Midterm 2 Flashcards
Henry Molaison (patient HM)
o Man who had his amygdala and HC removed. He developed a case of retrograde amnesia and was found to also have good nondeclarative memory after he did a series of mirror drawings and over time he remembered them even though he did not have recollection of knowing these drawings cerebellum shrunk too
Hippocampus
A medial temporal lobe structure that is important for learning and memory. Converts short term declarative memory into long term declarative memory
Study in Science: hippocampal neurogenesis and forgetting
o More neurogenesis the less likely you were to remember something (seen in infants). Experiement where mice were shocked and the ones with less neurogenesis remembered what happens at that setting (measure # of neurons).
Delayed non-matching-to-sample task
o Measure memory in monkeys by having them identify which object was not seen previously. They show the monkey a key and one other object and under the other object they hide a piece of food. They have a delay of 8-10 sec before they will let monkey choose which one had food. If damage to HC like HM this will be very hard.
Patient NA
Like HM but he had a sword put up nose and hit part of brain. He too had anterograde amnesia and a better nondeclarative memeory because of it. Had damage to Dorsomedial Thalamus and Mamilliary body both parts of HC.
• Dorsomedial thalamus (T)
limbic system structure connected to hypothalamus that has to do with memory decoding
Mammilary body (T)
limbic system connected to HC. It may serve as a processing system connecting HC and nearby cortex to thalamus to cortical sites
Korsakoff’s syndrome
o Degenerative disease with damage to the limbic system esp mammillary body and dorsomedial thalamus. They fail to recognize some objects they see repeatedly. They make up (confabulate) what things are by filling in the blanks with false info
o Cause: lack of vitamin thiamine (alcoholics)
• Give them thiamine to prevent it in future but cannot reverse damage done.
Patient KC
• A patient who sustained damage to the cortex that renders him unable to form and retrieve new episodic memories. Was in a motorcycle accident at age 30. Can no longer retrieve any personal memory of his past, but his general knowledge remains in tact. Damage to the left frontoparietal and right parieto-occipital cerebral cortex, and severe shrinkage of the hippocampus and nearby cortex. The bilateral hippocampal damage accounts for his anterograde declarative amnesia.
Episodic memory
Memory of a particular incident or particular place and time
Semantic memory
• Generalized declarative memory, such as knowing the meaning of a word without knowing where or when you learned that word
Basal ganglia
• A group of forebrain nuclei, including the caudate nucleus, globus pallidus, and putamen, found deep within the cerebral hemispheres. They are crucial for skill learning. Sensorimotor skills, perceptual skills and cognitive skills all take place here.
priming
o Change in view of stimuli because you’ve seen it before. Like seeing ST and thinking stomp becausae you recently saw that word instead of assuming it would be start
-Evident in HM
Cerebellum
A structure located at the back of the brain, dorsal to the pons, that is involved in the central regulation of movement and in classical conditioning
place cell
at HC contains many neurons that selectively encode spatial location AKA place cell. Activated in specific location if move place cell tells HC and brain is re-mapped.
o Birds who hide food have high place cells
What is Working memory made up of?
STM + other stuff (episodic buffer; central exec)
Two neural correlates of working memory
o Neural synchrony—how well neurons an networks are simultaneously activated
o Higher in slow wave sleep and WM
Superior autobio memory
think about past and can recall most events
Reconsolidation
o When you are giving a memory back to LTM after you could have changed it or altered it
o Can create false memory by feeding someone line like saying “did you see the broken car window” instead of “is the window broken”
o Used in hyponosis
Neuroplasticity
o Memories and events that require formation of new synapses or neurons. How CNS changes in response to environment
Synaptic changes that underlie (some) memory
o More frequently used synaptic sites take over less used synapses receptors
o Increase number of NT coming through in a successful synapse
o Start up post synaptic receptors that are not being used if one is successful
Environmental enrichment/impoverishment & dendrites
o UC—housed one rat in small cage
o IC—houseed multiples rates in normal conditions
o EC—housed multiple rates in better conditions
o Found that in EC
• Higher cortex in somatosensory visual areas
• More dentric branches on neurons
• More neurons in HC
• Better recovery from brain damage.
Hebbian Synapse
pre and post synaptic connection becomes stronger because they are repeatedly activated together
Synaptic plasticity & habituation
o ST—aplysia retracts gill when squirted with water but after a while it takes longer for it to retract it because less NT will respond to it
o LT—aplysia squirted over time will respond less quickly until after days it does nothing in response
Synaptic plasticity & associative learning (Fig 13.20 generally – not names of nuclei)
o (CC) bunnies blink at tone and it is then paired with a buff of smoke. Found that HC is not needed for this but rather the cerebral circuit. US/CS converge in cerebellum
Long-term potentiation (LTP): outcome, physiologically
o NMDA usually blocked by Mg 2+ but repeated AMPA activation. Depolarization drives out Mg2+ and Ca rushes in cause an increase in LTP and increased AMDA receptors to membrane and NT increase
LTP structure
• The synapse becomes more responsive. The postsynaptic cell now has a stronger response, as more transmitter is released and more AMPA receptors are present.
LTP & NMDA receptors
Block NMDA prevent new LTP because blind glutamate agonist
LTP & AMPA receptors
o Binds to glutamate agonist AMDA
Retrograde Transmitter
Diffusible gas that travels back synapse and alters pre-functioning. Released by post when strongly stimulated and increase Ca to ensure more glutamate will be released
Emotion
o How body responds to certain events
o Subjective mental state accompanied by distinctive behaviors as well as involuntary physiological changes.
Schater-Singer experiment
• People were injected with epinephrine (adrenaline) and told either that it would have no effect on them or that it would make their heart race. They then were told to fill out forms and were exposed to a helper who either acts angry or happy while filling out the forms. Subjects who were warned that the injection might affect heart rate reported no emotional reaction. Subjects who were not warned reported intense emotional reactions. Among the subjects that were not warned about the effects of the injection, they tended to experience the emotion that their helper embodied. Conclusion: our cognitive analysis of the environment affects which emotion we experience.
• Facial expressions & core emotions
o Facial expressions are universal and there are a list of core emotions except surprise and disgust
o Superfacial nuscle—smiling
o Deep facial—skin attatch to bone produce large movemt of facial nerve
• Facial feedback hypothesis (T)
o (james lange—body tells us emotion)Changing facial expression can change mood to corresponding feeling
Purpose of (some) emotions (T; p. 309-311)
• Emotions act as motivational programs, gathering together distinct physiological and behavioral components to form unified responses to specific adaptive problems.
• Limbic system
o Compromised of brain nuclei to make a network that deals with emotion
o If damaged impair emotion
o Includes HC and amygdala and hypothalamus
• Kluver-Bucy Syndrome (T)
o Amygdala damage. Rats that used to fear and show stress to humans now make no expression. Now ate variety of objects and have innapropriate sexual behavior
Amygdala
o Processes fear
o Touch each temporal lob and have diff nuclei w/ spec connections. Sensori info travels to it via channels where it passes through thalamus and is directed
Patient SM
• Had damage to both her amygdalas. She is unafraid of snakes and spiders, and robbers with knives. Her other emotions are intact, but she shows fairly little sympathetic response to fearful stimuli and produces almost no startle response to a sudden, loud noise. She also is bad at recognizing facial expressions in others, but can recognize other emotional expressions.
2 routes of amygdala
o From thalamus for fear (fast)
o Or from sensory cortex to making a memory
Lateral and Central Amygdala
• Two diff routes to amygdala
o Both send info to lateral amygdala
• This sends info to central amygdala
This sends info to where in body it needs to go
PFC emotions and decisions
impairment in social decisions making even though intellect is okay
Stress
upset homeostasis
Alarm reaction
o What happens in response to stressor first off. Sends body to semantic response and triggers fight/ flight releasing norephonrine and epinephrine or hypothalamus stim anterior pituitary to drive out adrenal cortex to release cortisol
HPA- axis
o Hypothalamus-Pituitary-Adrenal
o H tells P via CRH to secrete ACTH which tells A to release Cortisol
o For slow stress response
o Process of body stress ends up with cortisol giving info to immune system
Adrenal gland
o In stressor it decides whether it will be quick or slow response
o Release hormones in response to stress
Norepinephrine
NT released by adrenal medulla in alarm reaction. In fight/flight response accelerates activity of body.
Epinephrine
released by adrenal medulla in alarm reaction fight/flight. is a hormone to boost HR and be synaptic transmitter.
Cortisol
o Hypothalamus drives adrenal cortex to realease hormones like this
o Slower part of stress response but is hormone that excites body
Epigenetic regulation
o Change in gene expression rather than encoding region of gene. Long lasting change in adrenal steroid recognition
o Mothers touch helps calm us down and
o If deprived of mom cannot handle stress
topics of stress research
o Affects on: • Cognitive ability • Emotion • Decisions • health o Relief o Hormones o Individual diff (why some get PTSD others don’t)
Caveats about oxycotin
o Makes people with autism more social
o Affects differ and some can be neg can promote fear
Structural changes in brain & schizophrenia
o Larger lateral ventricles
o Thicker corpus callosum
o Less grey matter (sensory perception)
Schizophrenia
o Psychotic; where you have delusions/ hallucinations (pos) and you are socially withdrawn(neg)
Typical Neuropleptics
various antipsychotic drugs are classified as this
Atypical Neuropleptics
drugs that don’t have many DA receptors. They avoid motor side affects. Selectivly block seratonin and other receptors
neural activity regions for depression
o Blood flow increased in prefrontal cortex and amygdala; parietal lobe activity down
neural activity of bipolar disorder
ventricles increaase, grey matter decrease
Tricyclics (T)
o Inhibit reuptake of MAOs so they are more present.
Benzodiazepines
o Used for anxiety; GABA receptor in CNS. Bind to GABA receptor non-competitivly. Boost GABA mediated postsynaptic inhibition
Propanolol
o Used to treat PTSD by helping not associate emotion with remembering. Beta blocker that blocks epinephrine and norepinephrine. Blocks emotional aspect of memory and lessens adrenaline response. Only works in reactivated situation
SSRI and OCD
disfunction of serotenergic NT plays role in depression which accompanies OCD
Cingulotomy (T)
o Lesions that interrupt cingulate cortex. Small lesions replace anterior part of internal capsule. Helps anxiety
Simultagnosia
Narrowing of focus spotlight so you cannot focus on more than one object at a time. be found in balliants syndrome (difficulty steering gaze.)
Testing split-brain individuals (L, and Fig 15.13)
o Can respond verbally to stumli on right visual field because interhemisphere transfer not needed.
Fusiform gyrus (T)
o Something damaged that results in unrecognition of faces. It is where occipital and temporal corticles meet.
