Exam 2 Flashcards
1
Q
recreational drugs
A
- all recreational drugs elevate dopamine transmission (via diff mechanisms) in the nucleus accumbens, driving their pleasurable effects
- this fact is critical for understanding the mechanism of addiction
2
Q
alcohol: biphasic effect
A
- initial stimulant phase involving the situation of dopamine pathways
- euphoria, pleasure
- a more prolonged depressant phase invovling increase in GABAergic activity
- social disinhibition, motor control, attentional myopia
- inhibitory neurotransmitter
3
Q
alcohol: chronic alcohol abuse
A
- cells of superior frontal cortex, cerebellum and hippocampus show particularly prominent pathological changes
- excessive binging suppresses neurogenesis in hippocampus (memory)
- korsakoff syndrome: chronic memory disorder caused by deficiency of thiamine (vitamin B-1) secondary to alc abuse
4
Q
alcohol: changes following ‘quitting’ chronic alc abuse
A
- after a month of not drinking you see significant neuroplasticity changes and brain volume
- enlarged ventricle = smaller brain volume, slight reduction in ventricles after just a month
5
Q
marijuana
A
- derived from cannabis sativa plant - main active ingredient is THC
- not well studied
- brain contains cannabinoid (CB) receptors that mediate effects of THC
- high concentration cross diverse brain areas
6
Q
marijuana: endocannabinoids
A
- analogs of THC produced in brain that activate CB receptors, such as anandamine
- endocannabinoids are critical for many functions, including brain development
- runner’s high
7
Q
marijuana: THC
A
- mimics anadaminde, binding to cannabinoid type 1 receptors (CB1)
- THC vs cannabidiol
8
Q
marijuana: basal ganglia
A
- motor control and planning as well as initiation and termination of action
- where emotion, motivation and motor movement converge
- heroin, marijuana bc it targets receptors in this area
- also targets cortex, hippocampus, cerebellum, amygdala
9
Q
marijuana: edibles vs smoking
A
- method of ingestion is highly important
- smoking is a very fast and powerful way to get to the brain
- edibles have a delayed effect bc it takes longer to metabolize in the blood stream
10
Q
marijuana: brain function
A
- persistent cannabis users show cognitive decline from childhood to midlife: prospective design (ruling out preexisting deficits)
- marijuana reduces reward-relates brain function which may help explain some motivation deficits associated with sustained use
11
Q
opiods examples
A
- opium poppy
- morphine (extracted from opium
- heroin (synthesized from morphine)
- fentanyl
12
Q
opiates
A
- highly addictive substances generated from poppy flower
- morphine, the psychoactive substance in opium is an effective analgesic
- heroin, oxycontin and vicodin are derivates of morphine
- opioid receptors in the periaqueductal gray are central to the analgesic effect
- brain generates its own morphine-like compounds - endogenous opioids (endorphins) to help regulate pain
13
Q
stimulants: cocaine
A
- blocks monoamine transporters, slowing reuptake of monoamine nT so they accumulate in synapses throughout the brain (especially dopamine)
- generates a strong increase in dopamine transmission in mesolimbocortical reward circuit, especially nucleus accumbens
- crack is a smokeable form of cocaine - that enters blood stream more rapidly and this is more addictive
- by removing the salt from cocaine it makes it more powerful and addictive
14
Q
stimulants: amphetamines
A
- synthetic stimulants like amphetamine (speed)
- minor effect, much safer
- adderall
- dompaine receptors in the prefrontal cortex
- unless it is snorted
15
Q
stimulants: methamphetamine (meth)
A
- multiple mechanisms of action on monoamines (especially dopamine)
- work first in the axon terminals, causing larger-then-normal release of NT as well as release in absence of action potential
- then interferes with the reuptake and degradation of monoamine NT in synaptic celft
16
Q
amphetamine tolerance
A
- tolerance develops quickly, leading to rapid increase in dosage to obtain effects
- leads to symptoms resembling paranoid schizophrenia
- dopamine salience model of schizophrenia
17
Q
caffeine
A
- adensoine is typically co-released with certain NT (catecholamines) as a neg feedback mechanism
- when actived, presynpatic adenosine autoreceptors reduce subsequent NT release
- caffeine blocks adenosine autoreceptrs for catecholamines resulting in elevated and sustained release of catecholamines (dopamine, norepinephrine, epinephrine)
18
Q
hallucinogens
A
- alter sensory perceptions in dramatic way
- structure of LSD resembles serotonin and LSD evokes visual hallucinations by activating serotonin receptors in the visual cortex
- alterations in resting state functional connectivity associated with ego dissolution
- increases connections btw brain regions that are close to each other but weakens connections between brains that are further apart: similar to sleep and dreaming
19
Q
hallucinogens: LSD and depression treatment
A
- increases in reward-related brain function in the ventral striatum and is being considered for treatment of depression
- need to be very cautious about the use of LSD in both research and treatment
- these drugs may interact with latent risk factors for mental health problems in ways that we don’t yet understand
- possible that it causes ppl to unfreeze their ego and that’s what lowers levels of depression: ego dissolution (loose boundaries w body and start to feel like you’re one w the world)
20
Q
hallucinogens:ecstasy
A
- MDMA, hallucinogenic amphetamine derivative
- like LSD it stimulates visual cortical serotonin (5-HT-2A) receptors
- stronger mood feeling than LSD
- increase in prolactin causes sensory tactile experience
21
Q
hallucinogens: dissociative drugs
A
- produce feelings of depersonalization and detachment from reality
- phencyclidine (PCP, or angel dust) and ketamine (Special K) are both NMDA-type glutamate receptor antagonists
- ketamine is being used for treatment-resistant depression, effects are marginal
- short-term effects exist but long-term changes are fairly minor
- ketamine first targets glutamate in the PFC which then modulates dopamine in the striatum via “top-down” PFC-striatal projections
22
Q
addiction
A
- all forms of addiction hijack the mesolibocortical dopamine reward circuit
- down-reg of D2 dopamine receptors in the nucleus accumbens drives excessive ‘wanting’ and craving
- neuroadaptive responses
23
Q
functional vs metabolic tolerance
A
- functional tolerance - reduction of the number of receptors on the postsynaptic membrane to bind to that receptor
- brain actually needs that substance to feel normal
- gone from homeostasis to asteosatsis - Metabolic tolerance - the more you take something the more efficient the body becomes at excreting it
24
Q
addiction: reinforcement learning
A
- first time - big bump in dopamine, opioids and cannabinoids drives the pleasure
- Eventually no longer responds to the juice but rather the prediction of the juice
- Wanting and desiring the substance, a sense of free will escapes
- Often the person doesn’t want the substance anymore but the dopamine cues are so overpowering that they have to do it
25
risk for addiction
- reward hyposensitivity model: low on endogenous dopamine are more likely to seek outside of themselves what they aren't producing themselves
26
sensation and perception: historical perspective
- john locke: how we perceive experiences is shaped by our enviornment
- immanuel kant: noumenal vs phenomenal world
- berkeley: entire world is a fabrication of the mind
27
senstation + percp: input to the brain
- only input our brains recieve from the 'real' world is series of action potentials passed along neurons of sensory pathways
- how nerves turn energy (light, touch, etc) into nerve impulses is understood: sensory transduction
- the pathways those nerve impulses take to reach the brain are known
- less is known about how we generate an experienced perception from these nerve impulses
28
senstation + percp: bottom-up vs top-down perception
bottom up: perceiving stimuli based on sensory input without preconceived ideas
top-down: perception as a constructed hallucination - brain is generating it, evolutionary adaptive based on our personal history and learning experiences
29
sensation
- the registration of physical stimuli from the environment by sensory organs
30
perception
- subjective interpretation of sensations by the brain
- our visual experience is not an objective reproduction of what is out there, but rather a subjective construction of reality manufactured by brain
31
sensory systems and responsiveness
- restricted range of responsiveness
- frequency range for hearing, which varies with species
- elephants hear low frequencies that humans don't
- whereas cats hear high frequencies that human don't
- species evolve diff sensory abilities in response to differing ecological processes
- our perception of a flower is diff from other animals
- bc their eyes have diff perceptions of light
32
senstation + percp: sensory transduction
- an adequate stimulus is the type of stimulus to which sensory organs are particularly adapted
- the conversion of sensory energy from an adequate stimulus into a local change of membrane potential in a sensory receptor cell (a generator potential)
33
senstation + percp: generator potentials
- similar to EPSP
- if generator potential exceeds the firing threshold, action potentials are generated that travel via sensory nerves
- instead of chemical ligand (NT) opening ion channels, here mechanical alterations to neuronal membrane of Pacinian corpuscle opens sodium channel
- Mechanism by which something in the environment enters the body
- Touch receptors
34
senstation + percp: labeled lines
- all sensory info from all systems is encoded by action potentials that travel along peripheral nerves to CNS
- how do action potentials code diff kinds of sensations (vision vs touch)
- each nerve input to the brain reports only a specific type of info
- labeled lines occur both across diff sensory systems and within specific sensory systems
35
sensation + percp: topographical organization
location of peripheral sensory neuron maps directly onto specific cells in cortex
36
senstation + percp: location
- neurons at all levels of visual and touch pathways from surface sheet of recepotrs to cerebral cortex
- arranged in orderly, maplike, manner (labeled lines)
- primary somatosensory cortex invovles a somatotopic map that is spatially organized neural representation of the body
- vision involves a similar retinotopic map
37
levels of sensory processing + thalamus
- thalamus is central relay station of info to cortex for most sense
- info abt each sensory modality sent to separate division of thalamus
- cortical modulation of sensory info: brain can modulate info it receives - inhibit activity in ascending sensory axons (ex. pain)
- in CNS cortex can direct thalamus to suppress some and emphasizes other info
- olfaction doesn't go through thalamus
38
levels of sensory processing + thalamus: mice study
- new study in mice suggests that some photoreceptors in the retina bypass the thalamus and send direct signals to 59 brain regions including regions involved in homeostasis (ex. hypothalamus) and emotion (ex. amygdala)
39
intensity: range fractionation
- specialized cells sensitive to varying levels of intensity, as the strength of stimulus increases, additional sensory neurons "recruited"
- multiple neurons can act in parallel - as the stimulus strengthens more neurons are recruited
- a single neuron can convey stimulus intensity by changing the frequency of its action potentials
40
sensory receptor adaptation: tonic receptors
- tonic receptors: show slow or no decline in action potential frequency to a maintained stimulus - ex. pain receptors
41
sensory receptor adaptation: phasic receptors
- display adaptation and decrease frequency of action potentials to a maintained stimulus
- ex. olfactory receptors, tactile receptors
42
sensory receptor adaptation: adaptation
- progressive loss of receptor sensitivity as stimulation is maintained
- many systems emphasize change in external world, which is most relevant for behavior and survival
43
visual system overview
- vision is our (humans and non-human primates) primary seosry experience
- approx 1/3 of human cerebral cortex is devoted to visual analysis and percp
- we perceive reality at a level of analysis that was adaptive for survival
- detect motion within range of speed appropraite to locomotion of animals (bullet too fast, clock too slow)
- perceive objects as solid
- visual perp is as much top-down as bottom-up
44
structure of the human eye: overview
- elaborate with optical functions (capturing light and forming detailed spatial images) and neural functions (transducing lihgt into neural signals and processing those signals)
45
structure of the human eye: retina
- light- sensitive surface in back of the eye consisting of photoreceptor cells (rodes and cones) and other neurons
- translates light into action potentials: transduction
- neural signals in retina converge on retinal ganglion cells, whose axons give rise to optic nerves and generate action potentials
46
retina: fovea
- region at the center of the retina that is specialized for high acuity and color vision
- receptive field at the center of the eye's visual field (point of fixation)
- receives direct light input that does not pass through other cells or blood vessels
47
retina: bipolar cells
- receive input from photoreceptors
- rods, cones and bipolar cells involve graded, local potentials
48
retina: photoreceptors overview
- rods have maximal absorption at 496 nm, but do not contribute to color perception
- 3 types of cone pigments absorb light over a range of wavelengths
49
retina: photoreceptors - scotopic system
- rods, allow night vision
- high convergence as info from many rods converge onto scotopic retinal ganglion cell: large receptive fields
- high sensitivity, can see in dim light, but low acuity
50
retina: photoreceptors - photopic system
- cones, allows color vision
- little convergence as photopic retinal ganglion cells receive input from only 1 cone (or very few): small receptive field
- low sensitivity, required bright light, but high acuity (sharp vision)
51
retina: photoreceptors - phototransduction
- light particles strike the discs and are captured by photopigment receptor moleculues
- cascade of events produces hyperpolarization of rods and cones
- disc structure of rods and cones contributes to their sensitivity
- photoreceptors are depolarized in dark, so are continually releasing NT (glutamate)
- light triggers a hyperpolarization of the cell, so it releases less NT
- graded NT release: magnitude of hyperpolarization determines the reduction in NT release
- no action potentials
52
retinal ganglion cells + optic nerve
- neural signals in the retina converge on retinal ganglion cells (RGCs), the only retinal cells that generate action potential
- RGC axons form optic nerve, sends info to brain along several pathways
53
optic nerve: geniculostriate system
- conscious vision
- retina → lateral geniculate nucleus (LGN) of the thalamus → striate cortex (primary visual cortex, V1) → other visual cortical areas
54
optic nerve: topographic projection or retinotopic mapping
- mapping that perserves the point-to-point correspondence btw neighboring parts of space
- ex. retina extends a topographic projection onto the cortex
55
optic nerve: retinohypothalamic pathway
- circadian rhythm
- retina → tiny suprachiasmatic nucleus (SCN) of the hypothalamus
56
extrastriate cortex
- occipital lobe is composed of at least 6 diff visual regions
- primary visual cortex (V1: striate cortex)
- primary input from lateral geniculate nucleus
- secondary visual cortex (V2; extrastriate cortex)
- visual cortical areas outside the straite cortex
- V4: color, V5: motion
57
patient Ji - V4 lesion
- loss of perception of color
- no longer dreamed in color
- couldn't even imagine it
58
patient LM - V5 lesion
- lost ability to see motion
- fluid appeared frozen and to jump when being poured
- people disappeared when they moved and then reappeared when still
- difficulty tracking convos bc they could not see movements of speaker's lips
59
dorsal visual stream
- projects to vision-related areas of parietal cortex
- for assessing location of objects (where) and guiding our movement toward (or away from them)
- the where or how pathway: how action is to be guided toward objects
60
ventral visual system
- projects to vision-related areas of temporal cortex
- for identifying objects (what)
- what pathway
61
prosopagnosia
- face-responsive region of the right inferior temproal cortex called the fusiform face area (FFA), identified with fMRI in healthy patients
- prosopagnosia inability to engage the FFA to recognize faces
- secondary to inferior temporal damage
- unable to recognize familiar faces, but can describe facial characteristics and identify objects
- can recognize familiar ppl for nonfacial cues (ex. voice)
62
types of chemical communication
- Synaptic communication
- Endocrine communication
- Pheromone communication
- Allomone communication
63
hormone
- chemical usually secreted by an endocrine gland, conveyed by the bloodstream and regulates distant target organs and tissues
64
hormones: endocrine gland
- secretes hormones into bloodstream to act on distant targets
65
classes of hormones
- Peptide hormones
- Amine hormones
- Steroid hormones
66
two main mechanisms of hormone action: peptide
- receptors embedded in cell membrane bind to hormone, activating second-messenger system that affects various processes inside the target cell
67
two main mechanisms of hormone action: steroid hormones
- longer lasting effect
- diffuse passively, bind to molecules inside target cells
- steroid-receptor complex, bind to DNA and alter the expression of certain genes (genomic effect)
68
hormones: hypothalamus
- critical for hormone regulation, bridge btw brain and peripheral and central hormone system (neuroendocrine system)
- neural region central to homeostasis that links nervous system to endocrine system
69
hormones: pineal gland
- sleep
70
hormones: pituitary gland
- bridge btw brain and body
- proximal to hypothalamus
- half of it is in the tissue of the brain and half is outside the brain
- central endocrine glad, serves as bridge btw hypothalamus and periphery
71
hormones: posterior pituitary gland
- releases two hormones
- cell bodies in the hypothalamus produce oxytocin or vasopressin
- axons from these neurons pass through the pituitary stalk
- terminate on the capillaries of the posterior pituitary
- when action potential arrives at the terminal, oxytocin or vasopressin is released from the terminal directly into the bloodstream
72
hormones: posterior pituitary gland - vasopressin
- critical for initiating contractions at birth
73
hormones: posterior pituitary gland - oxytocin
- implicated in a broad range of social, maternal, affilative bonding
- lactation and the 'letdown reflex' and uterine contractions during childbirth
- in animals facilitates monogamy
- trust and romantic attachment: neuromodulatory of dopamine
- intranasal oxytocin elevates empathy, generosity, bonding and 'in group' affiliation, may elevate 'out group' distancing
- modulates dopamine: imp role in rewarding aspects in social situations
74
hormones: anterior pituitary gland
- Cascade of intermediary hormone release, messenger hormones than then bind on other glands of the body that say to release the actual hormones needed
- Neuroendocrine cells in the hypothalamus bind to blood cells on the hypothalamic-pituitary vein system - releasing hormones
- Arrive the anterior pituitary gland causing the release of tropic hormones go into general circulation, directionless, go where blood goes
- In case of cortisol they’ll start to circulate around the adrenals and bump into a receptor that is an ACTH that facilitates the release of cortisol from the adrenals which is then released systematically through the body
75
hormones: anterior pituitary gland - tropic hormones
- travel through the bloodstream to regulate endocrine glands throughout the body
- don't affect tissue in the way standard hormones do, go through the blood
- eventually bind to endocrine glands in the periphery
76
hormones: anterior pituitary gland - regulation of hormones
- neg feeedback circuit
- receptors
- other nuclei invovled in brain regulation: hippocampus in cortisol reg
77
hormones: neuroendocrine cell
- neuron that releases hormones into local or peripheral circulation
78
stress biology: sympathetic activity stage 1
- immediate stress response mediated by noradrenergic system involving activation of CNS neural activity and sympathetic nervous system
79
stress biology: sympathetic activity stage 2
- subsequent stress response is hormonal involving secretion of stress hormone cortisol via the hypothalamic-pituitary gland adrenal (HPA) axis
- CRH: corticotropic releasing hormone for the cascade of cortisol
80
stress biology: sympathetic activity stage 2: ACTH
- ACTH: adrenocorticotropic hormone, tropic hormones that release cortisol
- secretion of cortisol has similar effect to activation of sympathetic nervous systemL pupil dilation, elevated heart rate, immune system suppression
- prepare body for defense
- more sustained than SNS
- chronic stress/HPA activity associated with stress-related illness (ex. cardiometabolic and inflammatory illnesses)
81
hippocampus + cortisol: negative feedback loop
- Release of something inhibits subsequent release, self-regulatory
In this case release of cortisol inhibits subsequent release by binding to glucocorticoid receptor
Cortisol
- A lot of these receptors are in the brain, cortisol gets into the brain tissue and binds to glucocorticoid receptors, in the thalamus and hippocampus
In the short term, good because it accentuates memory but with chronic stress it can have neurotoxic effects, feedback loop goes off the rails and people have a hard time regulating cortisol
82
chronic cortisol as neurotoxic
- chronic stress/cortisol release has neurotoxic effect on hippocampal neurons and suppresses memory
- kills cells in the hippocampus and reduces hippocampal neurogenesis
- why stress-related mental illnesses target hippo and result in reduced mem
- depression associated w excessive cortisol
83
sleep: circadian rhythm
- pattern of behavior, biochemical or physiological fluctuation that has a 24-hour period (hormone levels, body temp, drug sensitivity)
- most common rhythm
- mammals: slightly longer than 24 hours
84
sleep: ultradian rhythm
- rhythmic biological event with a period shorter than a day, usually from several min to several hours (ex. bouts of activity, feeding, hormone release)
85
sleep: infradian rhythm
- rhythmic biological event with a period longer than a day (ex. menstrual cycle, animal breeding behavior)
86
sleep: social zeitgeber and entrainment
- sun, alarm, clock, roommate etc
- zeitgeber: cues from environment that regulate your rhythm, particularly on 24 hour clock as supposed to 24.12
- entrainment: synching the body's internal clock to external cues like light/dark cycle
87
sleep: SCN
- biological clock, lesions to SCN protion of hypothalamus eliminate circadian rhythms
88
sleep: melatonin
- as night approaches the pineal gland secretes the hormone melatonin
- informs brain about day length and entrainment (synch) of circadian rhythms
- exogenous melatonin as standard treatment for sleep disorders, chronobiotic slightly advancing the circadian phase by 30 min to 1 hour
89
retinohypothalamic pathway
- retina → the tiny suprachiasmatic nucleus of the hypothalamus
- entrainment pathway consists of specialized retinal ganglion cells that project on to SCN via the retinohypothalamic tract
- cells do not rely on trad photoreceptors (rods and cones) but a photopigment called melanopsin
- some ppl who are blind have intact retinohypothalamic pathways and are able to keep rhythm in tact, some don't
90
REM sleep
- paradoxical sleep, brain is super active
- body has no muscle tone and is paralyzed (atonia) other than moving eyes
- brainstem profoundly inhibit motor neurons via GABA transmission: motor neurons are hypoerpolarized
- REM behavior disorder: body is acting out dreams, body is not paralyzed during this stage, dangerous
91
non-REM sleep
- more resotrative and very slumbered
92
sleep stages
- waking
- EEG is desynchronized
- high frequencies with low amplitude is also called beta activity
- stage 1
- alpha rhythms appear during relaxation
- sharp waves called vertex spikes appear
- stage 2 (50% of total sleep)
- brief period of sleep spindles and K complexes
- sleep walking
- stage 3
- slow-wave sleep is recognized by large slow delta waves
- REM (20% of total sleep)
- despite deep muscle relaxation, the EEG activity in REM sleep resembles that of waking
93
sleep myths
- myth: we only dream during rem sleep: imp distinctions btw rem and non-rem dreaming
- fact:
- night terror: wake up in state of panic, prominent in young kids
- nightmare: bad dream
- sleep paralysis: when you wake up in REM
94
sleep across species
- nearly all mammals display both REM sleep and slow-wave sleep
- certain marine mammals such as dolphins do not display REM sleep
- atonia of paradoxical sleep likely incompatible with need to come to the surface of water to breathe
- certain marine mammals such as dolphins, as well as birds display unilateral sleep
- one hemisphere of the brain is in paradoxical sleep and the other have is not, allowing them to stay afloat
95
sleep: across the life span
- takes approx 16 weeks for a newborn infant to establish a 24 hour sleep rhythm
- REM sleep is more prevalent in infants
- early in life we sleep a great deal, about half of that time is spent in Rem sleep
- by adulthood we average about 8 hours of sleep, 20% of that is Rem
- sleep decreases over the course of life
96
sleep: slow-wave sleep across the life span
- 50% reduction in slow wave sleep in 60 yr olds, absence of slow wave sleep in 90 yr olds
- slow-wave sleep critical to memory consolidation and growth hormone secretion
97
biological functions of sleep: energy conservation
- slow-wave sleep in particular is metabolically conservative
- small mammals with high metabolism sleep more
98
biological functions of sleep: ecological niche adaptation
- safer to sleep during the evening to protect us
99
biological functions of sleep: body and brain restoration
- growth hormones central to cell reproduction and regeneration secreted in slow-wave sleep
- immune system processes occur at night
- prolonged sleep deprivation can be fatal via infection
- glial cells 'flush out brain waste' during sleep
100
sleep: memory consolidation
- brain doesn't store new info during sleep (ex. only remember a dream if u wake up and recall it consciously)
- sleep is critical to consolidating mems experienced before bed
- ppl perform better on verbal learning task after 8h of sleep vs 8h of daytime
- slow wave: declarative (factual) memory
- REM sleep: perceptual skills learning (ex. visual discrimination tasks)
101
sleep: brain's connections shrink during sleep
- synapses become larger during the day as part of learning but maintaining these synapses is metabolically demanding and unstable
- brain downsizes these synapic connections by up to 20% during sleep
- not all synapses are scaled down: certain ones remain unphased and these correspond to strong connections/mems
- synpases are scaled down are recently active ones that are not highly linked to anything relevant
- so the brain's microglial cells trim unnecessary synaptic connections to maximize the relevant ones
102
sleep: defensive activation theory
- if brain cells are not active they may die bc they don't store energy
- spend close to 1/3 of life asleep
- REM sleep as mechanism to prevent takeover of the visual cortex
- dreams as meaning of life vs objective
103
emotion
- feeling state that tends to facilitate or inhibit motivated behavior
- emotion-inducing stimuli can be internal (cognition, emotion, sensation) or external
- evolved to prepare us to deal quickly w most vital events in our lives
104
feeling, mood, affect
feeling: transient, less intense than emotin
mood: diffused, mild and longer-lasting emotional episodes
affect: general term encompassing emotion, feeling and mood
105
maclean's limbic system theory
- neocortex: cognition
- parts identified in reptiles and birds
- limbic system: emotion
- never well defined, overly general model
- believed there was no connection btw reason and emotion
- largely based on hypothalamic connectivity, but was soon discovered that hypothalamus was connected to neocrotex
- challenged idea of cler distinction btw limbic and neocortex
106
threat-circuitry: amygdala
- modulates every area of the brain
- response to both neg and pos stimuli
107
threat-circuitry: amygdala - SM
- amydgalectomy
- had cognitive reps of feelings, but didn't have feelings
- emotional faces: seeing whites of eyes are sig in understand there is something salient in environment
108
threat-circuitry: amygdala - low road
- retinal ganglia cells to thalamus to amygdala (excluding the visual cortex)
- but also direct pathways from retina to amygdala without thalamus
109
threat-circuitry: amygdala - provocateurs
- facial expressions, snakes and spiders
- innate or learned
- biological preparedness
110
threat-circuitry: basolateral amygdala
- light, tone, smell, touch and shock
111
hypothalamus links
- links nervous sytem to endocrine system
- regulated body temp, hunger, thirst, sleep, drives, stress response, ANS
112
threat-circuitry: amygdala - outputs
- noradrenergic: modulates the locus coeruleus
113
threat-circuitry: amygdala - fear conditioning
- unconditioned stimulus
- conditioned stimulus +: predicted the bad
- conditioned stimulus -: predicts the absence of the bad
114
threat-circuitry: BNST
- bed nucleus of the stria terminalis (BNST)
- amygdala and BNST for the ;extended amygdala'
- amygdala implicated in short term threat/defense responses (fear)
- BNST implicated in sustained threat/defense
115
threat-circuitry: insula
- role: re-representation of interception (brain-body bridge)
- disgust
- depression and anxiety are associated w elevated amygdala, BNST and insula activation
- psychopaths show limited fear conditioning in the amygdala
116
threat-circuitry: anterior cingulate cortex (ACC)
- Identifies discrepancies in our models of the universe
- Positive prediction: mediate senses and wires the appropriate area of the brain to produce a response through glutamate NT
- Negative prediction: cingulate will communicate in GABAergic and suppress dopamine
117
reward/pleasurable emotion circuity: mesolimbocortical dopamine pathway
- wanting/effort: dopamine
- depression suppresses the I want this (working) not the please areas
- effor expenditure more than pleasure
- leaking and pleasure: opioids and endocannabinoids
- reinforcement learning: dopamine
- reward prediction error: dopamine and GABA
118
reward/pleasurable emotion circuity: bipolar/mania vs depression
- risk for bipolar disorder and mania is associated with increased ventral striatal/nucleus accumbens activation to reward cues
119
executive/cognitive control circuity: prefrontal cortex
- dorsolateral prefrontal cortex
- ventromedial prefrontal cortex: preconscious regulatory processes
- both cognition and emotion
- maintains rep of goals (particularly in ambiguous situations
- biases other areas of brain to facilitate task-appropriate behavior
- makes you do the right things when its hard
120
executive/cognitive control circuity: emotion regulation
- reappraisal: forcing a diff perspective
- preventing emotions form affecting actions
- attempting to function 'normally' in situations
- implementation of a conscious or nonconscious process to start, stop or modulate the trajectory of an emotion
- emotional reg is triggered when the emotional reaction itself becomes the target of valuation
121
executive/cognitive control circuity: emotion regulation - explicit regulation in lateral PFC
- explicit: conscious effort, active monitoring and is associated with insight and awareness
- involves lateral portions of the PFC
- lateral PFC also involved in:
- cognitive and exec control processes (response inhibition, conflict monitoring, task switching)
- working mem
- goal-directed behavior
122
executive/cognitive control circuity: emotion regulation - implicit regulation in lateral PFC
- evoked automatically, runs to completion without conscious monitoring, can happen without insight or awareness
- involves ventromedial portions of PFC
- ex. fear inhibition, regulation of emotional conflict, moment to moment homeostasis
- fear-extinction in classical conditioning paradigms
123
efferent outputs from amygdala: uncinate fasciculus
- connects amygdala and PFC
- top-down reg of our emotion from frontal cortex to prefrontal cortex
124
efferent outputs from amygdala: extinction of conditioned fear response
- high vmPFC correlates with successful extinction to the conditioned stimulus
- unlearning fear is driven by top-down suppression of the amygdala by the vmPFC (mammals w lesions to vmPFC never unlearned conditioned fears)
125
efferent outputs from amygdala: emotional reg + neg affect in depression
- healthy controls use prefrontal cortex to try to dampen neg emotions
- depressed ppl try to use prefrontal to dampen but they actually generate more neg emotion
- "upregulate" neg emotion
126
efferent outputs from amygdala: emotional reg + pos affect in depression
- when depressed ppl look at smtg positive they dampen pos emotions
- down regulate pos emotion
127
neurodevelopment: midbrain
- superior and inferior colliculi (sensation, perception)
- tegmental area and substantia nigra (dopamine)
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pre-natal growth
- first phase of dev: more than 250,000 neurons per min during height of prenatal growth
- by day 25: neural tube has developed, eventually scopes come off and spread out to fill rest of brain
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neurogenesis
- brith of new neurons, ventricular zone in neural tube region lining cerebral ventricles, providing neurons in early dev and glial cells throughout life
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pre-natal dev: synpatogenesis
- establishment of synaptic connections as axons and dendrites grow
- neurotrophic factors: target-derived chemicals that facilitate cell migration and synaptogenesis
- brain-derived neurotrophic factor (BDNF)
- growth cones are attracted toward neurotrophic factors and "pull" the neurons towards the cells
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adult neurogenesis
- in the dentate gyrus of the hippo plays important rle in declarative and spatial mem and conditioning
- expeirience modulates neurogenesis = neuroplasticity
- exercise enhances
- meditation and hippocampal volume
- stress and depression reduces neurogenesis
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dendrate gyrus
- apoptosis
- critical for brain dev
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brain dev: synapse rearrangement, modeling and pruning
- loss of some synapses and dev of others
- neurotrophic factors play imp role in synaptogenesis
- microglial cells are central to synaptic pruning
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dev of emotional brain
- subsequent dev of prefrontal cortex after traumatic childhood show that experiences affect the amygdala
- amygdala dev very early and 'teaches' the brain and body about the extent to which world is safe and trustworthy
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adolescent brain: threat/defense - amygdala
- amygdala hyperactive during adolescence
- due to effect of gonadal hormones
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adolescent brain: reward/pleasure - ventral striatum
- hyperactive
- normative biological profile that has been selected to pick a mate
- those who don't show this hyperactivity are at risk for depression
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adolescent brain
- elevated threat reward and self referential thinking
- harder time taking long term perspective bc dorsolateral prefrontal involved in explicit emotion regulation is not yet fully matured
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dev of prefrontal cortex
- cell death and synapse rearrangement/pruning results in reduced gray matter density in the PFC
- gray matter density highest when young, steadily decreases until 50s and slight increase around 80
- increased myelination
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becoming an adult
- involves the maturation of pathways btw prefrontal cortex and emotion gen
- facilites exec control and emotion reg
- adolescence is characterized by 'asynchrony' btw elevated neg and pos emotions and still dev PFC
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becoming an adult time scale
- good to become adult but not too soon
- healthy control display pos amygdala-PFC relationship during childhood that becomes neg as age
- institutionalized child display neg relationship during childhood, age-inappropriate reg of amygdala
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stages of memory
- Incoming info through senses
- Senroy buffers (ex. Iconic memory) - filters stuff
- Encoding
- Short-term memory/working memory
- Consolidation of STM into LTM
- Performance
- Retrieved from LTM to STM
- Loss of info from STM or LTM
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LTM; declarative
- things you know that you can tell others = hippo-dependent
- consolidation of 'what' info and transfer from STM to LT
- spatial mem
- encoding, consolidation and retrieval of declarative mems
- memory trace: persistent change in the brain reflects the storage of a memory
- LTM stored throughout the cortex
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LTM: non-declarative
- things you know that you can show by doing = hippocampus independent
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damage to hippocampus
HM
- hippo and anterograde amnesia
- less ability to form new declarative mems
- loss window of 5 years around surgery
- damage to pathways connecting to hippo also assoicated with anterograde amnesia
- dorsomedial thalamus and mammillary bodies
- Korsakoff's syndrome
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hippo + spatial mem
- place, grid cells
- taxi drivers vs bus drivers: taxi drivers had larger volume of hippo
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areas of the brain and memory
- basal ganglia: habit formation
- motor cortex
- cerebellum
- ventral striatal dopamine signaling central to reward conditioning
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amygdala and memory
- activity in amygdala modulates declarative memory
- electrical stimulation of amygdala alters memory
- norepinephrine injected into amygdala and epinephrine/cortisol release from adrenal glands during times of distress enhances memory
- injecting beta-blockers (propanolol) block emotional modulation of memory
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memory: reconsolidation
- return of a memory trace to stable long-term storage after it has been temporarily made changeable during the process of recall
- every time we have a memory it is being "reconsolidated" or recreated
- individuals with PTSD admininstering of beta-adrenergic antagonist propranolol during trauma recall reduces symptoms
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memory: blocking reconsolidation
- inital memory formation and reconsolidation invovles protein synthesis
- injecting a protein snythesis inhibitor (anisomycin) into the rat amygdala blocks the reconsolidation of conditioned of fear response
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synaptic plasticity: effective synapse
- after training, each action potential in relevant neural circuit causes an increaseed release of transmitter molecules
- either more transmitter is release from axon terminal
- or the postsynaptic membrane becomes large and/or more sensitive to transmitter
- synapse enlarges both pre and post synaptically and repeatedly activate together forming stronger more stable synaptic connections
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synaptic plasticity: neural circuit
- interneuron modulates polarization of axon terminal and causes release of more transmitter molecules per nerve impulse
- neural circuit not only increases size but also number of synaptic contacts
- more frequently used neural pathways take over synaptic sites formerly occupied by less active competitor
- experiences modulate synaptic plasticity
- enriched environments more strongly modulate basal dendrites, the enviro has less of an effect on apical dendrites
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hebbian synapse
- strengthened when it successfully drives that postsynaptic cell
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LTM potentiation and memory consolidation
- cells that fire together wire together
- if axons in the circuit are stimulated only once every sec, size of the response in its postsynaptic neurons is quite stable
- after brief tetanus the EPSP response increases markedly and remains high
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LTP
- stable and enduring increase in the effectiveness of synapses flowing repeated string stimulation: cellular mechanism of memory
- occurs in hippo and other brain regions
- most studied form occurs at synapses that use the excitatory NT glutamate
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LTP: NMDA
- LTP is critically dependent on a glutamate receptor subtype called NMDA receptor
- treatment with drugs that block NMDA receptors prevent new LTP, but it does not affect synaptic changes that have already been established
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LTP: AMPA
- glutamate NT binds to AMPA receptor, sodium rushes in, small local graded potential change
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LPT: NMDA and AMPA pathway
- mechanism in which cells that fire together wire together
- doesn’t have standard receptor that other AMPA receptors have, but with consistent and sustained excitatory potential, sustained voltage is going to change the structure
- Magnesium ion is in the NMDA receptor, blocking the inflow of these ions, magnesium pops out
- Calcium flows in acting as a second messenger binding to protein in the intracellular portion of the cell, end result = more AMPA receptors
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LTP activity
- evidence suggests that the same mechanism effects whether new synapses are formed or old synapses are retracted
- cells synchronously because they fire together, drive the postsynaptic neuron to fire
- cells fire at random, they rarely cause the postsynaptic neuron to fire
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language: aphasia: non-fluent
- impairment in language production and/or understanding that is caused by brain injury
- damage to left anterior speech zone (broca's) causes nonfluent aphasia: cannot produce a lot of language
- nonfluent aphaasia: difficulty w speech production but not language comp
- hemiplegia involving paralysis of one side of body is common
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language: aphasia: fluent
- damage to left posterior speech zone
- fluent aphasia is characterized by impairment in language prod and/or understanding
- producing lots of language but its not intelligible
- verbal output, but contain paraphasias like sound substitutions and or word substitutions
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consciousness: physcialism
who you are and what you are is made of phsycial stuff and the midn energes from the bra
