exam 3 Flashcards
(129 cards)
1
Q
homeostasis
A
optimal, stable and balanced internal environment
- deviations of homesostasis cause changes in motivation
2
Q
negative feedback
A
restoring set point turns off response
- ex: thermostat uses neg feedback control, inclusion of sensor and response system, heat from system provides neg feedback inhibiting thermostat
3
Q
redundency
A
multiple systems that perform the same feneral function provides fail safe mchanism for vital functions
4
Q
behavioral compensation
A
adjusting behavior to achieve homeostasis
- ectothermic lizards: huddling, moving to shade or sun, making nests
5
Q
allostasis
A
process by which the body responds to stressors in order to regain homeostasis
- used to maintain optimal functioning
- stability thru change
6
Q
allostatic load
A
wear and tear on the body
- new set point of homeostasis for brain with constant stress
7
Q
energy balance and nutrient intake
A
brain uses glucose for energy, with or without help from insulin
- body uses glucose for energy but needs insulin to use glucose
- glucose shuttled back and forth by hormones regulated by brain
- brain integrates glucose and insulin levels w other info to monitor appetite (not sole signal monitors)
8
Q
why is losing weight difficult
A
set point for body weight is strict
- 80% of food energy spent on basal metabolism: heat production, cellular activity, maintaining memberane potentials
9
Q
metabolic adaptation
A
biggest loser ex
- decrease in weight and metabolism makes upfor itself again over time
- human hypothalamus responds to nutrients
10
Q
appetite
A
controlled by hypothalamus in arcuate nucleus
11
Q
ventromedial hypothalamus
A
- satiety center
-VNM lesioned rats over eat
12
Q
lateral hypothalamus
A
- hunger center
- LH lesioned rats experience satiety
13
Q
arcuate nucleus
A
headquarters of appetite
holds neurons- leptin, insulin, ghrelin, PYY, GLP-1, NPY, POMC which are vital for regulating hunger
14
Q
insulin
A
-from pancreas which brain can detect
- acts as short term signal to tell us to slow/stop eating
-inhibits NPY neurons
15
Q
ghrelin
A
- from stomach
- high levels when hungy
- stomach growling
- excites NPY neurons, promotes appetite and food seeking
16
Q
PYY
A
produced by intestine
- created thru digestion
- acts to shut down feeding
- inhibits NPY neurons
17
Q
GLP-1
A
- produced by intestines
- acts to shut down feeding
- stimulates POMC neuron, reduces appetite
18
Q
NPY neuron
A
- hunger neuron
- when activated causes you to want to eat
- works in opposition to POMC
19
Q
POMC
A
satiety, no eating
- opposed to NPY
- gets to voluntary motor system, causes us to exhibit behavioral food seeking
- increases metabolism
20
Q
orexin/orexigenic neurons
A
- lateral hypothalamus
- coordinate increased appetite and food intake signals
21
Q
somnambulism
A
sleep walking
- sleep disorder
22
Q
enuresis
A
bed wetting
- sleep disorder
23
Q
nucleaus of solitary tract
A
- brainstem nucleus that reveices visceral and taste info via cranial nerves
24
Q
thermoregulation
A
how we control body temp
- food burned to maintain internal temp- takes a lot of calories
25
temp detection/ thermosensitive neurons
- free nerve cells have specialized receptors to tell temp
- skin surface receptors, body core receptors, hypothalamus/pre optic area POA receptors
- spinal cord, brainstem, hpothalamus/pre optic are POA
26
physiological effectors
- thermogenesis: burning body tissue or inhibiting burning to change temp
- blood flow may change; vasoconstriction or vasodilation
- water evaporation; sweating, panting
-shivering
27
behavioral effectors
- postural change; reduce exposed surface
- temp choice; heat seeking, cold seeking
-altering microenvironment; nesting, huddling, air conditioning
28
circadian rhythm
diff body functions rise and fall over 24 (almost 25) hour period
29
increased during the day
body temp
cortisol
blood pressure
30
increased during the night
metalonin
growth hormone
testosterone
prolactin
31
entrainment
process of shifting rhythm to a stimulus
32
zeitgeber
cue used to synchronize (i.e light)
33
suprachiasmatic nucleus
- in hypothalamus above optic chiasm
- cells make clock and cycle
-recieves entraining light stimulation from eye via retinohypothalamic pathway
-vital for circadian rhythms
-brain transplants prove SCN contains a clock
- location of endogenous clock
34
retinohypothalamic pathway
uses glutamate as neurotransmitter
35
components of circadian system
-entrainment pathway w/ specialized retinal ganglion cells containing melanopsin that projects to SCN via retinohypothalamic tract
- cones and rods provide vision
- to thalamus for form vision
36
melatonin effect
sunlight enters eye thru retino hypothalamic tract to suprachiasmatic nucleus to superior cervical ganglion and back to pineal gland to make melotonin
37
molecular clock in flies and mice
- clock and cycle initiate and enhance expression of period and cryptochrome
- PER and CRY accumulate thru out the day
- repress their own transcription
- degrade over night
38
clock and cycle
- proteins made in SCN that bind together to form dimer, and that DNA promotes transcription of cryptochrome and period
39
period
key circadian protein, regulates daily rythms of behavior and physicology
- inhibit activity of Clock and Cycle (BMAL1)
40
cryptochrome
key circadian protein, regulates daily rythms of behavior and physicology
- inhibit activity of CLOCk and Cycle (BMAL1)
41
sleep
patterns differ by sex and change w age
- humans become late risers at puberty
42
waking stage
mix
of high frequenceis with low amplitudes; beta activity
43
stage 1
alpha rythms
- vertex spikes/shar waves
- hear rate slows, muscles relax, eyes roll about slowly, lasts several minutes
44
stage 2
brief periods of sleep spindles and K complexes
45
stage 3 SWS
dreams
- motor skill learning and consolidation of declarative memory
- large amplitude delta waves
46
REM sleep
- every 90-110 minutes
- sleep activity resembles waking stage
- eyes dart rapidly
- muscles relax
- called paradoxical sleep
- perceptual learning
47
night of sleep
waking to rem to non rem to rem to waking to non rem to rem etc
- sleep in babies; stable at night does not appear until 16 weeks
48
sleep and age
- we sleep a lot early in life and half is REM sleep
- adulthood; 8 hours, 20% REM sleep
- elderly; severe reduction in SWS and frequent awakenings
49
fatal familial insomnia
becomes impossible for individual to sleep, which leads to their death
50
functions of sleep
- energy conservation
- niche adaptation
- body and brain restoration
- memory consolidation
51
niche adaptation
sleep serves adaptive function, organizms sleep the amoun they to and way they do to promote their survival
52
body and brain restoration
waste and byproducts cleared out
53
memory consolidation
- brain replays events during sleep
- evidence of memory function in SWS
-memory enhancement function present when we sleep
54
nonassociative learning
presentation of particular stimulus alters the strength or probability of a response and includes habituation
55
basal forebrain
-regulates SWS by releasing GABA into tubermammillary nucleus in hypothalamus
- electrical stimulation of basal forebrain makes animals sleepy while lesion induce insomnia
56
brainstem
- regulates waking stage
- contains ascending arousal system projecting monoaminergic axons to brain
- electrical stimulation promotes wakefulness and alertness, lesions produce sleep states
57
medulla
- REM sleep
- subcoeruleus, ventral to locus soerculeus sends projections to promote rem sleeo
- medullary axons projecting to spinal cord inhibit motot neurons to they cannot fire, causing muscle atonia
58
hypothalamus
main coordinator of sleep
- region w neurons that use hypocretin as neurotransmitter send axons to other three sleep centers to coordinate them
- enforce sleep pattern
- loss of hypocretin can lead to disorganized sleep llike rem like muscle atonia while awake; narcolepsy
59
insomnia
inability to sleep or stay asleep
60
narcolepsy
excessive drowsiness
- associated with loss/lack of orexin containing neurons in lateral hypothalamus
61
disorders of sleep-waking schedule
jet lag, grave yard shift etc
62
dysfunctions associated w sleep
sleep walking, night terrors etc
63
hippocampus
- deep in temporal lobe, in medial temporal memory system
- body GPS
- vital learning and memory center
- Patient HM; crucial to short term and long term memory, unconscious motor sensors separate from conscious understanding, declarative and procedural are diff parts of brain, implicit vs explicit
64
procedural memories
basal ganglia and cerebellum
65
sensorimotor learning
basal ganglia cerebellum and motor cortex
- eye blink conditioning; cerebellum
66
anterograde amnesia
cannot make new memories and carry them forward
67
engram
neuronal encoding that provides a physical location for a memory
- plastic change in brain gives memories a physical location
68
process of memory
- sensory info in sensory buffers
- encoded into STM
- consolidated to LTM w rehearsal
- memory pulled from LTM to STM when performing task
-info forgotten at any stage
69
stages of memory
-sensory
-STM
-LTM: explicit; declarative-episodic, semantic; Implicit-procedural
70
long term potentiation
increase of communication that lasts for a long time
- synaptic connections between neurons become stronger w frequent activation
- found in rabbit brain
71
rabbit experiment
LTP
- axons from cortex; create activity in system
- recording activity shows liively hippocampus
- day later cortex and hippocampus communicate more efficiently
- week later even better
72
LTP normal synaptic transmission
- synapse releases glutamate via two receptors
- AMPA, NMDA
73
AMPA receptor
one of the glutamate receptors in LTP
- cation: positive ion channel
- opens when glutamate activates it, sodium releases, neuron is hyperpolarized
74
NMDA receptor
blocked by magnesium ion under normal conditions
- induces increased number of postsynaptic AMPA receptors when activated in ltp
75
Induction of LTP
- synapse releases glutamate
- learning event is so strong that post synaptic side depolarizes to eject magnesium out of NMDA
-NMDA lets in calcium, a lot changes
- calcium activates 2nd messengers, changing functions of neuron and dna
- AMPA receptors inserted into membrane
76
LTP properties
-input specific
- coincidence (timing important)
- requires NMDA receptor
- calcium dependent
- 2nd messengers
77
LTP expression
- insertion of AMPA receptor allows twice as much calcium
- increased communication
- more AMPA receptors
-better ion conductance
78
LTP changes
- some cells fire synchronously, strengthening synapses that fire
- some cells fire at random and rarely cause firing, loss of ineffective inputs
- pre and post synaptic changes
- structural changes; # and size of synapse and dendritic spines
- increase AMPA receptors
- requires NMDA, calcium and magnesium ejection
- vital to learning and memory
79
learning and LTP
learning can occlude LTp
- learning event cant be replicated
80
cellular consolidation
consequence of synaptic and biochemical events initiated by original experience
-depends on protein synthesis
- time frame of hours
- like ltp, consolidates memory itself
81
systems consolidation
consequence of interaction btwn hippocampus and cortex
- time frame of days to years
- like H.M
- hoe memory moves around thru time
82
delayed non matching to sample task
- declarative memory task
-hippocampal lesions cause mild impairments
- hippocampus is vital to spatial memory, navigating environment
- part of brains gps
83
place cells
cells in hippocampus that tell location
- only fire in specific location
- requires experience
- hippocampus can map out an entire environment using neurons
- entorhinal cortex
84
grid cells
neurons that form grid like representations of environment believed to be important for feeding info to hippocampus
- entorhinal cortex
85
speed cells
encode how fast an animal is moving in a direction
- entorhinal cortex
86
head direction cells
cells that can tell which direction one is facing
- entorhinal cortex
87
phineas gage
personality change due to extreme brain damage
- emotions are adaptive, functional states
88
james lange theory
bodily response evokes emotional experience
-stimulus
-perception/interpretation
- specific pattern of autonomic arousal
-emotion experienced
- autonomic response triggers emotion
89
cannon bard theory
brain must interpret situation to decide which emotion is appropriate
- stimulus
-perception/interpretation
-general autonomic arousal and particular emotion experienced
- autonomic response and emotional experience are simultaneous
90
inferring an emotional state
- behavior: posture, aggression
- neuroscience measures: brain activity, manipulating brain areas
- physiology: changes to cardiovascular function, breathing rate, sweating
- subjective experience: feeling, part of emotional state, how do you feel
91
characteristics of emotions
- adaptive, functional
- central, causative states
- stimuli from in or outside body can induce changes in brain
- relationship between emotional states and behavior
- interpretation of signals bys brain can lead to changes
- drive/ motivation
-context/environment
- volitional control; disconnecting internal emotion from what is expressed
92
changes in brain from interpreted signals
- observed behavior
-subjective reports
-physiology
-cognitive changes
-somatic responses
93
core features of emotions
- scalability: intensity
- valence: good or bad
- persistence: response to stimulus can outlast stimulus
- generalization: conditioned response to object exhibited in presence of similar stimuli
- global coordination: when stimuli induces changes, you get behavior, hormones, sympathetic response
- social communication: most prominent behaviors are changes in the face
94
sham rage
- frontal cortex acts to inhibit strong emotional reactions
- connections between frontal cortex and hypothalamus severed, rage response seen
- anterioir and osterior hypothalamus severed, rage resposne seen in hypothalamus
- cortical connections
95
limbic system
system of structures in the brain that is important for emotions
-amygdala, hippocampus, fornix, anterior thalamus
- subcortical system that generates emotional responses
- prefrontal cortex has large part
96
kluver bucy syndrome
damage to medial temporal lobe produces
- emotional blunting: lack of appropriate response to stimuli
- hyperphagia: extreme weight gain
-innapropriate sexual behavior
- visual agnosia: inability to visually recognize objects
97
autonomic nervous system and emotion
very vital and part of emotional response
- interoceptive feedback: brain is always interpreting what is happening in the body
98
neural activity when watching facial expressions
increased activity in primary motor cortex and premotor cortex
99
cultural differences in facial expressions
-western and non western literate groups agree abt represented emotions
- people from isolated non literate groups are less likely to agree
100
fear
we know most about how brain generates fear
- evolutionary purpose of protecting from harm, promoting survival
101
fear process
threatening stimuli
- fear state
- behavior, hormones, sympathetic response
102
amygdala
perception of threat, and behaviors all involve amygdala
- receives infro from sensory thalamus and sensory cortex in lateral region
- cortical info; perception, 'high road'
- info to central amygdala sends info to other areas
103
associative learning
necessary for survival, approaching good and avoiding bad
104
fear and anxiety
1 in 3 experience clinical anxiety disorder in lifetime
28.8% prevalence
105
urback wiethe disease
skin calcification disorder that leads to loss of amygdala
- little to no fear
106
optogenetics
way of controlling activity of neurons with light
- proteins derived from organisms use dif wavelengths of light to perform physiological procedures
107
circuitry of fear
periaqueductal gray; involved in behavior elicited by fearful stimulus
- ventral lateral; freeze
- dorsal lateral; flight
108
sham rage; aggression
hypothalamus- aggression and mating
- testosterone involved in aggression
109
neural mechanisms
- emotions produce widespread brainactivation
- all areas involved in emotions involved in other functions
- no one brain structure linked to emotions
-variability in neural substrates
110
stress
-hypothalamus releases factors from pituitary to other factors in blood stream
- hormones: epinephrine, norepinephrine, cortisol
111
hippocampus and stress
glucocorticoid receptors in hippocampus mediate stress
- stress effects; shrinking of dendrites, reduced neurogenesis
112
mental illness
15.4 million adults SMI
59.1 million adults MI
113
stressors
social stress, microbes, toxins, impaired nutrition
114
body defense systems
immune system, genetic factors, endocrine factors, NS, memory and perception, coping/appraisal strategies
115
lobotomy
1930s-70s disconnecting frontal cortex from other parts with ice pick
116
electroconvulsive therapy
1938- present
electrical stimulation to head
- induction of minor seixure to disturb neuronal connections to improve mental health condition
117
chlopromazine
1952
first antipsychotic
- receptor blocker at dopamine synapses (dopamine antagonist)
- first receptor blocker identified
118
schizophrenia
trouble distinguishing reality from fantasy, expressing and managing normal emotions and decision making
- psychosis, emotional dysregulation, impaired motivation, neurocognitive impairment
- accelerated loss of gray matter in adolescents
- ventricular enlargement
- change in neuro transmission in prefrontal cortex
- mesolimbic pathway of dopamine transfer; more dopamine= more psychosis
- reduced metabolic activity in frontal lobes
119
gaba hypothesis (schizophrenia)
interplay btwn excitatory and inhibitory neurons generate gamma oscillations that are crucial to generation of slow fluctuations in neural activity that underlie functional brain networks
120
glutamate hypothesis (schizoprenia)
schizophrenia may be result of hypofuntional NMDA receptors on GABA interneurons in cerebral cortex- may lead to overactivation of downstream glutamate signaling ventral tegmental area
121
depression
despair, hypoactivity, sleep problems, withdrawal, lack of apetite
- causes: genetics, stress
- little to no time in stage 3 sleep
- enter REM early and more
- increased activity in prefrontal cortex and amygdala, low activit in pariet and posterior temporal cortex
- SSRIS, atypical antidepressants, tricyclics, heterocyclics, monoamine oxidase inhibitors, ketamine, transcranial magnetic stimulation, CBT
122
ketamine and depression
acts on postsynaptic glutamate neurons on GABA neurons, preventing GABA activation, more glutamate available for action potential
- improved glutamate improves synaptogenesis
123
monoamine hypothesis
decreased monoaminergic activity is key variable in depression
- antidepressants- increase monoamine accumulation; norepinephrine and serotonin
124
sex differences in depression
biopsychosocial explanations, endocrine function, males mask depression w substance abuse
125
dopamine hypothesis
schizophrenia results from excessive levels of synaptic dopamine or excessive postsynaptic sensitivity
- role of glutamate in schizophrenia also
126
typical neuroleptic drugs
potent dopamine D2 receptor antagonises
127
atypical neuroleptics
affinity for serotonin receptors
128
thalamus
low road in fear processing
- project to lateral nucleus
129
sensory cortex
high road in fear processing
- project to lateral nucleus
