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4 monoamines
- dopamine
- serotonin
- epinephrine
- norepinephrine
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main brain structure dealt with emotion
amygdala
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james lange theory
event-appraisal or cognitive aspect-action or behavior interacted physiogically-emotional feeling of fear
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pure autonomic failure
- no emotions
- completely/ to little reactions to
- nervous system doesnt control regular reactions
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panic attack
hard to breathe and heart race
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insula w/ what emotion
- part of the limbic system
- for disgust and taste
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behavioral activation system
- left hemisphere (frontal and temporal lobes)
- dealt with happiness and anger
- low/moderate automatic arousal
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behavioral inhibition system
- right hemisphere (frontal and temporal lobes)
- increase arousal, inhibits actions, and to stimulate fear/disgust
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more activity in left hemisphere w/ emotion
happier
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activity in right hemisphere
- prone to unpleasant situations
- soically withdrawn and less satisfied
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right vs. left hemisphere w/ emotions
right is more linked to emotions expressing and recognizing
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damage to right temporal cortex
trouble recognizing emotions
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phineas gage and prefrontal cortex damage
- poor decision making
- loss of emotion along with burst of anger
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ventromedial prefrontal cortex
- center for guilt
- damage people dont feel guilty
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parts of the limbic system
thalamus, globus pallidus, caudate nucleaus, putamen, hippocampus, amygdala
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testosterone effects on emotion
decrease in recognition of emotion in faces but increase responses in emotional ares of brain
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turnover
amount of a NT that is released and replaced like reuptake of serotonin
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low serotonin release is linked with what emotion
generally more aggresive and angry
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high vs low serotonin reuptake and aggression
low- die easier, more fighting but can become more dominant with that aggresion. remove inhibition.
high- less aggressive but is fine and low key status. inhibit impulses
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serotonin comes from
break down of trypyophans in protiens
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diet alterations to level serotonin
increase consomption of tryptophan or decrease consomption of high amino acid that work with tryptophan in the brain.
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movement of fear through the brain
senses from temporal lobe (auditory and visual cortex) go through the thalmus- baso/lateral amygdala-central amygdala-pons-reflex
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where is the startle reflex located
pons
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stria terminalis
connects nuron tissue in the amygdala with other limbic systems
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kluver-bucy syndrome.
- damaged amygdala
- monkeys were less scared of usual things
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emotion with faces experiment
easier to understand directed towards viewer except fear is understood better from a side
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when looking into a fear faced
people with damaged amygdala....
focus on nose/mouth instead where it rely all on the eyes
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panic disorder
frequent anxiety attacks and arousal of the sympathetic nervous system
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sympathetic vs parasympathetic
- para- calms
- sympa- helps and raises arousal "fight or flight"
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men vs woman and age with anxiety
higher in woman and in adolescents
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brain structure involved with anxiety
abnormalities in the hypothalmus
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NT involved with panic disorder
no release of gaba- more orexin
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orexin and gaba
orexin is used for arousal and staying awaka and gaba inhibits this from overpowering
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drugs used to treat anxiety
benzodiazepine (valium, librium, xanax)
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how do drugs work to treat anxiety
release more gaba to stop orexin
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when Gaba receptors open up
- chloride channels fluctuate easier
- hince why chloride is a chenical in the benzodiazapines
- hyperpolarize cell and inhibit the potential
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other recreational drug that helps anxiety
alcohol
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alocohal and benzodiazopine
anti anxiety medication that binds to GABA a to open up chloride channel and to inhibit
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general adaptaion syndrome
3 stages
- 3 stages to stress
- alarm
- resistance
- exhaustion
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alarm stage
readying the body with moderate emergency activity.
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resistance stage
- sympathetic system slows down,
- release of cortisol to keep up alertness
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cortisol
released by adrenal cortex to bring down sympathetic nervous system and to keep up alertness
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exhaustion stage
vulnerable inactive stage. no stage
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HPA axis
hypothalmus, pituitary and adrenal cortex
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stress and the immune system
- high amounts can impair it and harm you
- low amounts can increase and build memory as well
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leukocytes
white blood cells
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b cells in the immune system
- bone marrow release
- antibodies that recognize antigens and attacks unfamiliar ones
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antigens
protiens your body makes and regognizes
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t cell
- thymus gland
- mature and multiply
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natural killer cell
attack infected cells and tumor cells. kill all intruders where b and t attack certain ones
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cytokines
from hypothalmus to give alert that there is a problem or feeling ill
produce fever, loss of hunger, less sex drive, and more sleepy
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stress on the hippocampus
high activity of cells can make it hard to remember and higher metabolism and cause apoptosis or overstimulation. more cytokines released.
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ptsd patients or anxiety hippocampus
smaller hippocampus
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ptsd cortisol levels and smaller hippocampus
- lower than normal
- naturally have small hippocampus to begin with leading to easier access to ptsd
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agoraphobia
fear of public places and having a panic attack in front of others
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early onset depression linked to genes
will have higher chance of depression and other inherited psychological disorders
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late onset depression and genes
high probability circulatory prorblems
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serotonin gene expressing depression
short form- react to stressful situations by being depressed but no absence of stress does not decrease depression
in other words can still be randomly depressed and does not increase chance of happyness
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postpardum depression
depressed after birth
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depression links with the 2 hemispheres
decreased activity in left hemisphere and increased in right
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3 types of antidepressants
tricyclics, monoamine oxidase inhibitors, and selective serotonin reuptake inhibitors
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tricyclics
block the transporter protien that allow the 4 monoamines to reuptake
leaving NT in the synaptic cleft- and stimulating post synaptic neuron
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bad effects of tricyclics
- block histamine, ach, and sodium channels
- leading to drowzy, dry mouth and biofunction, and heart irregulatory. most unpleasant side effects
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MAOI vs SSRI
SSRI- focus on serotonin
MAOI- block the enzyme monoamine oxidase in presynaptic terminal from breaking down the monoamines into their metabloic sources
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myth serotonin levels in depression
a myth. people who are depressed may have higher serotonin and is just irregular
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bdnf
brain derived neurotrophic factor
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brain derived neurotrophic factor
neurotrophins for brain plasticity, learning, and growing new neurons in hippocampus
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antidepressants and bdnf
spring of new neurons and neurogensis. better learning.
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reaction with antidepressants
immediatly but mood correlated may take weeks to change
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ECT
- elecrical compulsive therapy
- used in schizo and epileptic people
- everyother day for 2 weeks small shock.
- helps depression unless relapsed
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depression and sleep
people who are depressed, sleep less. more REM sleep and waken earlier.
being sleep deprived may help the depression till next time. more practical to sleep earlier so you can wake earlier
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ECT in right hemishpere
unless moderated can lead to sufficient memory loss
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bipolar characteristics
mania with depressed states
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mania charcteristic
restless, rambling speech, and no inhibition
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lithium salt
- treat bipolar
- mood stabilizer
- stabilize glutamate- mania activator
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2 ways treat bipolar
anticonvulsant drugs and lithium
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seasonal affective disorder
messed up circadian rhythem and seasonal depression.
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treating sad
bright lights
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schizophrenia
delusins, hallucinations, disorganized speech and or behaviors, weak social, speech, and emotional responces.
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negative and positive symptoms of schizophrenia
positive- present behaviors that should not be there (delusions and hallucinations)
negative- symptoms that are not there that should be (weak emotion, social, and speech life)
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hallucinations come from
disorganized connections between cortex, cerebellum, and thalamus
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men and woman with schizophrenia
more common in men
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differences in brain with schizophrenia
- less grey and white matter
- larger ventricles (fluid space)
- small thalmus
- prefontal cortex and hippocampus are small
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left vs right hemishphere in schizophrenia
left is usually larger but in schzo its equal or right side is largee
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why does it take longer to see schizophrenia
late development of the prefrontal cortex
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chlopromazine
releives dellusions and hallucination
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treating schizophrenia
block dopamine receptors
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dopamine and schizo
turnover is elevated- faster release and reuptake with quicker synthesizing
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glutamate and schizophrenia
- low release of glutamate
- dopamine inhibits glutamate
- increase of dopamine and decrease of glutamte have same effect
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glutamate and dopamine
- dopamine inhibits glutamate
- glutamte excite neurons that inhibit dopamine
- low glutamte and high dopamine is equally effective
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