1 - Non-associative learning

learning

gaining new knowledge about the world and ourselves through our senses

memory

keeping that knowledge over time

Multilevel

Learning and memory work at three levels: molecules, neurons, and behaviour. It all shows up in behaviour which is what we measure

Equipotentiality

Karl Lashley's idea that any part of the cortex can store memory. He lesioned rats' cortex: location didn't matter, but more damage meant worse performance on a rat maze running task. Lashley was searching for the engram, the physical trace of a memory.

Equipotentiality criticism

Big lesions also damaged vision and movement, so rats may fail for non-memory reasons, also contradicted by Broca, Wernicke, and HM

Brcoa/Wernicke

Mid-19th century neuroscientists studied patients with lesions - linking language production (Broca - posterior inferior frontal gyrus) and processing (Wernicke - posterior superior temporal gyrus) to specific regions - suggested memory may also be localised.

HM

Henry Molaison studied by Brenda Milner from the 1950s. He had amygdala, entorhinal cortex and hippocampus removed on both sides and could no longer form new memories

Engram

The idea that specific brain regions can store specific memories - the opposite of equipotentiality

HM criticisms

One case only - several structures were removed at once, it showed regions are needed to form memories, not that memories are stored there - bro also had epilepsy and an atypical brain

Aggregate field hypothesis

Memory is stored in the bioelectric field made by many neurons' combined activity (Lashley and others)

Synaptic plasticity

Memory is stored by changes in the connections between neurons (Ramon y Cajal, Hebb)

Tractable

A behaviour simple enough to link neural changes causally to learning - by the 1960s this was needed to separate the two hypotheses

Types of learning

Simple - nonassociative (habituation, sensitisation) and associative (classical, instrumental). complex - latent, observational, etc....

STM vs LTM

STM lasts minutes to hours. LTM lasts days, weeks, or longer

Nonassociative learning

The simplest learning - you learn about one stimulus on its own. It's found across the animal kingdom, even in Hydra which has no brain

Habituation

A reduced response to a repeated stimulus . In rats - a sudden stimulus makes the rat jump. With repeated presentation, the startle gets smaller. In infants - orienting, the infants look towards a new stimulus, and with more repetition, they look less

Habituation criticism

In the orienting and rat examples we only observe this behaviour - a weaker response could mean learning, but it could also mean tiredness, boredom, or the sense organ adapting

Why do we use simple systems to study habituation/sensitisation?

Habituation is conserved across animals, some invertebrates have simple, accessible nervous systems

Sensitisation

An increased response, usually after a strong or noxious stimulus. In Aplysia, the trigger is a tail shock

Why does a response get weaker in habituation?

The path is environmental stimulus -> sensory organ -> sensory neurons (SN) -> interneuron (IN) -> motor neuron (MN) -> muscle -> behavioural response. there are three competing hypotheses

Why does a response get weaker?

H1 - Sensory adaptation, the sense organs get less responsive. The change happens at the start (sensory organs/neurons)

H2 - Habituation - the central nervous system learns to respond less. change in the middle (interneurons/CNS)

H3 - motor fatigue, the muscles get tired. change happens at the end (muscular/skeletal side)

criticisms for H2- habituation

Habituation is proof by elimination - showing H1 and H3 are false makes H2 more likely, but doesn't directly prove it

Habituation in Neohelice grantula

Crabs found in Argentina. experiment - a shadow passes overhead like a predator and the crab shows an escape response. This reduces over trials. Tomsic et al., 1991 used a bowl with dim illumination, a moving shadow and a transducer to measure the crabs movement

Ruling out H3 - motor fatigue

GABA relaxes the muscles, and glutamate contracts them. Habituation cannot be explained by motor fatigue because in the absence of motor response, the escape response habituates. If muscles are relaxed by GABA they cannot be getting tired from responding.

Ruling out H1 - sensory adaptation

Researchers used calcium imaging and intracellular recordings of the LG neurons (lobula giant neurons) across repeated stimuli (Beron de Astrada et al., 2013). the early visual pathway stays responsive - LG neuron activiy falls within the behaviour, with photoreceptors and peripheral cells not adapting, so the change is in the CNS.

Criticism - LG activity tracking behaviour is correlational - one species and stimulus - occurs in CNS is still fairly broad

Why is Aplysia californica (sea hare) good for studying nonassociative learning?

1. simple nervous system - its 'brain' has 10,000 neurons ish - a rat brain has 200 mil, human 100 bil

2. big, identifiable neurons - 1mm across, so you can place electrodes on single cells. organised in ganglia, number of nerve cells behind behaviour can be small, and the same cell can be found across different animals

3. simple behaviours such as the gill and siphon withdrawal (GSW) reflex. a touch stimulus to the siphon activates sensory neurons (SN) which synapse onto motor neurons (MN) that control the gill muscles, causing contraction

Aplysia criticism for studying NA learning

big advantage is causal access to the circuit. limitation is generalisation - its a sea slug with one reflex, so findings need support from vertebrates

Habituation in Aplysia

Carew et al., 1972 - repeated gentle siphon touches (4 sessions daily, 10 trials each) cause habituation. The gill contraction becomes weaker and shorter - this is behavioural evidence

Cellular mechanism of habituation

Castellucci and Kandel, 1974 - habituation is homosynaptic (the change happens in the same pathway being stimulated, the SN-MN synapse) and caused by synaptic depression (reduced release of synaptic vesicles from the synaptic neuron). Fewer vesicles means a weaker signal to the motor neuron, so the gill moves less

Synapse-specific

Only the repeatedly stimulated pathway weakens - the mantle and siphon pathways are unchanged and still respond normally. This supports habituation being real learning and not general fatigue

Short vs long term habituation

Castellucci et al., 1978 - one session of 10 trials gives habituation lasting several minutes. Four sessions over 2 days gives long-term habituation lasting up to three weeks, relying on fewer SN-MN synaptic contracts. Short term = synapse works less well. Long-term = synapse physically changes - the same pattern appears in sensitisation

Habituation (strength)

A good example of multilevel evidence - the behaviour changes, and the matching change is seen in a single identifiable synapse, linking th levels

Habituation (limitaiton)

The long-term result shows a correlation between fewer active connections and long-term habituation. Its strong in this system but not proof of cause - correlational

Sensitisation in Aplysia

Training 4 shocks per day for 4 days, with siphon touched 5,12 and 26 days after. The gill withdrawal reflex was stronger, and sensitisation was seen even 3 weeks after training. The simple manipulation/accessible circuit make it good for studying molecular basis

Cellular correlate of sensitisation

Brunelli et al., 1976 - compared touch only with sensitised animals (tail shock plus touch) - sensitised animals showed bigger synaptic potentials and bigger behaviour

Facilitating interneuron

Sensitisation - relays tail-shock information and releases serotonin (5-HT) onto the sensory neuron at an axo-axonic synapse. think of the tail shock as an alarm, the interneuron carries the alarm and turns up the volume on the sensory neuron

S-A-c-P

1. Serotonin activates adenylyl cyclase (AC) in the sensory neuron, which raises cAMP, activating PKA. 2. PKA then inactivates K+ channels, so more Ca2+ enters during action potentials 3. this increases the pool of available vesicles and boosts release machinery 4. this promotes Ca2+ channel opening. more glutamate is released onto the motor neuron on a siphon touch, so the gill withdraws more strongly - but this increase in neurotransmitter only lasts about 2.5 minutes

Long-term sensitisation (hours to days)

Requires gene expression - and shows growth of new SN-MN connections. Long-term sensitaiton involves repeated serotonin pulses, PKA signalling into the nucleus, CREB (transcription factor) and new protein synthesis.

Sensitisation criticisms

Uses an aversive tail shock - its a clear case of the meaning of a stimulus changing the response, but it snot exactly the same as the repeated stimulus definition earlier on