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
2
Q
DIF FORMS OF LEARNING
A
- NON-ASSOCIATIVE
- habituation; sensitisation - ASSOCIATIVE
- classical/operant conditioning - OBSERVATIONAL
- imitation; stimulus enhancement; social learning - TOOL USE
- play; latent learning; insight; view-baed navigation - IMPRINTING
3
Q
OBSERVATION LEVELS
A
- BEHAVIOUR
- consequences of actions/interactions w/stimuli/emotions/knowledge resulting from experience - NEURONS
- neural network activity - SYNAPSES
- interactions between individual neurons; synaptic plasticity - REGULATORY/STRUCTURAL GENES
- (de)activation; modulation of expression patterns
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
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
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
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
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
9
Q
MEDIAL TEMPORAL LOBE
A
- facts & events
- declarative
- LTM
10
Q
NEOCORTEX
A
- priming
- non-declarative
- LTM
11
Q
REFLEX PATHWAYS
A
- non-associative
- non-declarative
- LTM
12
Q
STRIATUM
A
- procedural
- non-declarative
- LTM
13
Q
AMYGDALA
A
- emotional
- classical conditioning
- non-declarative
- LTM
14
Q
CEREBELLUM
A
- somatic
- classical conditioning
- non-declarative
- LTM
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
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
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
CAREW (2005)
- 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
CLASSICAL CONDITIONING
- 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
CLASSICAL CONDITIONING: CONTROL GROUPS
- backward pairing
- unpaired presentation of CS/US
- only CS
- only US
28
BRANDT ET AL. (2005)
- medulla/lobula = visual processing
- antennal lobes = olfactory processing
- mushroom bodies = multimodal sensory integration; learning; memory
- proto/deutero/tritocerebrum = central processing; executive functions
29
MENZEL & MULLER (1996)
- 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
HAMMER & MENZEL (1995)
- 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
HAMMER (1993)
- 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
HEISENBERG (2003)
- drosophilia brain:
1. optic lobes
2. suboesophageal ganglion
3. antennal lobes
4. mushroom bodies
5. central complex
33
NEUROGENETICS
- dissection of components of synaptic plasticity/manipulation of individual neurons
- naturally occuring allelic variations/mutations (rare) = artificial selection of lines
34
INDUCED MUTATIONS
- 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
SIEGEL & HALL (1979)
- 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
TULLY & QUINN (1985)
- 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
PLOMIN (2000)
- 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
DROSOPHILIA MUTANTS AFFECTING: 2ND MESSENGER CASCADE IN CELL
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
DROSOPHILIA MUTANTS AFFECTING: PROTEIN SYNTHESIS
dCREB2-b
- blocks protein-synthesis dependent LTM
- control = CXM (protein synthesis inhibitor)
RADISH
- affects enzymes involved in cytoskeletal rearrangement
- influences neuronal/synaptic morphology
40
KEENE & WADDELL (2007)
- 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
SUMMARY
- 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
flashcards
Decks in class (10)
# Cards
-
Nerve Cells & Behaviour39
-
How Vision Guides Action20
-
Visual Processing26
-
From Receptor Signal to Perception34
-
Similarities & Differences Between Senses25
-
How Hearing Guides Action18
-
Sensory Learning & Memory Formation41
-
Spatial Learning27
-
Vocal Learning30
-
From Sensory Plasticity to Behaviour25
