Unit 4 Exam Flashcards
pattern of behavioral, chemical, or physiological fluctuation in 24 hours
circadian rhythm
yearly patter
circannual pattern
less than 24 hours
ultradian pattern
master clock with sleep and temperature patters. where is it found
SCN (supra schismatic nucleus). Hypothalamus
triggered from within
endogenous
when relying on endogenous. maintaining its own personal cycle. think person in dark (a little over 24 hours)
free-running
zeitgeber
“time giver” (light)
retinohypothalamic tract
light > retina > SCN
pineal is inhibited by light, which makes
melatonin
there are specialized retinal ganglion cells that go straight to the
SCN
entrainment pathway through which light affects SCN (2)
through retinohypothalamic tract OR retinal ganglion cells
genes that regulate in 24 hours. Protein products degrade. Proteins activate other clock gene transcription
clock genes
explain mechanism of clock genes
clock and cycle dimerize, and each turn on CRY and PER, producing two proteins which come together and then turn off BOTH CRY AND PER
per gene is also activated with
glutamate receptors coming from retina…
SCN Lesion then transplant
loses rhythm, then gains rhythm of transplant
Slow wave sleep
Stages 3 & 4 (sync activity of neurons)
Decrease in heart rate and breathing
1 thru 4
REM sleep
High brain activity, muscle tone low, dreams!
Most of SWS? Most of REM?
First half, second half
biological functions of sleep
energy conservation, avoid predation when inefficient, memory consolidation, restoration of body processes (adenosine, beta amyloid)
what memory does REM consolidate?
Implicit
what memory does SWS consolidate?
Explicit
builds up when ATP is used, binds to receptor on terminal and prevents glutamate being released, makes sleepy
adenosine
adenosine receptor antagonist, accumulates. delays clock
caffeine
brainwashing
cerebralspino fluid clearing out debris. deeper in sleep.
what makes us sleep?
circadian signals, homeostatic mechanisms, neural controls. Can all be overridden by FEAR or HUNGER
Circadian signals
Clock genes/proteins, melatonin
Regions that Promotes wakefulness
Brainstem, hypothalamus (sleep promote), and forebrain.
Which brain regions coordinate REM
pons and midbrain
Dreams most vivid, external stimuli often incorporated
REM
Activation synthesis hypothesis
Dreams are a result of cortex attempt to make sense of random brain activity
Brain regions active during dreaming
1 sensory inactive > hallucinations.
PFC inactive (memory weak, logic lacking, judgment lacking).
Amygdala active > emotions
Hypothalamus active > motivations and drives
Consequences of sleep deprivation
Sleepiness, negative affect (tangry), poor vigilance, poor executive functioning, decreased immune, microsleep
Benzodiazapines
GABA receptor agonists. Not normal sleep. Suppress SWS and REM. Poor sleep
Non-Benzo
GABA receptor agonists. Doesnt interfere with REM
Non-restorative sleep
Insomnia
Onset, Maintenance, termination
Falling asleep, maintenance, and termination
Inability to sleep during sleep. Causes?
sleep apnea. caused by genetics, hormones, obesity, aging.
Moving of limbs every 30 seconds
periodic limb movement disorder
Moving around during REM bc no paralysis
REM behavior disorder
symptoms of narcolepsy
Sleepiness and sleep attacks, cataplexy, sleep paralysis, hypgagonic hallucinations (dreaming while awake)
loss of muscle tone
cataplexy
Fear >
Anger >
Disgust >
> Escape
Fight
Avoidance
Darwin’s Evolution of Emotions
Expressions of emotions comes out of behaviors that indicate what an animal is to do next. If its beneficial, it will get better. 1
What are emotional displays for?
Survival and communication.
Facial expressions are
Innate, universal
brief expressions reveals true feelings & breaks through false ones
microexpressions. Different muscles are involved in fake and real emotions
Volitional facial paresis
Can’t be faked
Emotional facial paresis
Can’t be real
Imitation of facial expression is innate as a mechanism for
empathy? See > Imitate > FEEL
Emotional states
Perception (cognition), physiological response (action), Feeling (emotion)
Modern biopsychological model
all emotional states interact together
Brain regions involved in emotion
Cortex (PFC, Insula, Cingulate), Amygdala, Hypothalamus, Brainstem (PAG)
Hypothalamus, Amygdala, and PAG in emotion
Amygdala feels emotion, to hypothalamus, and to PAG (organizes behavioral responses)
PFC in emotion
assessment of situation. Inhibits Amygdala (knee jerk reaction)
Present stimulus with adverse shock, animal presents body tone of fear or defense. Requires Amygdala
Fear Conditioning
Context Conditioning requires
amygdala and hippocampus (spacial memory)
Low serotonin turnover leads to
High aggression. Serotonin excites PFC. Outward and inward. Also low in clinical depression
Prenatal exposure to nicotine
Convicted sons of aggression
Twin studies of emotion/aggression
MZ & DZ same in adolescence. (more controlled)
MZ more aggressive in adulthood.
Acute physical stressors
Lions
Chronic physical stressors
Drought, famine, parasites
Psychological, social stressors
Traffic, relationships, care-giving, mortgage, debt
Combined set of behavioral and physiological adjustments that an individual makes in response to current and predicted environmental stressors. Requires prior experience or knowledge
Allostasis
Body’s attempt to restore balance.
Stress response. Trigger general adaptation syndrome (threats to a body and its response)
Three stages of general adaptation syndrome
- Alarm (SNS)
- Vigilence (HPA)
- Exhaustion (immune/nervous system spent, tired, inactive)
Two System Model of Stress:
SNS:
HPA Axis:
SNS: Energy for immediate expenditure
HPA Axis: hormones from adrenal cortex
Factors that affect stress response
intensity, control, duration, support, perception to cope, personality, gender, age
Low nurture mice moms leads to elevated stress
LOW glucocorticoid receptors (weak negative feedback)
High nurture mice moms leads to reduced stress
High glucocorticoid receptors — know how to manage stress. Robust negative feedback
Long term stress on reproductive system
Decreased libido, menstrual cycle, bad sexual performance
Long term stress on Limbic system
Prolonged cortisol in hippocampus, explicit memories, Expansion of amygdala
Long term stress on immune system
Mobilize survival so less immune
Diathesis-stress model: diathesis
Genetic/constitutional predisposition
Diathesis-stress model: stress
environmental trigger
Psychiatric disorders characterized by mood or emotion
Depression and mania
Major Depressive Disorder
Emotional, somatic, Cognitive
sadness/helplessness.
ADHEDONIA
Emotional
Little pleasure.
Adhedonia
Low energy, sleep patterns, weight loss/gain, psychomotor agitation/retardation
Somatic
Feeling worthless/guilt, can’t imagine happinesss, death, suicide, decrease in concentration
Cognitive
How many symptoms present for Major Depressive Disorder
BOTH Emotional and 3 other for 2 weeks
mild persistent depression, emotional/cognitive, can worsen
Dysthymia
Responds to pos/neg experiences (sensitive to negative . Weight gain/hypersomnia/appetite. SSRI’s and psychotherapy
Atypical depression
Depressive symptoms 1 month after birth, Decrease in estrogen
Postpartum depression
Occurs in the winter, reduction in sunlight, decreased serotonin and melatonin,
Seasonal affective disorder
Full manic/depression
Bipolar 1
Full depressive/not full manic
Bipolar 2
Mild depression and manic
Cyclothymia
Symptoms of mania
restless, excitement, laughter, self-confidence, distracted, loss of inhibition, verbal memory
Block reuptake of serotonin
SSRI
serotonin and norepinephrine uptake inhibitors
SNRI
block breakdown of serotonin and catecholamines
MAOI
prevent reuptake of serotonin, norepinephrine
tricycles
Treatment for bipolar disorder
Lithium
Depression untreated with drugs may result in proliferation of monoamine receptors
Monoamine theory of depression
Bridges the gap between drug effect at synapse and behavioral effect. Depression results from a decrease of neuroplastic processes* in the amygdala, PFC, and hippocampus > neuron loss & other neural pathology
Neuroplasticity theory of depression
Non-pharma cures for depression
Deep brain stimulation, sleep deprivation, exercise, electrocolvultive therapy, cognitive behavioral therapy
Positive Behavioral Symptoms (SZ)
Delusions, Hallucinations, Disorganized symptoms
Negative Behavioral Symptoms (SZ)
flat effect (not emotional tone), avolition (no volition), associality (no social), anhedonia, alogia (no speech)
Cognitive symptoms (SZ)
Attention, executive function, working memory, cognitive flexibility
less activity in frontal lobes
Hypofrontility (SZ)
many genes involved
polygenetic
Diathesis-Stress Model
genetics + trigger = depression/stress
Brain abnormalities in SZ
increased ventricles, thinning of cortex, heterotopias
small displaced grey matter probably migrating during prenatal but never made it to cortex
heterotopias
Dopamine Hypothesis of SZ
Dopamine transmission is elevated in some brain regions (NA). D2 receptor
OLD SZ DRUGS
D2 receptor antagonist, only positive symptoms, movement
NEW SZ DRUGS
D2 antagonist, both -/+ symptoms.
dopamine receptor seen in SZ
D2. Increased dopamine