Exam 3 cards 1.0 COPY Flashcards
- What types of learning/memory are preserved in people like H.M. who have bilateral hippocampal damage (what types of things can they still learn, even though they won’t be aware of their learning, and why)? What types of neuropsychological tests are used to determine what they can still learn?
What is lost if hippocampus is damaged?
H.M. (1953, 27 y.o): intractable epilepsy >bilateral medial temporal lobectomy… how did he change?
Seizure frequency decreased
IQ increased
Working short term memory was intact
Long term memory, EXPLICIT (declarative):
Retrograde amnesia (2-3 years)
Anterograde amnesia
What learning/memory is preserved?
IMPLICIT:
Motor learning tasks (e.g. “mirror-drawing” – fig. 11.2) (cerebellum)
Classical conditioning (CS tone + US airpuff > eyeblink) (amygdala)
Repetitive priming tasks (“incomplete pictures”—Fig. 11.3)
But each time H>M was tested, he had no EXPLICIT memory of doing the task previously!
…such “unconscious” types of learning/memory rely on cerebellum (learned movement), basal ganglia (habitual movement, memory, learning), amygdala (conditioning), sensory cortex - explains why H.M. acquired new implicit memories despite his lack of awareness of learning new things
- What is the difference between retrograde and anterograde amnesia? What are some common causes of amnesia?
Retrograde amnesia: old memories are lost
Anterograde amnesia: Cannot retain new memories
II. Other causes of amnesia
A. Stroke (may cause only transient memory loss)
B. Korsakoff’s syndrome (in 1-2% of alcoholics, due to thiamine deficit)
C Alzheimer’s
• more general memory deficit (not just declarative LTM), +
working memory impairment
D. Concussion (Fig. 11.5) Usu. short period of retrograde amnesia
variable anterograde amnesia
E. Seizures (incl. those induced by ECT)
F…. “childhood amnesia”
- Describe what learning is in terms of changes in “synaptic strength” (LTP, LTD), including what nt, what receptors, and what ion channels are involved, and how these function under conditions of transient (brief) activation vs. strong or repeated activation. What are some pre- vs. post-synaptic mechanisms of synaptic strengthening/weakening? How can you develop/strengthen circuitry in your own brain, for example, to retain memories of Psych 372 material (or to improve your memory of anything)?
- Long-Term Potentiation (LTP): long-lasting facilitation of synaptic transmission (“strengthening of neural connections”)
observed in various brain areas; most prominent in hippocampus
- 3 ionotropic glutamate receptors: AMPA (on Na+ ion channel), NMDA (on Ca++ ion channel), kainate
- Low-level (transient) excitation of post-synaptic neuron occurs via glutamate binding to AMPA rec. > Na+ influx → A.P.
- glutamate also binds to NMDA rec., but its Ca++ channel is blocked by Mg++, so no Ca++ influx - High-level (sustained, strong) excitation of post-synaptic neuron dislodges Mg++ from Ca++ channel, so glutamate binding to AMPA & NMDA rec’s >Na+ and Ca++ influx > A.P. + Ca++-dependent protein synthesis
- Protein synthesis → synaptic strengthening:
a Post-synaptic neuron: synaptic contact strengthens = dendritic spine widens, more AMPA rec. synthesized & inserted into dendritic spine membrane
b. Pre-synaptic neuron: more glut. synthesized, released
More glut released
Wider dendrite with more receptors
Synaptic connections are constantly forming/strengthening and weakening/disappearing
Long-Term Depression (LTD): weakening of synaptic connection (e.g. due to AMPA receptor loss decrease neuro transmitter)
- Explain, on a neuronal or circuitry level, how a behavior or emotion becomes classically conditioned. For example, how can a tone come to elicit a flinch after the tone has been presented with a shock to the skin several times? Make sure you can distinguish between UCS, CS, UCR, CR (identify them in some examples you come up with yourself).
C Example: fear conditioning
- UCS (shock) >>>>> UCR (flinch): single sensory neuron excites motor neuron + “low level excitation
- If a particular tone is heard at the same time shock is experienced: two sensory neurons (one auditory, one somatosensory) that synapse on single motor neuron fire at same time = “High level excitation” >>> LTP occurs, strengthening tone-to-flinch synaptic connection
- Later, tone Cs alone will trigger flinch CR, because there is a stronger synaptic connection.
How might this explain hyperreactivity to noise in those with PTSD
- What is the role of the hippocampus in learning/memory (and what is the evidence for this role)? Include the different types of cells that have been discovered in this brain area, and how their firing can contribute to the experience of “déjà vu” for a place or person.
III. Brain Areas Crucial for Learning/Memory
A. Hippocampus (+ medial temporal cortex):
Episodic memory formation: link SENSORY PERCEPTION (sights/sounds/smells, etc.) toPLACE and TIME
“place cells”: where did event happen?
“time cells”: when did event happen? (flow of events)
“concept cells” who/what is this? (e.g. people, ideas)
[e.g. what do you recall about your h.s. graduation?]
hippocampal “place cells”
Electrode implanted into hippocampus to record single neuron firing….. When does neuron fire the most (ticking noise = A.P.)?
https://www.youtube.com/watch?v=vOJKID4ukbY
…when you move to a new place, your hippocampal cells rapidly acquire “place fields” so gradually you “know” where you are no matter how you are oriented in that place (i.e., your hippocampus creates spatial maps)
What is déjà vu?
• Associated w/ hippocampal place cell firing..
…these cells fire, causing you to think you’re somewhere familiar
…same for concept cells: when they fire, cause you to think you’re seeing a particular familiar person or thing
- What is the role of the amygdala in learning/memory, and what is the evidence for this role?
Amygdala: crucial for emotional learning • e.g. fear conditioning
- What are the differences in learning/memory deficits between someone with bilateral hippocampal damage vs. someone with bilateral amygdala damage vs. someone with prefrontal cortex damage?
- Describe the different stages of sleep in terms of EOG, EMG, and EEG, and describe how the relative length of sleep stages change as sleep progresses.
Sleep stages
A cyclic pattern and are 90 min cycles as night progresses, less deep sleep, more REM
Sleep stage measures (polysomnography)
- EOG: electrooculogram
- EMG: electromyogram
- EEG: electroencephalogram
- Describe the main two theories of sleep; what is the evidence supporting each theory?
Why do we sleep?
- Adaptation Theory: sleep conserves energy, at times when species is most vulnerable to threat
“prey species sleep less than predators”
b. Recuperation theory: body and or brain requires recovery from daily activity (energy use).
Neither theory explains this fully
- Describe the impact of sleep deprivation on physical, physiological, mood, cognitive functions.
- Impact of Chronic sleep deprivation
- On physical performance: small increments (e.g slight clumsiness, decreased reaction time)
- On physiology: increased susceptibility to illness, disease (immune suppression, metabolic dysregulation)
- On mood: increased irritability, lower mood
- On cognition: Decreased vigilance particularly for boring tasks
- Decreased executive function
Increased microsleeps!
However most “lost sleep” isn’t made up (e.g randy gardner)
- Compare/contrast the apparent importance of REM vs. deep sleep – what happens when people are deprived of only REM or only deep sleep?
REM-deprivation: results in REM rebound on subsequent nights, Except if substitute short period of wakefulness for each REM stage (i.e “default theory”) >>> suggests REM not crucial?
In contrast, deep sleep (stage 3) always made up after total sleep deprivation, and short-sleep nights have same deep sleep time as longer sleep nights (brain gets more efficient getting to stage 3) so getting deep sleep most important?
REM cant be made up, deep sleep is always made up.
- Explain what the suprachiasmatic nucleus does, and describe where it’s located.
Brain mechanisms of sleep
- Retina>>> SupraChiasmatic Nucleus (SCN, part of hypothalamus): “master clock”, maintains circadian rhythm of brain (entrained by light)
- What is the reticular formation (“reticular activating system”), and how does neural activity in this area change on a circadian basis, and during REM sleep?
Reticular formation, “ARAS”
(medulla/pons/midbrain)
- input from SCN and other sensory systems
- Output to thalamus > cerebral cortex
- Key “alertness” nuclei:
- Locus ceruleus (LC: NE-releasing)
- Raphe (5-HT releasing)
- How would drugs that alter NE or 5-HT affect sleep/wake cycles.
Also activated during REM, to:
Generate visual images (“PGO waves”)
Trigger eye movements (>superior colliculus)
Relax core muscles (inhibit spinal motor neurons)
- What are “PGO waves” and when do they occur?
PGO waves are internally generated during REM> visually vivid dreams
Pons > geniculate > occipital lobe
- Describe the various causes of insomnia. How can sleep in someone who has depression differ from someone who does not have depression? How do strong stimulants like amphetamines interfere with sleep?
Sleep disorders
Insomina
Causes:
Sleep medication overuse
Sleep apnea
Leg movement disorders (e.g “restless legs syndrome”)
Depression/anxiety
Sleep cycles in depression
Longer to fall asleep, more awakenings, less deep sleep: decreased sleep efficiency also short latency to long duration of first REM (They have more REM initially which shortens through out the night)
Meds can also disrupt sleep
Locus curuleus decreases firing at night, so brain NE and alertness decrease; some antidepressants prevent reuptake of NE > so increase synaptic NE levels… thus can cause insomnia
Raphe: similar circadian rhythm; SSRIs increase synaptic 5-HT
Stimulants such as amphetamines also increase synaptic NE, 5-HT, DA levels
Caffiene = adenosine antagonist
Amps block reuptake and increase synthesis of MAOs
- Describe the sleep disorders narcolepsy and REM behavior disorder. Explain a biological cause of each disorder.
arcolepsy (a type of hypersomnia)
- Symptoms (dysregulation of REM):
Daytime sleep attacks (abrupt, lasting minutes, REM sleep)
Cataplexy (in some people): loss of muscle tone while awake (secs to mins)
Sometimes, “sleep paralysis” (cant move upon falling asleep or waking) and wakeful dreaming although this can happen in those without it.
- Cause genetic and environmental (triggered by viral infection (?) or toxin exposure in genetically vulnerable people) >> loss of orexin-releasing neurons in posterior hypothalamus, which normally coordinate RAS neurons that control REM onset/offset
- Treatment: stimulant and lifestyle changes
REM behavior disorder: REM without muscle atonia
- Loss of neurons in RAS that normally inhibit spinal motor neurons (or loss of normal input to RAS neurons?)
- … Commonly co-occurs with dementia, parkinsons and other progressive neurological disorders (2% older adults, M>F)
- What is the corpus callosum, and where is it located?
Inter hemispheric communication
- Corpus callosum: axons of cerebral cortex neurons that communicate with neurons in opposite hemisphere (coordination between, right visual field, somatosensory, motor, cognitive neurons).
* 10 percent larger in left handers (less lateralization of function in left than right handers) - Split brain phenomenon (callosotomy)
Why can split brain person:
Only say what they saw when
- Why is it more difficult to draw two different objects simultaneously, one with each hand (or to pat your head with one hand while rubbing your tummy with the other), as opposed to operating one hand at a time, or doing the same thing with both hands simultaneously?
Motor cortex can work independently but the crossing in the corpus callosum from both hemispheres causes interference
- Describe the testing that has been conducted in “split-brain” patients that has revealed lateralization of language processes. Which hemisphere is dominant for language comprehension and production? If visual information processed by the non-language-dominant hemisphere cannot be revealed verbally, how can we determine if the split-brain patient “knows” it?
Why can split brain person:
Only say what they saw when word/pictures is in right visual field?
But write/draw with left hand what they couldn’t say?
- Where are Broca’s and Wernicke’s areas located? Has modern research supported the initial idea that these very small areas of cerebral cortex are responsible for language production and comprehension, respectively?
The dotted line is where modern research believes speech is implicated instead of the small specific areas.
Damage to L hemisphere language areas: aphasia= lack of communication ability
- Broca’s (expressive) aphasia: most strongly associated with extensive left posterior frontal lobe damage
* R posterior frontal damage : possible prosody (intonation, emphasis, rhythm) in speech - Wernicke’s (receptive) aphasia: most strongly associated with extensive Left parietal temporal junction damage
* Typically , fluent grammatically correct speech that isn’t meaningful, poor comprehension, using wrong words and nonsense words. Cant tell that they are not making sense.
- What’s the difference between expressive and receptive aphasia?
Damage to L hemisphere language areas: aphasia= lack of communication ability
- Broca’s (expressive) aphasia: most strongly associated with extensive left frontal lobe damage
* R frontal damage : possible loss of prosody (intonation, emphasis, rhythm) in speech - Wernicke’s (receptive) aphasia: most strongly associated with extensive Left parietal/temporal damage
* Typically , fluent grammatically correct speech that isn’t meaningful, poor comprehension, using wrong words and nonsense words.
- According to Ekman, what are the 6 primary emotions indicated by our facial expressions? In what other ways do we express emotion besides facial expression, and are there cross-cultural differences in emotional expression?
“Primary” Emotions
- >6 (Ekman):
Disgust
Surprise
Sadness
Fear
Joy
Anger
How else do we express emotion, besides face?
Cross-cultural differences in body language
Cultural diversity in emotional expression/interpretation
Western Caucasian participants relied more on eyebrows and mouth whereas East Asian participants relied more on eyes (and gaze change)
- How does the autonomic (especially sympathetic) nervous system contribute to emotional experience?
Neural basis of emotions
- Autonomic (sympathetic) nervous system: does it contribute to our emotional experience?
- HR and BP increase most with negative emotions (fear, anger, disgust); decrease during sadness
- Do quadriplegics experience emotion similarly to those with intact spinal cords? Experience them just a little less intense
- Trace the path of neural communication involved in the emotional experience you are likely to have upon seeing (and hearing the voice of) the person who viciously assaulted you 3 months ago (start at the retinas/ears, end at sympathetic n.s. and PAG). What brain area is crucial for your conditioned emotional response to the PLACE where the assault happened? What brain area would be crucial in your decision-making process regarding whether or not to openly express your fear of a person who assaulted you, and to pursue legal action against them?
- VTA: increase activity ssociated with joy, reward- DA release to PFC and other areas
- Amygdala (fear, anger, disgust): to visual, somatosensory, auditory input (from thalamus and cortex to amygdala)
- Hypothalamus (any strong emotion>stress): activates SNS and HPA axis (HPA= hypothalamus-pituitary-adrenal)
- PAG (fear,anger): coordinates defensive reactions (freezing, fleeing, pain suppression)
Hearing the teachers voice triggers anger: Ears> MGN> Auditory cortex> Amygdala
Now do the sight of the teacher: eyes> LGN> visual cortex> Amygdala
Now do the classroom where you were wronged: Place cells in hippocampus> Amygdala
Now do why you suppress your anger: Prefrontal cortex > amygdala
- What is life like for people who do not have amygdalae?
Generally fearless to their own detriment.
- Describe the “fast” vs. “slower” physiological components of the stress response. What is the adaptive value of these responses (i.e., how do they help you cope with stressful situations)?
Stress:
- Hypothalamus activates both SNS and HPA axis: both support coping responses to stressors (Hypothalamus-pituitary-adrenal)
- SNS: NE,E released > rapid response to support fight /flight
Increased HR/BP, expand bronchial passages> increase O2 and glucose to large muscles and brain
Pupil dilation> increased light to retina to sharpen vision
Liberation of stored nutrients (e.g. glycogen from liver) > provide extra energy
… but prolonged activation can exhaust bodys resources, tax cardiovascular system, impair digestion
- HPA: cortisol released> slower, more sustained coping response; shunts resources from energy-demanding tasks such as immune system activity and learning, so you can continue to deal with stressor.
- Explain how long-term stress can adversely affect your health, including biological mechanisms underlying these detrimental health effects.
- Short term SNS and HPA activation (hrs to days) not harmful, can even boost immune function (e.g. cortisol decreased inflammation) and enhance learning (brain NE increased LTP)
- But sustained HPA activation (weeks to years) can seriously compromise health and learning/memory
- Cortisol receptors on immune cells, and in hippocampus, PFC (can inhibit LTP)!
- Describe the major positive and negative symptoms of schizophrenia, and discuss the evidence for the various “ultimate” causes of this disorder.
- Positive symptoms (presence of unusual behaviors/thoughts) ; e.g
Delusions, Hallucinations, Disorganized speech and thought
- Negative symptoms (loss of usual behaviors/thoughts); e.g.
Flattened affect
Schiz. Is not a unitary disorder
Ultimate causes: Genetic risk (many genes implicated): e.g. COMT gene codes for enzyme that breaks down DA/E/NE; SYN@ gene codes for synaptic vesicle protein (which regulates nt release); GRIN2A, GRIA3 code glutamate receptors
And/ or early environmental insults: e.g. pre-natal (esp. 2nd trimester) viral exposure (e.g. rubella, flu), malnutrition and/or birth complications (hypoxia).
- What are some possible “proximate” causes of schizophrenia, and what is the evidence to support these hypotheses?
Proximate causes:
DA hypothesis: excessive activity at DA receptors contributes to positive symptoms
DA antagonists can reduce positive symptoms; DA agonists can increase positive symptoms
D2 receptor binding predicts drug potency
Glutamate hypothesis: abnormal glutamatergic activity contributes to symptoms (e.g., glutamate antagonists, PCP, and ketamine can trigger symptoms)
Progressive loss of neurons and neural connections, especially in the hippocampus and temporal, frontal, parietal cortex.
MRI scans = schizophrenia?
Lieberman et al. (2018): correlation between hippocampal activity and delusional severity
- What are the primary pharmacological treatments for schizophrenia, and how are they believed to work?
treatments
Primarily anti-psychotic meds: all DA (D2) antagonists
Side effects of blocling DA rec?
Movement disorders (dyskinesias)
Hormone dysregulation
Cognitive behavioral therapy
- Describe the major symptoms of unipolar depression (both major, and seasonal affective types) and bipolar depression. Discuss the evidence for the various ultimate causes of these disorders.
Depressive Disorders (past-yr U.S adult prevalence – 10%)
- Major (Unipolar) depression: persistent sadness, fatigue/lethargy hopelessness, anhedonia, sleep disturbance
Ultimate causes:
Genetic risk (heritability – 40%): many genes contribute: e.g. 5-HT transporter gene, 5-HT2 receptor gene explain <1% of the variance
Environmental triggers: trauma/abuse, chronic stressors (also: lack of daylight; pregnancy)
- What are some possible proximate causes of unipolar depression, and what is the evidence to support these hypotheses?
Proximate causes: gray matter loss, decreased activity in the frontal and cingulate cortex, hippocampus, amygdala
Monoamine hypothesis: hypoactivity at monoamine synapses
Drugs that increase 5-HT, NE (DA) can alleviate depression
Autopsy shows increased 5-HT, NE receptor density in brains of depressed.
Neuroplasticity hypothesis: loss of neural growth, connectivity (e.g. nerve growth factors like BDNF decreased)
Raphe (5-HT) and locus coeruleus (NE) decrease and increase activity in a daily rhythm… dysregulated in depression.
- What are some pharmacological and non-pharmacological treatments for unipolar depression, and how are they believed to work?
Treatments:
Anti-depressant meds:
- 5-HT agonists: SSRIs block 5-HT reuptake
- Monoamine (5-HT/NE/DA) agonists: tricyclics prevent reuptake of monoamines; MAOI’s prevent enzymatic degradation of monoamines
- Ketamine (2019): glutamate antagonist; rapid effects>> Stimulates increase glutamate receptor # (for treatment-resistant depression only; intranasal or i.v; in patient only; repeat at 3-6 weeks) also causes Increased BDNF g nerve growth factor
If meds/psychotherapy ineffective (-40% of patients):
ECT: effective in 70-90%, but amnesia, relapse common
Deep brain stimulation: e.g. stimulate anterior cingulate or nucleus accumbens (mesolimbic DA reward pathway)
–remission in up to half of patients, may last years
- What are some pharmacological treatments for bipolar depression and how are they believed to work?
- Bipolar disorder: depression alternating with mania (poor judgement, racing speech, inflated self esteem, euphoria/extreme optimism, risky behaviors, agitation/aggression, little sleep)
Ultimate cause: genetic (heritability 80-90%)
Proximate cause: ??
Treatment: “mood stabilizer”
To decrese neural excitability (prevent mania)
Anti seizure meds (e.g Tegretol): Na+ channel blockers
Anti psychotics (e.g. Zyprexa): DA antagonists
Lithium: alters intracellular signaling…
Impact of lithium on neuro transmitters: increased GABA neurotransmission, decreased glutamate, DA antagonist too neurotransmission
CBT
- Describe several major types of anxiety disorders, and discuss the evidence for the various possible causes of these disorders.
III. Anxiety Disorders: chronic or intermittent fear in absence of immediate threat (incidence 15-30%) e.g. PTSD: nightmares, flashbacks, sleep disturbance, hypervigilance
- Ultimate caueses:
- Genetic risk: heritability 30-50%
- stressful event(s): e.g. trauma in the case of PTSD
- Proximate causes (PTSD):
- HPA axis dysregulation (also observed in 40-60% depressed individuals) >chronically high cortisol.
- Amygdala hyperactivity; (too) strong connectivity w/cingulate?
Berry et al (2019): people with lower trait anxiety show greater DA activity (-) in amygdala and anterior cingulate, and less connectivity between these brain areas.
People with PTSD show increased amygdala and cingulate activity, decreased PFC activity than controls
- What are some treatments for anxiety disorders, and how are they believed to work?
Treatments: psychotherapy effective, to learn coping/management strategies (=brain re wiring= LTP/LTD!), although meds are often used, e.g.
Benzodiazepines (Xanax, valium) : gaba agonists
SSRIs 5-HT agonists
