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Comparative Approaches > Sensory Learning & Memory Formation > Flashcards

Sensory Learning & Memory Formation Flashcards

1
Q

LEARNING & MEMORY

A
  • learning = process of acquiring new info
  • memory = ability to store/retrieve info
  • changes in beh/emergence of responses caused by previous individual experience
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2
Q

DIF FORMS OF LEARNING

A
  1. NON-ASSOCIATIVE
    - habituation; sensitisation
  2. ASSOCIATIVE
    - classical/operant conditioning
  3. OBSERVATIONAL
    - imitation; stimulus enhancement; social learning
  4. TOOL USE
    - play; latent learning; insight; view-baed navigation
  5. IMPRINTING
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3
Q

OBSERVATION LEVELS

A
  1. BEHAVIOUR
    - consequences of actions/interactions w/stimuli/emotions/knowledge resulting from experience
  2. NEURONS
    - neural network activity
  3. SYNAPSES
    - interactions between individual neurons; synaptic plasticity
  4. REGULATORY/STRUCTURAL GENES
    - (de)activation; modulation of expression patterns
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4
Q

WHEN DOES ENVIRONMENT START TO INFLUENCE BEH DEVELOPMENT?

A
  • innateness = inherited; unlearned/spontaneous beh actions/responses present after birth; NOT to be opposed to learning (aka. be careful of NVSN fallacies)
  • learning/synaptic plasticity occurs across life span/development in all animals as they experience/sense/interact w/their environment
  • ie. chicks/ducks move/vocalise days before hatching
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5
Q

SELECTIVE BREEDING

A
  • bright/dull rats bred for solving maze task
  • aka. are maze-bright rats smarter > maze-dull rats?
  • artificial selection experiment on maze-running ability in rats
  • aka. can we conclude that lvls of intelligence = based on dif genotypes?
  • some heritable factors allow selection over generations that change average phenotype in offspring
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6
Q

COOPER & ZUBECK (1958)

A
  • environmental conditions can mask genetic variation & produce similar phenotypes
  • enriched environment improved performance of maze-dull rats
  • Q: does genotypic variance matter for beh of rats?
  • A: may completly/partially depend on type of environment
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7
Q

DRICKAMER ET AL. (2002)

A
  • beh/cognitive performances of individuals during development/across life are shaped by interdependent processes of gene-environment interactions/non-genetic inheritance effects
  • aka. epigenetic mechanisms by which heritable factors change gene expression in offspring
  • ie. maternal body/postnatal care via cellular processes ie. DNA methylation/small-coding RNA/histone modification
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8
Q

CLARK ET AL. (2017)

A
  • dif brain regions = involved in learning/memory
  • subcortical areas play important role in memory formation/recall
  • critically involved regions:
    1. MEDIAL TEMPORAL LOBE
    2. NEOCORTEX
    3. REFLEX PATHWAYS
    4. STRIATUM
    5. AMYGDALA
    6. CEREBELLUM
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9
Q

MEDIAL TEMPORAL LOBE

A
  • facts & events
  • declarative
  • LTM
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10
Q

NEOCORTEX

A
  • priming
  • non-declarative
  • LTM
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11
Q

REFLEX PATHWAYS

A
  • non-associative
  • non-declarative
  • LTM
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12
Q

STRIATUM

A
  • procedural
  • non-declarative
  • LTM
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13
Q

AMYGDALA

A
  • emotional
  • classical conditioning
  • non-declarative
  • LTM
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14
Q

CEREBELLUM

A
  • somatic
  • classical conditioning
  • non-declarative
  • LTM
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15
Q

GRADY ET AL. (1995)

A
  • learning & memory changes as we age
  • newly born neurons (neurogenesis) may aid learning
  • with aging humans experience decreases of dif memory types incl. spatial memory/navigational skills due to loss of neurons/connections; ie =
    1. reduction of cholinergic inputs to hippocampus/cortex (neuromodulator acetylcholine (ACh) critical for memory)
    2. white matter (myelinated axons) can change in older subjects to allow task-dependent learning in specific regions dif to younger ones
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16
Q

AMREIN (2015)

A
  • adult hippocampal neurogenesis in natural populations of mammals
  • decline of cell proliferation w/chronological age
  • possible functions = repair/plasticity
  • new neurons can be born in adult brain aka. evidence overturns old dogma
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17
Q

BARKER ET AL. (2011)

A
  • how comparative studies contribute to understanding function of adult neurogenesis
  • adult neurogenesis in both vertebrate/invertebrate brains
  • fish/amphibia = neurogenetic cells in many brain areas
  • reptiles/birds/mammals = neurogenesis largely in lateral ventricles/hippocampus (mammals); cells migrate throughout telencephalon (olfactory bulb (HVC))
18
Q

GALEF (1984)

A
  • field obvs can point to areas where organisms express special competences suggesting existence either of reflinements of known learning processes/previously unsuspected learning mechanisms
  • lab investigations of plasticity can expand/limit range of acceptable proximal explanations of changes in beh observed in field
  • field studies thus can direct lab research on animal learning toward potentially fruitful investigation areas while lab research can provide assistance to field workers in understanding beh/neurobiological mechanisms that may be responsible for acquisition/development of adaptive responses
19
Q

CAVEGN ET AL. (2013)

A
  • habitat-specific shaping of proliferation/neuronal differentiation in adult hippocampal neurogenesis of wild rodents
  • Q: can adult hippocampal neurogenesis be linked to environmental conditions a species lives in?
  • mole rats live in subterranean tunnel systems; among suface-dwelling rodents, South-African rodents live in challenging habitat
20
Q

CELLULAR MECHANISMS OF LEARNING: HEBB’S RULE

A
  • learning changes properties of synaptic transmission
  • when axon of cell A is near enough to excite cell B & repeatedly/persistently takes part in firing it = some growth process/metabolic change takes place in 1/both cells so that A’s efficiency (as 1 of cells firing B) is increased
21
Q

CAREW (2004)

A
  • homo/heterosynaptic plasticity
  • faciliation (augmentation/post-tetanic potentiation); name depends on effect duration/experimental system (ie. LTP)
  • experimentally studied since 1950s following Hebb’s prediction (aka. Hebbian synapse theory)
22
Q

SMALL NEURAL CIRCUITS IN APLYSIA

A
  • buccal ganglion
  • cerebral ganglion
  • pleural ganglion
  • pedal ganglion
  • abdominal ganglion
23
Q

NON-ASSOCIATIVE LEARNING

A
  • habituation of gill withdrawal response
  • sensitisation = tail shock precedes siphon touch (ie. prior to habituation training)
  • initial response = higher than in group that doesn’t esperience sensitising stimulus
  • no temporal association between stimuli; aka. non-associative learning
  • spaced trials = more effective than massed trials in training; aka. better LTM
24
Q

PINSKER ET AL. (1973)

A
  • long-term sensitisation
  • lasted 3 weeks
  • pretraining = habituation training (siphon touch)
  • training = 4 tail shocks p/day over 4
  • R = retention trials (siphon touch)
25
Q

CAREW (2005)

A
  • structural changes associated w/LTM
  • LTM formation requires protein synthesis/degradation
  • transient changes in activity of intracellular signaling cascades
  • LTM sensitisation -> activation of transcription factor CREB (cAMP-response element binding protein)
  • LTM requires synthesis (transcription of DNA -> mRNA & translation -> proteins)
  • CREB = transiently activated (phopshorylated) by biochemical cascades incl. cAMP/PKA
  • CREB initiates gene transcription; central gene in regulatory gene network for LTM in both vertebrates/invertebrates
26
Q

CLASSICAL CONDITIONING

A
  • neural mechanisms underlying classical conditioning (associative learning) = mostly studied in aplysia/rats/rabbits/honeybees/genetically tractable organisms (ie. mice/zebrafish/drosophilia)
  • conditioning experiments (ie. appetitive/eyeblind/taste/fear)
  • forward pairing effective in reinforcing CS
  • temporal contiguity = important
27
Q

CLASSICAL CONDITIONING: CONTROL GROUPS

A
  • backward pairing
  • unpaired presentation of CS/US
  • only CS
  • only US
28
Q

BRANDT ET AL. (2005)

A
  • medulla/lobula = visual processing
  • antennal lobes = olfactory processing
  • mushroom bodies = multimodal sensory integration; learning; memory
  • proto/deutero/tritocerebrum = central processing; executive functions
29
Q

MENZEL & MULLER (1996)

A
  • appetitive classical conditioninf of proboscis extention response (PER) w/odors in honeybee
  • olfactory honeybee system:
    1. mushroom body
    2. layeral proto-cerebrum
    3. antenna (60k receptors)
30
Q

HAMMER & MENZEL (1995)

A
  • VUMmx1 = identified neuron of reward pathway (US); unpaired neuron branching widely in bee brain
  • cell body lays in suboesophagal ganglion
  • VUMmx1 = octopaminergic; sucrose application -> excitation
  • arborisations in antennal lobe/mushroom bodies
31
Q

HAMMER (1993)

A
  • associative learning involves coincidence detection of US/CS
  • if odour (CS) = paired w/depolarisation of VUMmx1 neuron instead of sucrose -> bees acquire association between odour & reward
32
Q

HEISENBERG (2003)

A
  • drosophilia brain:
    1. optic lobes
    2. suboesophageal ganglion
    3. antennal lobes
    4. mushroom bodies
    5. central complex
33
Q

NEUROGENETICS

A
  • dissection of components of synaptic plasticity/manipulation of individual neurons
  • naturally occuring allelic variations/mutations (rare) = artificial selection of lines
34
Q

INDUCED MUTATIONS

A
  • transgenic inbred lines (ie. mice/drosophilia):
    1. KNOCK-IN/OUT
  • permanent loss/gain of function
    2. KNOCK-DOWN
    -reduced expression of gene
    3. PERMANENT KD
  • modification of DNA
    4. TRANSIENT KD
  • possible in species w/o transgenic lines
  • RNA interference (RNAi) w/double-stranded RNA segments (microRNA/small interfering RNA)
  • CRISPR/Cas9
35
Q

SIEGEL & HALL (1979)

A
  • conditioned responses in courtship beh of normal/mutant drosophilia
  • males kep in isolation before/during training trials; food chambers w/(training) or w/o (control) premated female
  • in test w/new premated female males = less likely to initiate courtship beh
  • knock-out of orb2 (2 mutant alleles tested) learn/form STM BUT not LTM (relative to wildtype control orb2); aka. suggests specific role of CPEB protein-synthesis dependent changes at synapse
36
Q

TULLY & QUINN (1985)

A
  • classical conditioning/retentio in normal/mutant drosophilia
  • olfactory shock-avoidance conditioning
  • groups of 40 placed in start tube; induced to new tubes by switching they away from light & inducing phototactic response
  • electric shock = tubes w/odour A; no shock = tubes w/odour B; rest tube = no odour/shock
  • test rest tube VS tubes w/odour
37
Q

PLOMIN (2000)

A
  • olfactory shock-avoidance conditioning in drosophilia
  • at cellular lvl molecules that act as coincidence detection = active in pre/post synaptic side of synapse
  • presynaptic = adenylyl cyclase (dependent on calmodulin (amplifies cAMP))
  • postsynaptic = AMPA/NMDA receptors
38
Q

DROSOPHILIA MUTANTS AFFECTING: 2ND MESSENGER CASCADE IN CELL

A

RUTABAGA
- affects Ca++/Calmodulin-dependent adenylate cyclase -> lower cAMP lvls
AMNESIAC
- affects neuropeptides in modulating/extending effects of 2nd-messenger cascades
DUNCE
- blocks cAMP phosphodiesterase -> v high cAMP lvls

39
Q

DROSOPHILIA MUTANTS AFFECTING: PROTEIN SYNTHESIS

A

dCREB2-b
- blocks protein-synthesis dependent LTM
- control = CXM (protein synthesis inhibitor)
RADISH
- affects enzymes involved in cytoskeletal rearrangement
- influences neuronal/synaptic morphology

40
Q

KEENE & WADDELL (2007)

A
  • drosophilia olfactory memory = single genes -> complex neural circuits
  • lots of genetic screens/reverse genetic approaches over > 30y revealed >80 genes involved in olfactory memory
  • mushroom body (MB) neurons form key neural circuits for olfactory memories
  • parallel/sequential use of dif MB neurons to dynamically process memory similar to mammalian brain
41
Q

SUMMARY

A
  • animals learn relations of stimuli/actions/outcomes based on coincidence/temporal contiguity/order
  • dif learning types
  • memories = encoded as changes in synaptic strengths/connectivities between neurons
  • memory formation = multi-step process
  • morphology of neurons/brain areas changes via synaptic phasticity/memory formation

Comparative Approaches (10 decks)

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