Chapter 14: Learning and Memory Flashcards
What does dyslexia result from? In what area of the brain is it?
neuron clusters/warts from birth; reduced activity in the tempo parietal cortex
What is eyeblink conditioning and what part of the brain is active during it?
a tone is associated with a puff of air; the cerebellum
What is fear conditioning and what part of the brain is active during it?
conditioned emotional response between neutral stimuli and unpleasant events; the amygdala
What is amnesia and what type of tasks do typical amnesia patients perform normal on?
the partial or total loss of memory; on implicit memory tasks
What is a learning set?
the “rules of the game”, how a problem can be solved in a given situation; is stored in memory
What is priming and what type of memory does it mostly relate to?
using a stimulus to sensitize the nervous system to a later presentation of the same or similar stimulus; implicit memory
What lobes are STM and LTM processed in?
frontal and temporal lobes respectively
Where are memories for colour stored?
the ventral temporal
Where are memories for motion stored?
the middle temporal gyrus
Where is episodic memory processed?
the frontal lobe but connections in various areas
What is shown in brain scans for those with highly superior AM?
an increase in gray matter in the temporal and parietal lobes
What did H.M. have removed? What was the result?
hippocampus, amygdala and some surrounding; could not form new explicit memories
Where is implicit motor memory located?
in the basal ganglia
What is the neural circuit for explicit memories?
major cortical areas both Perirhinal and Parahippocampal entorhinal hippocampus
Where is the entorhinal cortex and what does it do?
medial temporal lobe surface; it is the major route for neocortical input to the hippocampal formation; the integrative area
What happens if the entorhinal cortex degenerates?
Alzheimers
Where is the parahippocampal cortex and what type of information does it receive and relay?
along the dorsal medial temporal lobe surface; visuospatial memory
Where is the perirhinal cortex and what type of info does it receive and relay?
next to the rhinal fissure on the ventral surface of the brain; the visual stream
What are 2 possible ways for Alzheimers to develop?
1) Loss of cholinergic cells in the basal forebrain
2) Development of neuritic plaques in the cerebral cortex
What are neuritic plaques?
dead tissue with a central protein core surrounded by degenerative cell fragments
Where is spatial memory processed?
the hippocampus
What types of cells are in the hippocampus to process spatial memory? (3)
1) Place cells - certain location
2) Head direction cells - particular direction
3) Grid cells - tells us how big where we are is
What are the reciprocal functions of explicit memory and what is their purpose?
1) from the MT to the cortical layers - keeps sensory info alive
2) Back to the neocortex - keeps it appraised? (review this)
What is Korsakoff syndrome and what is it caused by?
both retrograde and anterograde amnesia resulting from diencephalic damage because of alcohol use and vitamin B deficiency
Where does consolidation of explicit memories take place?
in the hippocampus
What does the basal forebrain help do for explicit memories?
maintains activity levels in forebrain areas so that memories can be stored
What is the neural circuit for implicit memories? What is different about it from explicit?
sensory and motor info –> neocortex –> basal ganglia (also receives info from substantia nigra) –> ventral thalamus –> premotor cortex ; there is no feedback
What sends and receives info to and from the amygdala in the neural circuit for episodic memories?
the medial temporal cortex, basal ganglia and hypothalamus and PAG
Where do the hypothalamus and PAG exchange info with?
the amygdala and the frontal, parietal, temporal, occipital and cingulate cortices
What is long-term potentiation?
a long-lasting increase in synaptic effectiveness after high-frequency stimulation
What is long-term depression? What is it hypothesized to be a part of?
long lasting decrease in synaptic effectiveness after low frequency electrical stimulation; clearing out old memories
What is AMPA’s role in the LTP process?
it mediates responses when glutamate is released; if enough glutamate is released then it allows Na+ to enter and depolarize
What is NMDA blocked by and what does it allow to pass if depolarized?
blocked by Mg2+ and allows Ca2+ to pass
What are the 2 conditions that must be satisfied for NMDA to open?
1) Postsynaptic depolarized (Mg2+ displaced)
2) NMDA receptors activated by glutamate
What molecule plays the crucial role in LTP that is moderated by NMDA?
Ca2+
What effects does Ca2+ have in relation to LTP?
1) Increased responsiveness of AMPA
2) Formation of new AMPA receptors
3) Release of more glutamate
What is the BrdU technique used to detect?
new neurons in the mammalian brain?
What qualities of brain did enriched rats have compared to regular?
more dendrites, glial cells and blood capillaries; also more neurons in hippocampus and more
Where did amputated hand sensors move?
to the face –> increased sensitivity/responsiveness to face
What is dystonia?
a blending of finger representation that messes up hand movements because of overuse as well as vibrations moving through fingers (usually in musicians)
What type of people have more dendritic branches in Wernicke’s area?
college educated people and females
What happens if you block the methylation of DNA in hippocampus?
no memory
What effect does estrogen levels in women during their cycles have on the brain?
increased dendrite spines in the neocortex but less in the hippocampus
What do Neurotrophic factors do?
signal stem cells to turn in to neurons of glia
What does Nerve Growth Factor (NGF) do?
stimulates neuron growth and survival?
What neurotrophic factor plays a role in learning?
BDNF
What is drug-induced behavioral sensitization and what types of drugs cause it?
escalating behavioral response to repeated administration of a psychomotor stimulant; amphetamine, cocaine, caffeine
What does drug induced behavior sensitization do to the brain?
increases receptors/synapses in the prefrontal cortex and nucleus accumbens (dopamine areas); stops hinders learning of complex environments later
What are the 3 potential recovery solutions to Brain Injury?
1) Compensate with out body/brain parts
2) Grow new circuits
3) Lost neuron replacement
What does growing new circuits allow the brain to do? What can be done to result in it?
do more with less; deep brain stimulation and NGF (promotes growth)
What is a growth factor that is used to replace neurons? Where is it and what does it do? What else is needed?
epidermal growth factor; in ventricles; stimulates neuron and glia growth in the striata; trophic factors also needed
What are 3 things the brain is according to Dickson?
1) a sensory-motor integrator
2) dynamic and modifiable
3) a storage device
What are the 2 premises of neurobio?
1) NS operation is completely responsible for behavior and mind
2) Environmental influences that change/modify behavior must be reflected by functional changes
What did Muller and Pilzecker research?
rehearsal, consolidation and interference
What did William James research?
different aspects/types of memory
What was a saying that was famously said by Hebb? What was the backing of this?
cells that fire together wire together; that there was activity dependent enhancement of synaptic transmission (LTP)
Who first researched LTP? What were they studying?
Bliss and Lomo; transmission in the hippocampus
What are the 3 properties of LTP?
1) Cooperativity: threshold aspect of it
2) Associative: associate weak with strong so weak can bring LTP by itself
3) Specificity: LTP expressed only in active synapses and not nearby ones
After LTP is induced what is NMDA’s role?
it is not needed anymore; only useful for induction
What is Calmodulin dependent protein Kinase II? What does it do?
it is the “memory molecule” when activated promotes LTP and when inhibited stops LTP
What are the 3 phases of LTP?
1) Early - Induction: NMDA activation and Ca2+ dependence
2) Medium - expression: changes to receptors and release; local protein synthesis
3) Late - Maintenance: genomic involvement (translation dependent); possible anatomical changes
What is significant about the Aplysia’s gill withdrawal reflex? (3)
it shows habituation, sensitization and classical conditioning; a monosynaptic connection evokes the reflex; also has interneurons though that are modulatory
What happens during habituation to the presynaptic neuron?
decrease in width of action potential; less physical connections between neurons
What learning process is classical conditioning similar to at the cell level?
sensitization
What kind of process is required for memory at the cellular level?
protein synthesis and perhaps the transcription of DNA-RNA; memory requires gene expression that leads to new proteins
Where is the Memory trace located according to Karl Lashley? How did he come to this conclusion?
diffusely in the brain; by removing parts of the brain and realizing that it had the property of equipotentiality (parts could take over to do the same tasks
What did Ribot discover about amnesia?
the loss of memory is inversely related to the closeness to the injury
What did patient H.M. have removed and what was the result?
the medial temporal lobe (hippocampus, entorhinal cortex, parahippocampal cortex and amygdala) and then he had profound anterograde explicit amnesia but IQ actually increased
For a DNMS for rats what lesions were there a notable performance difference? Which weren’t there?
MTL noticeable; hippocampus not
What part of the brain is responsible for temporally ordering events?
the frontal lobe
Where is the damage for korsakoff syndrome?
medial thalamus and the medial hypothalamus (the medial diencephalon)
What lobe is central to long-term explicit memory formation?
the temporal lobe
What do concussions disrupt? Why?
the consolidation process; perhaps because it interferes with frontal lobe action
Where does the standard consolidation theory suggest memories are stored temporarily?
the hippocampus
What is the distributed reinstatement theory?
a learning episode rapidly produces a stored memory representation that is strong in the hippocampus but weak elsewhere
