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111 Cards in this Set
- Front
- Back
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consolidation
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moving short term memory into long term
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reconsolidation
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retrieve memory
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working memory
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memory in use, centered around hippocampus or prefrontal cortex
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working memory
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facts, events,
milliseconds, seconds moment to moment utilization of info hippocampus, prefrontal cortex |
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long term memory
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facts, events
years, decades acquisition of knowledge/experience dentate nucleus, posterior cortex |
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declarative memory
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knowing " this is my hair"
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semantic memory
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meaning of words
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working memory
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memory in use, currently happening
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reference memory
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details of an object, knowledge of college
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implicit memory
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where you parked
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procedural memory
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how you parked
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autobiographical memory
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knowing random dates
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exteroceptive memory
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specific dates, ft hood shooting
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skilled learning
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involves extrapyramidal motor system, like cerebelum and basal ganglia
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association cortex
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the more association areas in the cortex, the more advanced the species seems to be intellectually
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unilateral neglect/ contralateral
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cannot utilize information from one side of the environment, deals with associative cortices
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lession in prefrontal cortex
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hard to make new memories or to retrieve them, not storage site
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lession in the ANTERIOR part of the cingulate cortex
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affects memory
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lession in the POSTERIOR part of the cingulate cortex
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affects sleep
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mediotemporal lobe-specifically-occipitotemporal cortex
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facial recognition
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hippocampus
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3 inputs
1. occipitotemporal 2.parahippocampal 3. entorhinal * ( main one) |
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anterior portion of cingulate cortex
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wiping out about half of it severely disrupts memories
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posterior cingulated cortex
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important in sleep regulation
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occipital temporal cortex
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important in recognizing faces
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hippocampus
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new long term memories cannot be made if there is a lession in hippocampus, can still learn procedural memories
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alzheimer's destroys the hippocampus
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then destroys the entorhinal cortex and parahippocampus, cannot remember new information with this disease , but memories involving past experiences are unaffected,
Hippocampus in involved with consolidation |
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face recognition cortex
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occipital temporal cortex , neurons fire in response to seeing a face, if face is scrambled, they do not fire
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the hippocampus
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lots of calcium channels, highest order function
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hippocampal commisure
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hippocampus is bilaterally connected
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Electroconvulsive shock
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current is applied between the sides of the head, inducing seizures, this induces retrograde amnesia ( events before amnesia cannto be recalled)
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anterograde amnesia
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inability to make new memories
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HM
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had an experimental seizure, removed the entire medial temporal lobes, includes hippocampus, parts of amygdala, entorhinal cortex and parahippocampal cortex,
after surgery , no longer sufferered from seizures, but could not make new memories -only procedural memory( basal ganglia and cerebellum) no declarative memory loss of CA1 pyramidal neurons in hippocampus and pyramidal neurons in entorhinal cortex was enough to recreate HM symptoms |
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CA1 neurons
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CA1 neurons in hippocampus are most sensitive to oxygen diff.
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Hippocampus and memory
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memories pass through and possibly indexed by hippocampus, but not where memories are stored, consolidation
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protein synthesis and anterograde
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once memory has been made, blocking protein synthesis has no effect
At the end of the first day before sleep, blocking protein synthesis results in the fish no making long term memory Blocking protein synthesis seems to affect consolidation |
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Memory consolidation : increase in protein synthesis
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Protein synthesis inhibitor added before the training results in normal short term memory, has same effect as when protein synthesis inhibitor was added at the end of the first day
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wisconsin card sort
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tests for prefrontal lobe damage, particulary lateral prefrontal cortex
prefrontal cortex damage very common because of car accidnets |
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stroop test
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test the anterior portion of the frontal cortex, anterior cingulate cortex
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matching to sample
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posterior cingulate cortex
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nonmatching to sample
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activity seen in the orbitofrontal cortex
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aplysia slugg
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habituation for sensitization, poke slug after a while doesnt feel it anymore
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prefrontal lobectomy
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shoving probes up through the top of the eye sockets, and scrambling the prefrontal cortex
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amygdala
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known for its function involved in emotional arousal
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hippocampus
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highest density of high volatage gated calcium channels, as well as high numbers of many other receptors
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hippocampus is archicortical
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3 layered
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pyramidal cells
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primary output neurons of the hippocampus
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granule cells
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in the dentate gyrus
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CA1
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output neurons from the hippocampus, they synapse with the subiculum, which then goes back to the entorhinal cortex
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CA3
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pyramidal neurons which send outputs primarily to CA1 as well as some modulatory systems
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hippocampal circuitry
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feedback circuit
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consolidation
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most changes in the CA1 and CA3 neurons during consolidation, granule cells show very little change over time
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CREB
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acts to promote gene transcription
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short term potentiation
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increase in synaptic activity , less than 50ms.
Mechanism is pre-synaptic and deals with calcium in presynaptic terminal. More calcium leads to more NT release, does not last long because the cell has mechanisms to handle the excess calcium |
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long term potentiation
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increase in synaptic activity, 10 minutes to 10 days
Maintenance phase: has a high spike in potentiation and then slowly falls back down near base level. pre and post synaptic activity: calcium |
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Long term depression
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last at least 10 minutes, not more than 1 day, post synaptic activity: calcium
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cooperativity
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pairing /spatial summation: most individual synapses are too weak to cause post synaptic cell to fire. Requires cooperation of a number of synapses.
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Associativity
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timing/temporal summation. Action potentials need to be put together at about the same time. Can cause potentiation or depression of synapses
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Specficity
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discrimination/synapse specificity. Sets of synapses that have been paired should show increased responses.
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stress
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the effects of stress are cumulative,
hippocampus has the highest density for stress hormone, found in the pyramidal neurons in hippocampus Chronic stress=increased glucose utilization |
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stress can cause
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1. presynaptic dysfunction
2. postsynaptic dysfunction 3. excitotoxicity: death by glutamate glia cells beging to change pattern of activity , they begin to release a great abundance of syrine ( important for activation of glutamate receptors-NMDA receptors-which function as calcium channels) under these excitotoxic conditions over activation of NMDA receptors greatly increases the load of calcium on post synaptic cells, which may lead to apoptosis ( cell death) |
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neurochemical hypothesis for aging?
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cystoskeleton:
actin: gives shape and structure to the cell, can have abnormal variants Tau protein cleavage defects Accumulationof beta-amyloid proteins Impaired calcium homeostatsis :intracellular calcium increase each deacade of life |
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calcium
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intracellular calcium levels increase each decade of life( leads to calcification)
causes many changes structurally and functionally at the cellular level |
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genetic hypothesis
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cumulative mutations=disease
developmental programmed cell death ( apoptosis): certain stimuli can cause apoptosis to become re-initiated Telomerase loss |
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myelination
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decreases with age
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high blood pressure in aging
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has effects on the NS
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prion disease
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prion proteins build up in the brain and destroy it over time
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vascular dementias
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suffered after a stroke or injury
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parkinsonism
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loss of SN pars compacta DA neurons
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Huntington's dz
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trisomal CAG repeat, affects medium spiney neurons in basal ganglia
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progressive supranuclear palsy
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loss of cerebellar deep n, olivary n
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alzheimers disease
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reported incidence increasing
alzheimers tangles and plaques neurodegeneration beginning in hippocampus spreading to entorhinal , and other limbic cortices reactive astrocyte responses |
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in aging
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global major changes in synaptic transmission, increased sensitivity to glutamate
regional hyper/hypophosphorylation |
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global changes in cognition
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preserved functions, long term memory
severe impairments in consolidating new memories progressive retrograde amnesia, mood changes progressive impairment in activities of daily living end stage loss of control |
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alzheimers: beta-amyloid protein
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problems with cleaving amyloid proteins
Apo-E genes: a gene that is related to early onset of alzheimers |
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learning related plasticity
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occurs only in the pyramidal neurons
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post burst afterhyperpolarization : AHP
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an event that occurs after an AP is fired-makes cell more hyperpolarized after an AP. Using a calcium blocker on the cell membrane badly affects the current, proving it is a Ca-dependent current. , more calcium that enters the cell: larger/longer AHP
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animals that are learning successfully
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have reduced AHP
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aged AHPs are larger ( so they are slower)
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while young AHPs are smaller
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aging neurons have high levels of Calcium
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inside the cell, PKA pathway seems to account for this overall higher AHP in aged neurons
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calmodulin
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calcium binding protein that can bind with up to 4 different calcium ions per molecule
SK type potassium channels and calmodulin: interact, by gating the opening and closing of the channel, the more calcium that is bound to it, the longer the channel will stay open |
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short term memory
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does not depend on protein synthesis
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Long-term memories involve changes in protein synthesis and gene regulation
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, whereas short-term memories do not.
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potassium channels that generate the AHP
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SK-type potassium channels
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calcium sensor that binds 3 calcium ions per molecule
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hippocalcin
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blocking calmodulin
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we can in dose dependent fashion, affect the AHP. Blocking these sites can reduce AHP significantly
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SK-channel blockers
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Apamin
Dequilinium |
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apamin
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SK channel blocker, comes from honey bee venom. Can cross BBB. Dose dependently increases learning/memory. Reduces AHP amplitude
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Dequilinium
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SK channel blocker, from many plant sources, reduces AHP amplitude, consistenly increases firing activity of the pyramidal neurons
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Phosphorylation
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the SK channel and the unknown channel ( aka slow AHP channel) both modulated by phosphorylation. Phosphoryation closes these channels and reduces their activity.
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Muscarinic agonists: M1
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treatment with M! agonists results in faster learning. M1 agonists reduce underlying currents in a dose dependent fashion.
Increased phosphorylation, firing increases, AHP reduced, thus more excitable |
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mGluR1
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agonists for metabotropic glutamate receptors , AHP is reduced, neurons fire more and currents are reduced, faster learining
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NMDA receptors
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ionotropic receptors for glutamate. When glutamate binds to these receptors , they open allowing calcium ion inflow. Unique because they require 2 NTs: glutamate and serene
serine is dumped by glia cells |
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NMDA receptor antagonists
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block learning
Completely blocking NMDA receptors will block learning and memory in a dose depended fashion |
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Enhancing function of NMDA receptors
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increases learning
partial NMDAR agonists will enhance learning and memory A full agonists impairs learning/ just like an antagonists |
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D-cycolserine (DCS)
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was a partial agonist used for MNDA, animals learn faster
serine is a nt not released from neurons but glia displaces the serine that glial cells are releasing, resulting in activiating the NMDARs less than serene, redunces amt of calcium coming into post synaptic neurons |
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increasing PKA
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activity in hippocampus and pyramidal neurons also reduce AHP, facilitated by multiple Nts.
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conserved limbic system
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Conserved limbic mechanism necessary for many forms of learning/memory consolidation
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high Calcium
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potentian
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low calcium
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depression
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Criteria to support function of learning/memory
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• Changes in neuronal activity should CORRELATE with function changes
• TIME COURSE of neuronal changes should be appropriate • LACK OF NEURONAL CHANGES IN THE ABSENCE of functional changes • MANIPULATION of neuronal changes should alter functional changes |
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Ca Dependent K channels
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• Associated with learning
• Post-burst HP (after hyperpolarization) • BKA644 – makes you stupid • Can make AHPs smaller by learning • Slow AHP – less intense, longer-lasting |
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Eyeblink Pseudo
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• Same number of air puffs and tones, but change the timing between the tones and air puffs. Never learn.
• AHPs high |
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Rightward shift in AHPs
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• Control animals – evenly distributed
• After learning: shift to right |
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Fire activity – Accommodation
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• After learning – more excitable
• Slow learners – less excitable • IA/inhibitory avoidance (fear conditioning) strong connection between amygdala- basal lateral n of amygdala (fear memory), and HP (CA1) -AHPs get longer in older populations – less likely to learn. -learning reduces AHPS |
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spatial mapping
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-HP also plays a role in spatial mapping
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Corticospinal – voluntary movement
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Start at cortex
• 95% cross at pyramid • 5% ipsilateral |
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Rubrospinal – voluntary movement
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Start at red nucleus
• Cross immediately |
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neocortex
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§ 6 layered
§ Betz cells – pyramidal neurons in layer 5 that will travel from motor cortex to spinal cord § Input layer is 4 § Output layer is 5 |
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Basal ganglia
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Feedback loop, anticipation, and planning of movement
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3 layered cortex
§ Outer – molecular; where dendrites reside; also where all fibers come together § Middle – perkinje cells § Inner – granule cells |
Cerebellum
Ø Controls most movement and also mood Ø 3 parts § Anterior § Posterior § Archicerebellum (flocculonodular lobe) |
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purkinje
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3 layered cortex
§ Outer – molecular; where dendrites reside; also where all fibers come together § Middle – perkinje cells § Inner – granule cells |
