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GBB > Cognition And Memory > Flashcards

Cognition And Memory Flashcards

1
Q

HM

A
  • partially spared retrograde amnesia
  • impaired anterograde amnesia
  • MTL damaged (hippocampus)
  • working memory in tact
  • procedural memory in tact
  • difficulty with episodic, declarative memory
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2
Q

Redefining procedural memory pathway

A
  • hippocampus is not needed to process procedural memories

- log-term procedural memories are stored in basal ganglia, cerebellum and motor cortices

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3
Q

Declarative memory

A
  • episodic (events)

- semantic (facts)

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4
Q

Nondeclarative memory

A
  • skill learning
  • priming
  • conditioning
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5
Q

Cell assembly

A

-ensembles of neurons linked via hebbian synapses could store memory traces

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6
Q

Charles Sherrington

A
  • speculated that alterations in synapses were the basis for learning
  • changes can be presynaptic, postsynaptic or both
  • changes can include increase NT release or effectiveness of receptors
  • structural changes at the synapse may provide long-term storage
  • new synapses could form or Somme could be eliminated over time/training
  • training/experience might lead to synaptic reorganization
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7
Q

Memory storage requires neuronal remodelling

A

-lab animals living in complex environment demonstrated biochemical and anatomical brain changes from those I’m simpler environment

  • 3 conditions
    1. Standard condition
    2. Impoverished condition
    3. Enriched condition
  • animals in EC developed thicker cortex
    • enhanced cholinergic activity
    • more dendritic branches (esp on basal dendrites)
    • more spines suggesting more synapses
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8
Q

Storing information in NS

A
  • hebbian synapses occur when successful stimulation of a cell by an axon leads to enhanced ability to stimulate that cell in the future
    • increases in effectiveness occur because of simultaneous activity in the presynaptic and postsynaptic neurons
    • such synapses may be critical for many kinds of associative learning

-aplysia (invertebrate) studied due to large neurons

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9
Q

Habituation

A

-decrease in response to a stimulus that is repeatedly presented an accompanied by no change in other stimuli

  • results in a change in the synapse between sensory neurons and motor neurons
  • sensory neurons fail to excite motor neurons as they did previously
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10
Q

Sensitization

A

-an increase in response to a mild stimulus as a result to previous exposure to a more intense stimulus

  • changes at the synapse include:
    • serotonin release from a facilitating neurons blocks K+ channels in presynaptic neuron
    • prolonged release of transmitter from that neuron results in prolonged sensitization
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11
Q

Aplysia

A

-used to study plastic synaptic changes in neural circuits

  • has fewer nerve cells
  • can create detailed circuit maps for particular behaviours
  • shows habituation
    • squirts of water in siphon cause it to retract gills
    • habituation causes it to retract less
    • habituation caused by synaptic changes between sensory cell in siphon and motor neuron that retract gill
    • less NT release in synapse results in less retraction
    • over several days, habituated faster
      • represents long term habituation
    • number of synapses between sensory cell and motor neuron is reduced
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12
Q

LTP

A
  • first described by Bliss and Lomo (1973) at glutamatergic synapses in hippocampal formation
  • dorsal hippocampus of anaesthetized rabbit was exposed
  • high frequency stimulation of performance pathways fibres (inputs) to dentate gyrus cells produces an increase in amplitude of excitatory postsynaptic potentials
    • lasting for hours or days
  • high frequency stimulation cause LTP
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13
Q

Facilitation

A

-amplitude of postsynaptic response increases when postsynaptic cell is activated several time in quick succession

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14
Q

Tetanus

A

-brief increase of electrical stimulation that triggers thousands of axon potentials

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15
Q

LTP

A

-stable and enduring increase in effectiveness of synapses

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16
Q

LTP in hippocampus

A
  • tetanus drives repeated firing
  • postsynaptic targets fire repeatedly due to stimulation
  • synapses stronger than before
17
Q

Storing info in NS

A

-LTP occurs when one or more axons bombard a dendrite with stimulation

  • properties of LTP that suggest learning and memory
    1. Specificity
    • only synapses onto a cell that have been highly active become strengthened
  1. Co-operativity
    • simultaneous stimulation produces LTP much more strongly than one stimulation by single axon
  2. Associativity
    • pairing a weal input with a strong input enhances later responses to weak input
18
Q

Synaptic plasticity in hippocampus

A
  • LTP in hippocampal formation (hippocampus, dentate gyrus and subiculum)
  • hippocampus has CA1, CA2, CA3
19
Q

LTD

A
  • long term depression

- prolonged decrease in response at a synapse that occurs whe axons have been active at a low frequency

20
Q

AMPA receptors

A

-bind glutamate agonist AMPA

21
Q

NMDA receptors

A

-names after selective ligand NMDA

22
Q

Neurochemical changes of LTP in CA1 region

A
  • transcription dependent
  • Actinomycin D inhibited maintenance of LTP in rats
  • Actinomycin D inhibits transcription by binding DNA
  • glutamate activates AMPA-R
  • NMDA receptors dont response UNTIL enough AMPA-R are stimulated and neuron is partially depolarized (-35mV)
  • NMDA-R at rest have Mg2+ block on Ca2+ channels
  • repeated glutamate excitation of AMPA depolarizes membrane and Mg2+ block removed from NMDA
  • Ca2+ can enter NMDA and activate protein kinases
  • CaMKII causes more AMP-R to be produced
    • moves existing AMPA into active synapse
    • increase conductance of Na+ and K+ ions

-dendritic branching increased

23
Q

Neurochemical changes cont

A
  • strong stimulation of POSTSYNAPTIC cells releases retrograde messenger (CO or NO) that travels across synapse and alters function of presynaptic neuron
    • decreases AP threshold
    • increase release of NTs
    • expansion of axons
    • NT release from additional sites

-these increase sensitivity to glutamate to strengthen synapse

24
Q

CREB

A
  • activation of protein kinases also triggers protein synthesis
  • CREB (cAMP responsive element biding protein) activated
  • CREB binds to cAMP in DNA promoter region
  • CREB changes the transcription rate of genes
  • regulated genes then produce proteins that affect synaptic function and contribute to LTP (eg more AMPA and NMDA receptors)
25
Q

LTP as a part of learning and memory formation

A
  1. correlational
    • time course of LTP similar to that of memory formation
  2. Somatic intervention exp.
    • pharmacological treatments that block LTP impair learning
  3. Behavioural intervention exp.
    • training an animal in a memory task induces LTP
26
Q

HDAC inhibitors

A
  • TSA and sodium butyrate both enhance induction of LTP

- inhibit acetylation

27
Q

Contextual fear conditioning behaviour paradigm

A
  • animal in training chamber paired foot shock to light of being removed from box
  • contextual fear memories are stored within amygdala and area CA1 of hippocampus for at least 24. Hr after contextual fear conditioning
28
Q

HDAC inhibitors

A
  • increased histone h3-acetylation and enhanced the formation of long term contextual fear memory
    • enhance freezing behaviour

-HDACI (SB) did not effect animals ability to perceive and respond to foot shock

29
Q

DNMT inhibitor in hippocampus

A

-blocks formation of LTP

  • animals injected with DNMT-I (sits in replication fork to stop methylation)
    • did not effect animals ability to perceive and respond to foot shock

-DNMT-I specifically blocked formation of long-term contextual fear memory

  • injected with HDACI and then DNMT-I DO NOT show memory impairment
    • due to timing
    • treating with TSA opens chromatin and allow demethylation machinery to come in, then no DNMTs present to Change activity
    • demethylation has already occurred
30
Q

Histone acetylation in LTP

A

-DNMT activity not only necessary for memory and plasticity but that DNA methylation works in concert with histone modifications to regulate plasticity and memory formation in hippocampus

  • particular methylation patterns are important
    • DNMT inhibitor strips off all methylation
31
Q

Events

A
  • activation of AMPA
  • removal of Mg2+ from NMDA
  • influx Calcium
  • activate PKC
  • extracellular kinase
  • phosphorylation of CREB
  • recruitment of CBP
  • acetylation
32
Q

Molecular basis of aging-related memory decline

A

-decrease in spatial memory and navigational skills

  • causes:
    • impairment of coding and retrieval -less cortical activation in some tasks
    • loss of neurons and connection
  • deterioration of cholinergic pathways (provide input to hippocampus and cortex)
    • Ach pathways lost in Alzheimer’s
  • enhancing cholinergic transmission helps with memory tasks
33
Q

Improving cognitive functions

A
  • Nootropics
    • enhance cognitive function
    • AChE inhibitors
    • AMPAkines (bind AMPA-R and enhance hippocampal LTP) increase calcium
    • PKMZ needed for LTP and memory traces (retardation if impaired)
  • lifestyle factors
    • living in favourable environment (less glucocorticoid)
    • stimulating activities
    • having partner of high cognitive status
  • epigeneotype shaped by lifestyle
    • epigenetic mechanisms (ncRNA) involved in memory formation
    • diet and housing
    • aging associated with disruption of memory-triggered epigenetic changes
  • development of selective memory enhancing drugs
    • opposite: PTSD drugs to help
34
Q

Nootropic effects and benefits

A
  • yerkes-Dodson’s law
    • certain stimulants enhances cognition non low doses but at high doses results in cognitive deficits
  • difficult task
    • multiple pathways may be involved and if the drug only targets one pathway it may impair function overall
    • need selected paths working in coordinated fashion

-AMPA and NMDA have glucocorticoid receptors

GBB (9 decks)

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