella,herpes, etc.

Childhood infection w/ toxoplasmosis

What are some mild brain abnormalities sometimes seen in schizophrenia?

Small, variable

Thinner cortex, but same cell number, so what

is lacking? Fig summarizes 15 studies, 390 people

Most of cortex, depending on study

Left prefrontal and temporal

Increased ventricle size

Smaller thalamus Smaller cell bodies, esp. in hippo. & prefrontal

Larger sulci

What is cognitive dysmetria?

Cognitive dysmetria: a disruptionof the fluid coordination of mental

activity

What is the neurodevelopmental hypothesis of schizophrenia? .


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Neurodevelopmental Hypothesis: S is basedon abnormalities of the prenatal or neonatal nervous system developmentwhich can lead to abnormalities of brain anatomy & behavior

What neurotransmitters are likely involved in schizophrenia, and how are they

involved (is there too much transmission or too little)? What is the evidence for the

dopamine hypothesis of schizophrenia?

Dopamine: too much! This is the dopamine

hypothesis of schizophrenia. Antipsychotic drugs block dopamine receptor

Repeated doses of drugs of abuse that increasedopamine induce substance-induced psychotic

disorder (H&D)

Glutamate: too little! This is called

hypofrontility. Especially in prefrontal cortex

PCP (phencyclidine; angel dust) inhibits NMDA

receptors Positive & negative symptoms of

schizophrenia at high doses (again, substance-

induced psychotic disorder)

Serotonin Atypical antipsychotic drugs block serotonin

receptors

What drugs are used to treat schizophrenia?

Older ones (Thorazine and more)


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Only helped positive symptoms

Extrapyramidal side effects

(involuntary movements)

D2 R antagonists

Second-generation: atypical

antipsychotics Clozapine, Risperidone, etc.

Help positive & negative symptoms

Fewer extrapyramidal side effects Side effects: increased appetite,

weight gain, diabetes, effect on

prolactin leading to breast formation,

decreased immune function Also block D2 R, but maybe with

shorter timecourse than 1stgen.

drugs.

Also block serotonin 2A receptors

Efficacy and lack of side effects may

be due to balance b/t action on

dopamine and serotonin systems. One study showed that these drugs

decrease positive & negative


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symptoms but do not improve quality

of life.

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