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153 Cards in this Set

  • Front
  • Back
Parkinson's disease
rigidity, muscle tremors, slow movements, and difficulty initiating physical and mental activity
-basal ganglia that help start or stop movement are impaired
slow cognitive tasks
early symptom- loss of olfaction
depression and memory loss are common
causes of Parkinson's
gradual progressive death of neurons (esp. in substantia nigra) which sends dopamine- relasing axons to the caudate nucleus and putamen
they lose axons and therefore dopamine

loss of dopamine activity in the substantia nigra leads to less stimulation of the motor cortex and slower onset of movements
twin studies with Parkinson's
monozygotic twins- one develops early onset- the other is almost certain to get it

twin develops it after 50- your risk is the same regardless of mono or dizygotic
equal concordance for both kinds of twins implies low heritability
genes have a weak influence on risk of late onset parkinson's
Parkinson's and chemicals
can be caused by exposure to chemicals or drugs that damage cells of the substantia nigra
herbicides or pesticides (farmers)
MPTP (heroin like drug)

people who smoke or drink coffee are less likely to develop parkinson's, but it isn't the nicotine or caffeine portion of these things that have the effect
L-dopa treatment
l-dopa is a precursor to dopamine-->when you take it daily it reaches the brain and converts to dopamine

-doesn't help some people in later stages
-doesn't prevent further loss of neurons
-lots of side effects - nausea, restlessness, sleep problems, low blood pressure, repetitive movements, hallucinations, and delusions
other therapies
-antioxidant drugs to decrease further damage
-drugs that directly stimulate dopamine receptors
-gene therapy- using a virus to transfer into the rain a gene that increases dopamine synthesis
-neurotrophins to promote growth of remaining neurons
Huntington's disease
1 in 10,000 people in the US
motor symptoms begin with arm jerks and facial twitches then tremors start and develop into writhing
gradual extensive brain damage, esp in the caudate nucleus, putamen and globus pallidus but also cerebral cortex
protein coded in the gene that causes Huntington
mutation outside of the brain doesn't cause any issues
mutation in the brain- it occurs in neurons and impairs neurons in several ways
-increase nt release- sometimes causing overstimulation
-later it forms clusters that impairs the neuron's mitochondira
-impairs the transport of chemicals down the axon
endogenous circannual rhythm
an inner rhythm within birds that prepares them for seasonal changes
endogenous circadian rhythm
internal clock that makes people tired at certain points of the day (ie at night)
wake-sleep cycle but also have circadian rhythms for other things like eating, hormones, drinking, etc
generate a cycle close to 24 hours
the stimulus that resets the circadian rhythm
light is the dominant zeitgeber for land animals
exercise, arousal, meals, and temperature of the environment
These are particularly important for blind people who can't rely on light as a zeitgeber
social stimuli needs to be extreme (ie induce exercise or other vigorous activity) to work
jet lag
disruption of circadian rhythm due to crossing time zones
internal and external times don't match up
phase delay- stay up later and awaken late the next morning (east to west)
phase advance- sleep earlier and awaken earlier (west to east)-->this is harder
danger of repeated circadian adjustments
stress elevates adrenal hormone- cortisol
prolonged elevated cortisol damages neurons in the hippocampus
damaged hippocampus leads to impaired memory

ex: flight attendants with constant jet lag
Suprachiasmatic Nucleus (SCN)
part of the hypothalamus- above optic chiasm (where axons from each eye cross to the opposite side of the brain)
provides the main control of the circadian rhythms for sleep and body temp
damage to this area causes body's rhythms to become erratic
SCN rhythms are genetic and able to be maintained in any environment (ie during a transplant it stays the same)
controls activity level in the pineal and endocrine gland
retinohypothalamic path
extends from the retina to the SCN
Axons of that path alter the SCNs settings
retinal ganglion cells that have their own photopigment
recieve some input form rods and cones but even without enough input they respond to light
located mainly near the nose
they respond slowly to light so not to instantaneous changes

this explains how blind people and mole rats respond to light cycles
secreted by the pineal gland
influences both circadian and circannual rhythms
mostly secreted at night- increases about 2-3 hours before bedtime
extended period of unconsciousness caused by head trauma, stroke, or disease
little response to stimuli especially those that are usually painful
vegetative state
alternates between periods of sleep and moderate arousal although during the aroused state the person shows no awareness of surroundings
no ability to speak or comprehend speech
no purposeful activity
minimally conscious state
one state higher than vegetative
occasional brief periods of purposeful actions and limited amount of speech comprehension
brain death
no sign of brain activity and no response to any stimulus
physicians usually wait until someone has no brain activity for 24 hours before pronouncing brain death
electroencephalograph (EEG)
records an average of the electrical potentials of the cells and fibers in the brain areas nearest each electrode on the scalp
combination of EEG and eye movement records
presents a period of relaxed wakefulness for comparison
alpha waves
recorded during a polysomnograph
frequency of 8 to 12 waves per second
characteristic of relaxation not wakefulness
Stage 1
dominated by irregular, jagged, low-voltage waves
overall brain activity is less than relaxed-wakefulness but higher than other sleep stages
Stage 2
characterized by sleep spindles and K-complexes
sleep spindle
consists of 12-14Hz waves during a burst that lasts at least half a second
result from oscilating interactions between cells in the thalamus and the cortex
sharp wave associated with temporary inhibition of neuronal firing
Stages 3 &4
slow-wave sleep
neuronal activity is highly synchronized
by stage 4 sensory input to the cerebral cortex is greatly reduced and the few remaining sources of input can synchronize many cells
paradoxical sleep
deep sleep in some ways and light in others
part of the brain will be really active while other parts are completely relaxed
for non-humans
rapid-eye movement (REM) sleep
same as paradoxical sleep but for humans
EEG shows irregular, low-voltage fast waves that indicate increased neuronal activity
REM sleep in that case is light, but the body's muscles are the most relaxed during this period so it is also deep sleep
cycles about every 90 minutes
becomes more common towards the end of a night's sleep
part of the reticular formation that contributes to cortical arousal
releases acetylcholine and glutamate which excite cells in the hypothalamus, thalamus, and basal forbrain
maintains arousal during wakefulness and increases it in response to new or challenging tasks
locus coeruleus
small structure in the pons that is usually inactive, esp during sleep but emits bursts of impulses in response to meaningful events esp those that produce emotional arousal
releases norepinephrine widely through cortex which has large effect on brain
orexin or hypocretin
axons extend to the basal forebrain where they stimulate neurons responsible for wakefulness
necessary for staying awake not waking up
GABA + sleep
GABA is necessary for sleep because it inhibits synaptic activity- prevents stimulation in other areas of the brain
inadequate sleep
caused by noise, uncomfortable temps, stress, paint, diet, and meds
can also be caused by epilepsy, Parkinson's brain tumors, depression, anxiety, or other conditions
can also be caused by dependance on drugs to help you sleep or alcohol
sleep apnea
impaired ability to breathe while sleeping
causes sleepiness throughout the day, impaired attention, depression, and sometimes heart problems
lack of oxygen causes lost neurons-->can cause deficiencies in learning, reasoning, attention, and impulse control
frequent periods of sleepiness during the day
four main symptoms (not all are always present)
1. gradual or sudden attacks of sleepiness during the day
2. occasional cataplexy- an attack of muscle weakness while the person remains awake. often triggered by strong emotions such as anger or great excitement
3. sleep paralysis- an inability to move while falling asleep or waking- can be experienced outside of narcolepsy, but is less frequent
4. hypnagogic hallucinations- dreamlike experiences that the person has trouble distinguishing from reality often occurring at the onset of sleep

people with this lack the hypothalamic cells that produce and release orexin (makes you stay awake)
periodic limb movement disorder
characterized by repeated involuntary movement of the legs and sometimes arms
REM behavior disorder
people move around vigorously during their REM cycles and apparently act out their dreams
frequently this incudes defending themselves against attack and they may punch, kick, or leap around
most of them injure themselves, other people, or property
mostly in older people esp older mean with brain diseases like Parkinson's
night terrors
experiences of intense anxiety from which a person awakens screaming in terror
more severe than a nightmare
occur during NREM sleep
James Lang Theory
the autonomic arousal and skeletal actions occur before the emotion is registered
emotion has three parts- cognitions, actions, and feelings
occur in that order

people with weak autonomic responses should feel less emotions and increasing someone's responses should enhance emotion
pure autonomic failure
output from the autonomic nervous system to the body fails either completely or almost completely
heartbeat and other organ functions continue but the nervous system no longer regulates them
someone with this doesn't react to stressful experiences with change in heart rate, bp or sweating
they report having the same emotions, but they are less intense
they associate their emotions much more with cognition
Möbius syndrome
cannot move their facial muscles to make a smile
they experience the same happiness and amusement but they have trouble making friends because people don't respond well to the lack of smiling
limbic system
forebrain areas surrounding the thalamus
critical for emotion
insular cortex or insula
part of brain that is strongly activated if you see a disgusting picture or the facial expression of someone who is feeling disgusted
behavioral activation system (BAS)
marked by low to moderate autonomic arousal and a tendency to approach, which could characterize either happiness or anger

activity in the left hemisphere- happier, more outgoing, and more fun-loving
behavioral inhibition system (BIS)
increases attention and arousal, inhibits action, and stimulates emotions such as fear and disgust

activity in the right hemisphere- less satisfied with life, socially withdrawn, and prone to unpleasant emotions
right hemisphere is also more specialized than the left for interpreting other people's expressions of emotion
the trolley dilemma
a runaway trolley is headed toward five people on a track, the only way you can prevent their death is to switch the trolley onto another track where is will kill one person- would it be right to pull the switch

most people say it is right
the footbridge dilemma
you are standing on a footbridge overlooking a trolley track. a runaway trolley is headed towards five people. the only way to prevent their death is to push a heavy set stranger off the footbridge onto the track to block the trolley
would it be right to push him?

few say this is right
activates areas of the brain known to respond to emotions- prefrontal cortex and cingulate gyrus
the lifeboat dilemma
you and six other people are on a lifeboat in icy waters, but it is overcrowded and starting to sink. if you push one person off the boat will stop sinking and the rest of you will survive
is it right to push someone?

few say this is right
activates areas of the brain known to respond to emotions- prefrontal cortex and cingulate gyrus
the hospital dilemma
you are a surgeon and five of your patients will die soon unless they get organ transplants (each need a different one)
you haven't been able to find any organ donors but then a visitor to the hospital arrived that has all the right tissue types for your other patients
the nurse suggests killing them and using the organs to save the other five
would this be right?

almost no one says this is right
prefrontal damage
Phineas Gage
he exhibited impulsive behavior and made poor decisions
Antonio Damasio
expressed almost no emotions
he also made poor decisions that hurt many areas of his life
he could predict the outcome of certain decisions, but not the emotions that would accompany that
ie approval would feel good, trouble would feel bad
attack behaviors
depend on the individual and the situation
the first attack increases the probability of a second attack
Monoamine oxidase A- MAOa
enzyme that breaks down NTs dopamine, norepinephrine and serotonine thus lowering the available amounts
this interacts with childhood experiences- kids who experience severe maltreatment during childhood and have low levels of this exhibit much more antisocial behavior
startle reflex
response to an unexpected loud noise
happens extremely quickly
Ubrach-Wiethe disease
causes calcium build up in the amygdala- lack of fear responses and difficulty identifying other peoples emotional expressions
study of patient SM- she doesn't fear anything, she gets angry but not fearful
this is dangerous because certain situations you should react with fear (being held up at gun point) so you can respond appropriately
panic disorder
characterized by frequent periods of anxiety and occasional attacks of rapid breathing, increased heart rate, sweating, and trembling
extreme arousal of the sympathetic nervous system
much more common in women than men
more common in adolescents and young adults
genetic predisposition, but not linked to 1 gene

decreased activity of GABA and increased level of orexin (keeps you awake)
Valium, Xanax, etc
bind to GABAa receptor - by binding to more sites in the chloride channel this drug facilitates the effects of GABA
anti-anxiety effects in the amygdala, hypothalamus, and midbrain
general adaptation syndrome
alarm- initial stage
characterized by increased activity of sympathetic nervous system, readying the body for brief emergency activity
resistance- second stage
the sympathetic response declines but the adrenal cortex secretes cortisol- used to prolong alertness, fight infections, and heal wounds
exhaustion- final stage
individual is tired, inactive, and vulnerable because the nervous and immune systems no longer have the energy to sustain heightened responses
HPA axis
the hypothalamus, pituitary gland, and adrenal cortex
adrenocorticotropic hormone (ACTH)
after the HPA axis activates the hypothalamus it induces the anterior pituitary gland to secrete this hormone, which in turn stimulates the human adrenal cortex to secrete cortisol (enhances metabolic activity and elevates blood levels of sugar and other nutrients)
most important element of the immune system
known as white blood cells
three types:
B cells
T cells
and Natural killer cells
mostly found in bone marrow
secrete antibodies which are y-shaped proteins that attache to particular kinds of antigens (antibody generator molecules)
when these cells find an unfamilliar antigen they attack the cell
this can cause the body to reject organ transplants
mature in the thymus gland
several types of these cells attack the intruder directly and some help other types of leukocyte cells multiply
Natural Killer cells
attack tumor cells and cells that are infected with viruses
attacks all types of intruders
small proteins produced by leukocytes
combat infections and also communicate with the brain to elicit appropriate behaviors
the body's way of telling the brain that it's ill
deals with the ways experiences alter the immune system and in turn influences the CNS
Stress + the immune system
in response to a stressful experience the nervous system activates the immune system to increase production of natural killer cells and secretion of cytokines
the increase of these cytokines help combat infection but also make produce the same symptoms as being ill therefore prolonged stress has similar wear on the body as prolonged illness
Post-traumatic stress disorder (PTSD)
symptoms include frequent distressing recollections and nightmares about the event, avoidance of reminders of it, and vigorous reactions to noises and other stimuli
must last at least 1 month after the event

most people with this disorder have a smaller than average hippocampus, they show lower cortisol levels before and after the event
classical conditioning
Pavlov's dog
after several repitions
operant conditioning
reinforcer- any event that increase future probability of the event
punishment- any event that suppresses the frequency of the response
physical representation of what has been learned
concept that all parts of the cortex contribute equally to complex behaviors; any part of the cortex can substitute for any other
mass action
the cortex works as a whole and more cortex is better
memory loss
two types:
anterograde and retrograde
anterograde amnesia
inability to form memories for events that happened after brain damage
future memories
retrograde amnesia
loss of memory for events that occurred before the brain damage
episodic memories
memories of single personal events
impairment of these memories allows you to sometimes remember facts but not personal experiences
explicit/declarative memory
deliberate recall of information that one recognizes as a memory
Implicit memory
an influence of experience on behavior, even if you don't recognize that influence
procedural memory
the development of motor skills and habits
special kind of implicit memory
Case study: HM's memory
-normal working memory
-severe anterograde amnesia for declarative memory- ie difficulty forming new declarative memories especially episodic ones
-some degree of retrograde amnesia- mainly limited to episodic memories
-better implicit memory than explicit
-nearly intact procedural memory
hippocampus + memory
patients with damage to this area have trouble learning new facts but can acquire new skills
this area is critical for declarative memory- esp episodic
delayed matching-to-sample task
an animal sees an object (the sample) and then, after a delay gets a choice between two objects which it must choose the one that matches the sample

requires declarative memory- hippocampal memory reduces ability to perform well on this task
delayed nonmatching- to-sample task
an animal sees an object (the sample) and then, after a delay gets a choice between two objects which it must choose the one that doesnt match the sample

requires declarative memory- hippocampal memory reduces ability to perform well on this task
hippocampus + spatial memory
this area of the brain (as exhibited through a study of taxi drivers in London) plays a large role in spatial memory and can even grow depending on how long person was a taxi driver (thereby increasing their accuracy with spatial memory)
hippocampus + contextual memory
this area of the brain is very important for remembering details and context
recent memories are heavily dependent on this area and include a lot of detail which can degrade over time
as time passes memories become less dependent on this area and more dependent on the cerebral cortex
basal ganglia
gradual learning depends on this area-->ie learning patterns requires this area of the brain
Korsakoff's syndrome
brain damage caused by prolonged thiamine deficiency
mostly occurs in chronic alcoholics who go for weeks with only ingesting alcohol and no vitamins
thiamine= vitamin B1-->metabolizes glucose
deficiency leads to loss or shrinkage of neurons in the brain, esp the dorsomedial thalamus
apathy, confusion, and memory loss (like preforntal cortex damage)
major impairment of episodic memory and sparing of implicit memory (like hippocampal injury)
distinctive symptom of Korsakoff's syndrome
patients fill in memory gaps with guesses
generally the answer was true at some point but isn't any longer and they are usually more pleasant than current answers
occur in episodic memory questions not facts or nonsense
gradually progresses to more serious memory loss, confusion, depression, restlessness, hallucinations, delusions, sleeplessness, and loss of apetite

affects 5% of people between 65-74
people with down syndrome almost always get it if they live to old age
protein that accumulates inside and outside neurons
net effect is damage to dendritic spines, decrease synaptic input, and decrease plasticity

these damaged structures cluster into structures called plaques-->as these accumulate the cerebral cortex, hippocampus, and other areas waste away
tau protein
intercellular support structure of axons
high levels of amyloid-ß cause more phosphate groups to attach to tau proteins
these proteins then can't bind to its usual targets so it spreads through the body-->this magnifies the damage
semantic dementia
damage to the anterior and inferior regions of the temporal lobe cause this which is a loss of semantic memory
Hebbian synapse
a synapse that increases the effectiveness because of simultaneous activity in the presynaptic and postsynaptic neurons
decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli

ie if your clock chimes every hour you stop having as great of a response
an increase in response to mild stimuli as a result of exposure to more intense stimuli
long-term potentiation (LTP)
one or more axons connected to a dendrite bombard it with a rapid series of stimul- this burse leaves some of the synapses potentiated (more responsive to new input of the same type) for minutes, days or weeks
if some of the synapses onto a cell have been highly active and others have not then only the active ones become strengthened
nearly simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by just one axon
pairing a weak input with a strong input enhances later response to the weak input. in this regard LTP matches what we would expect of Hebbian synapses
in some cases a synapse that was almost completely inactive before LTP becomes effective afterward
long-term depression (LTD)
prolonged decrease in response at a synapse, occurs for axons that have been less active than others
corpus callosum
connects both halves of the brain
division of labor between the two hemispheres of the brain

left side- language
right side-dominant for recognizing emotion
in some severe cases of this disorder surgeons will cut the corpus callosum
this means that the seizures experienced for this disorder will only affect half of the body (since it can't cross to the other side) and has also effectively decreased the amounts of seizures these patients see
split-brain people
these individuals maintain their intellect and motivation and still walk without difficulty despite having their corpus callosum severed

they are actively able to split tasks between both sides of the brain
Williams syndrome
affects 1 in 20,000 people
mental retardation in most regards except that they speak gramatically and fluently
caused by the deletion of several genes from chromosome 7
leads to decreased gray mater- esp for visual processing

fascinated by faces- their fusiform cortex is twice as large
have severe anxiety or are quarrelsome and irritable (not good for social relationships)
language acquisition device
built in mechanism for acquiring language
nonfluent aphasia
language impairment caused by damage to Broca's area
have comprehension deficits when the meaning of a sentence depends on prepositions, word endings, or unusual word order-->ie the structure is complicated

also causes trouble when producing speech - omits prepositions and other grammatical connectives but includes mostly nouns and verbs

poor pronunciation
fluent aphasia
language impairment caused by damage to Wernicke's area
characterized by poor language comprehension and impaired ability to remember the names of objects
can still speak smoothly
speech is grammatical but often nonsensical, has trouble finding the right word- esp names of objects
specific impairment of reading in someone with adequate vision, motivation, and overall cognitive skills
more likely in boys
linked to at least 4 genes that produce deficits in hearing or cognition
linked to difficulty reading- understanding language is a combination of sound and reading

can also suffer auditory and attention problems
dysphonetic dislexics
have trouble sounding out words, so they try to memorize each word as a whole and when they dont recogonize the word they guess based on its context
dyseidetic dislexics
these readers sound out words well enough but they fail to recognize the word as a while
they read slowly and have particular trouble with irregularly spelled words

most severe of these cases suffer from damage that restricts field of vision

they experience lots of eye movements while reading (letter by letter)
belief that the mind and body are different kinds of substance that exist independently
universe consists of only one type of substance
view that everything that exists is material or physical
mental events don't exist at all
the view that only the mind really exists and that the physical world could not exist unless some mind were aware of it
identity position
the view that mental processes and certain kinds of brain processes are the same thing, described in different terms
phi phenomenon
if you see a dot in one position alternating with a similar dot nearby it will seem as though the dot is moving back and forth
inattentional blindness
if something in a complex scene slowly changes while you blink your eye you probably wont notice it unless you are paying attention to the particular item that changes
Stroop effect
the difficulty of ignoring the words and saying the color of the ink
spatial neglect
a tendency to ignore the left side of the body or left side of objects when there is damage to the right hemisphere
doesn't generally happen for damage to the left side
major depression (MDD)
sad, feeling worthless and helpless, lack of energy, contemplate suicide, have trouble sleeping, cannot concentrate, find little pleasure, and can hardly imagine being happy again

-5% of adults in the US
-moderate degree of heritability but no one gene
-people with early onset (before 30) have high likelihood of relatives with the disorder as well as anxiety disorders, attention-deficit disorder, alcohol or weed abuse, ocd, bulimia, migraines, and ibs
-people with late onset have high probability of relatives with circulatory problem
postpartum depression
after giving birth this disorder occurs
stress hormones peak late in pregnancy and ovarian hormones go through major changes around the time of delivery- might be cause
blocks the trasporter proteints that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after their release
result: prolongs presence of NTs in synaptic cleft
also blocks histamine receptors (drowsiness), acetycholine receptors (dry mouth and difficulty urinating), and sodium channels (causes heart irregularities)
selective serotonin reuptake inhibitor (SSRIs)
similar to tricyclics but only affects serotonin
ex: Prozac, Zoloft, Paxil
have milder symptoms than tricyclics but equally effective
Serotonin norepnephrine reuptake inhibitors (SNRIs)
block reuptake of serotonin and norepinephrine
monoamine oxidase inhibitors (MAOIs)
block the enzyme monoamine oxidase - a presynaptic terminal enzyme that metabolizes catecholamines and serotonin into inactive forms
this means the presynaptic terminal has more of this transmitter available for release
this is used after trying tricyclics and SSRIs
side effect: must avoid foods with tyramine (cheese, raisins, wine) because the combination of the two increases blood pressure
atypical antidepressants
everything besides MAOIs, SSRIs, SNRIs, and tricyclics
electroconvulsive therapy (ECT)
electrically induced seizures
doesn't work well for schizophrenia
people with severe MDD can respond well but only used if they don't respond well to drugs
downsides : memory loss (common), high risk of relapse within a few months
depression + sleep
most people with depression have altered sleep patterns (these occur before the depression)
got to bed at the normal time but awaken early and unable to fall back asleep
more eye movements than normal during REM

a full night without sleep is a quick fix for depression, but is short lived and increases sensitivity to pain
unipolar disorder
vary between normality and depression
bipolar disorder
alternate between depression and mania (characterized by restless activity, excitement, laughter, self-confidence, rambling speech, and loss of inhibitions)

also exhibit attention deficits, poor impulse control, and impairments of verbal memory
bipolar I disorder
full blown episodes of mania
bipolar II disorder
milder manic phases called hypomania- characterized by agitation or anxiety
treatment for bipolar disorder
stabilizes mood, preventing a relapse into either mania or depression
must be highly regulated- too little doesn't work and too much is toxic
seasonal affective disorder (SAD)
depression that recurs during a particular season
most prevalent near the poles where the winter nights are long
phase-delayed sleep and temp rhythms
most other types of depression are phase-advanced
treatments: very bright lights for an hour or more each day (effective at any time during the day)
deteriorated in everyday functioning (work, interpersonal relations, self care, etc) for at least 6 months and must show two of the following
disorganized speech (rambling or incoherent)
grossly disorganized behavior
weak or absent signs of emotion, speech, and socialization
unjustifiable beliefs such as "beings from outer space are controlling my actions"
false sensory experiences such as hearing voices when alone
positive symptoms v. negative symptoms
positive- behaviors are present that should be absent-->delusions, hallucinations, disorganized speech and behavior

negative- behaviors that are absent that should be present-->weak or absent emotions, speech or socialization
these are usually stable over time and difficult to treat
concordance + schizophrenia
-monozygotic twins have high concordance (agreement)
-about 50% concordance-->these twins could differ a couple genes or experience different environmental influences
-greater similarity between dizygotic twins than siblings
neurodevelopmental hypothesis
schizophrenia begins with abnormalities in the prenatal or neonatal development of the nervous system based on either genetics or other influences
relieves the positive symptoms of schizophrenia for most patients

blocks dopamine synapses
phenothiazines and butyrophenones
two chemical typs of antipsychotic or neuroleptic drugs
behavioral benefits of these drugs develop gradually over a month or more but symptoms generally return after stopping treatment

blocks dopamine synapses
dopamine hypothesis of schizophrenia
schizophrenia results from excess activity at dopamine synapses in certain brain areas
although the overall dopamine isn't higher the turnover is elevated (esp in the basal ganglia)
ie the neurons release dopamine faster
substance induced psychotic disorder
characterized by hallucinations and delusions, the positive symptoms of schizophrenia
occurs after repeated use of amphetamine or methamphetamine or cocaine
each of these increases or prolongs the activity of dopamine synapses
glutamate hypothesis of schizophrenia
deficient activity at glutamate synapses, esp in prefrontal cortex
dopamine inhibits glutamate release or glutamate stimulates neurons that inhibit dopamine release
therefore increased dopamine would produce the same effects as decreased glutamate
phencyclidine (PCP)
drug that inhibits the NMDA glutamate receptors
at low doses it produces intoxication and slurred speech
at larger doses it produces both positive and negative symptoms of schizophrenia
can produce a long lasting relapse for someone who has had schizophrenic periods
mesolimbocoritcal system
set of neurons that project from the midbrain tegmentum to the limbic system
also blocks dopamine neurons in the mesostriatal system that projects to the basal ganglia
tardive dyskinesia
characterized by tremors and other involuntary movement that develop gradually and to varying degrees among different patients
second generation antipsychotics
alleviate schizophrenia without producing movement problems
clozapine is most common type
more effective than older drugs at treating negative symptoms of schizophrenia
side effects: weight gain, impairment of the immune system