Emotion Flashcards
Default mode network
Part of the brain that is active while we are mentally inactive is the
Rerouting
New connections made between existing pathways
Sprouting
New axon & dendrite extends from an existing neuron to make new connections
Degenerative diseases
Existing neurons die off
-Alzheimer’s: Misfolded proteins build up
-Parkinson’s buildup of intracellular toxins
Coup/Contre-Coup
In closed head injuries, bruising occurs at two sites because brain hits the opposite site as well as
Ischemic stroke
Most common, from blood clot/obstruction of an artery
-Neurons not maintained, no access to oxygen/glucose
Hemorrhagic stroke
Less frequent, results from ruptured artery
-Neurons flooded with excess blood, calcium, oxygen, chemicals
Effects of stroke
Edema - fluid accumulation, increased pressure on brain
Disruption of Sodium-Potassium pumps
Immediate treatments for stroke
Minimize damage by cooling, tissue plasminogen activator that breaks up clots
Superficial facial muscles
Attach b/w points of facial skin
-Innervated by facial nerve
Deep facial muscles
Attach to bones, larger movements
-Innervated by motor branch of trigeminal nerve
Facial feedback hypothesis
Sensory feedback from facial expressions can affect mood
Folk Psychology
Stimulus > Perception/Interpretation > Emotion > autonomic arousal
James-Lange Theory of Emotion
Stimulus > Perception/Interpretation > Autonomic arousal > Emotion
Cannon-Bard Theory of Emotion
Stimulus > Perception > Emotion & Autonomic arousal
Schachter & Singer Theory of Emotion
Stimulus > Perception/Interpretation > Cognitive appraisal > Attribution of emotion responsible for arousal
Misattribution of arousal
Attributing false meanings due to similar reactions
Degeneracy
Different parts of brain able to do the same thing
Result of Prefrontal Lobotomy
apathy, lack of ability to plan, memory disorders, lack of emotional expression
Serotonin turnover
Amount of serotonin neurons release, absorb, and replace
-Low turnover associated with aggression
Testosterone & Aggression in animals
Removing testes > less aggressive behavior, strong correlation
Testosterone & Aggression in humans
Increased testosterone in puberty doesn’t increase aggression
High Road of fear/anxiety
From thalamus to sensory cortex/hippocampus, then to amygdala, uses perception
Low road in Fear/anxiety response
Thalamus > Amygdala
Toxoplasmosis
Parasitic infection in rats, can only reproduce in digestive system of cats
-Takes over part of CNS in rats & causes reduced fear of cats
Rabies
Viral infection spread through saliva,
-Increased saliva production
-Increased aggression
-Hydrophobia - fear of drinking water
General adaptation syndrome
Threats activate general response to stressors
Alarm stage of GAS
Increased SNS activity
Resistance stage of GAS
Sympathetic response declines, adrenals continue releasing hormones to prolong alertness
Exhaustion stage of GAS
After prolonged stress, body no longer has energy to sustain response
HPA Axis
Dominant response to prolonged stressors
-Hypothalamus responds to emotions & threats by releasing CRH
-Pituitary releases ACTH
-Adrenal glands release Cortisol
-Sympathetic activation: epinephrine & norepinephrine, cortisol drives negative feedback loop
Eustress
Good stress, helps focus
Endocannabinoids
Endogenous cannabinoid, NT that acts on CB-1 and CB-2 receptors, anti-anxiety effects
Dopamine
NT for reward/motivation behavior
Oxytocin
Hormone that has influence when we experience prosocial interactions
Endorphins
Hormones useful for pain dampening
MOD NED
Symptoms must occur most of the day, nearly every day
Areas of increased activation in depression
-Frontal lobes during cognitive tasks
-Amygdala during emotional processing
Negativity bias
gives negative events/thoughts proportionally greater impact in memory/psychological state
CBT
Looks at how thoughts, emotions, and behaviors are connected
ECT
Strong current used to cause controlled seizures
rTMS
Repetitive transcranial magnetic stimulation
-alters cortical electrical activity
Overall limitation of antidepressants
Strong placebo effect
First antidepressant drugs
MAO (Monoamine oxidase inhibitors)
How do MAO Inhibitors work?
-Enzyme inactivates monoamines: norepinephrine, dopamine, serotonin, raise level of them at the synapse
-originally irreversible
Tricyclic antidepressants
Block reuptake of serotonin & norepinephrine
SSRI Limitations
-serotonin discontinuation syndrome
-sexual side effects
-emotional blunting
-long lag-time
-^ Suicide risk (children/adolescents)
SNRI
Block reuptake of serotonin & norepinephrine, also for fibromyalgia
Buproprion
Reuptake of norepinephrine & dopamine
Vortioxetine
Inhibits serotonin reuptake, also antagonist for some serotonin receptors
Agomelatine
Agonist for melatonin receptors & 5-HT receptors
Reboxetine
Selective norepinephrine reuptake inhibitor, no effect in humans
Ketamine
Dissociative anesthetic, popular in veterinary medicine
Esketamine
Variant of esketamine, used as in-patient nasal spray
Positive symptoms
Hallucinations, delusions, disorganized speech, disorganized behavior
Negative symptoms
Weak emotion, speech, socialization
Cognitive symptoms
Limitations of thought/reasoning, may be due to impairments and working memory
Antipsychotic drugs for schizophrenia
Chlorpromazine (Thorazine) - first drug used, relieves positive symptoms of most patients
Antipsychotic/neuroleptic drugs
Tend to relieve schizophrenia and similar conditions
-2 chemical families: both block dopamine synapses
Phenothiazines
Antipsychotic/neuroleptic drug family that includes Thorazine
Butyrophenones
Antipsychotic/neuroleptic drug family that includes Haloperidol
Dopamine Hypothesis
Schizophrenia is due to excess activity at dopamine synapses in some brain areas - only helpful for explaining positive symptoms
Substance-Induced psychotic disorder (What does it support
Individuals experience hallucinations and delusions with repeated large doses of amphetamines, meth, or cocaine
-Supports dopamine hypothesis
