The Multi-Store Model, Hebbian Theory, Long Term Potentiation, Lashley's Mass Action Theory

What is the Multi-Store Model of Memory?

A model of memory proposed by Atkinson and Shiffrin → posits there are 3 separate memory stores and that information can transfer across these stores in a linear sequence (input, process, output) → wach store has a unique way of having information be processed (encoding), how much can be stored (capacity) and for how long (duration) → comprised of the sensory store, the short term memory, and the long term memory.

Who is Donald Hebb, and what was his influence?

Donald Hebb (1904-1985) was a Canadian theorist who helped shape biopsychology in the 20th century through his theory of ‘The Organisation of Behaviour’ (1949) which heavily influenced both neuroscience and computational science. He was influenced by Lashley, and taught Graham Goddard.

What is Hebb’s rule?

Cells that fire together, wire together (the law of synaptic plasticity)

What is Hebbian theory outlined in ‘The Organisation of Behaviour’?

Theory positing that each ‘psychologically significant event’ (sensations, perceptions, expectations, memories, thoughts, experiences) is a result of a particular pattern of activity in a group of interconnected neurons (cell assembly). The perception of an event involves the activation and firing of some cells, which will in turn create knock-on effects which activate some more cells → ‘When the axon of cell A is near enough to excite cell B, repeatedly and persistently taking part in its firing, some growth processes and metabolic changes takes place in one or both cells such that A’s efficiency as one of the cells firing B is increased.’

According to Hebbian theory, what is a ‘cell assembly’?

Where 2 or more cells are simultaneously active enough times to become associated enough for activity in one cell to facilitate activity in the other

According to Hebbian theory, how are long term memories formed?

Event occurs → certain cells fire together in a particular pattern (‘strengthening’ their connection when presynaptic and postsynaptic cells fire simultaneously) → while the event is in the short term memory, it’s functionally ‘reverberating activity’ in the neural network → when the event is recalled, those cells (as a ‘partial match’) repeat the firing pattern (this is called reactivation) → if this happens repeatedly (consolidation), synaptic strength increases and the memory is reinforced → the long term memory is stored by changing the strength of connections between neurons in a network

According to Hebbian Theory, what is the mark of an often-activated neuron?

Often-activated neurons have increased potential for activation (the more you access a memory, the easier it is to access)

According to Hebbian Theory, what is ‘reactivation’?

An imperfect (‘partial match’) re-expression of a perceptual experience during recall.

According to Hebbian Theory, ‘strengthening’ occurs when postsynaptic and presynaptic cells fire together, particularly repeatedly. What is then significance of ‘strengthening’?

Increasing synaptic connectivity (strengthening via consolidation) allows for associations of inputs (the associations between experiences/stimuli)

Using an example, explain ‘associated inputs’.

There is a strong synapse (in this case, from pain receptor axons) and a weak synapse (in this case, from the visual system). If you experience a visual input (seeing a crab) and a somatosensory input (pain from a puncture wond caused by the crab), cell A fires in response to the pain (presynaptic activity) and cell B fires in response to the visual input (postsynaptic activity), which increases the synaptic connectivity (‘firing together, wiring together’). This creates a greater association between the pain and the crab, meaning ‘pain’ and ‘crab’ are now associated inputs.

Associated inputs are also linked to what key psychological phenomena/theories?

Associated learning and fear responses

What is Long-Term Potentiation (LTP)?

A long-lasting increase in the strength of synaptic connections between neurons, used as evidence for models of synaptic plasticity including Hebb’s model.

How is LTP demonstrated?

Often using high-frequency electrical stimulation (HFS) that produces long-term alterations in the strength of synapses.

What does research on LTP demonstrate about synaptic plasticity?

Repeated HFS produces long-term increases in synaptic strength, as demonstrated by larger EPSPs (excitatory postsynaptic potentials, aka excitatory postsynaptic activation) → synapses and receptors change structurally, supporting neuroplasticity theories

Given that LTP is supported by evidence how does research test whether or not LTP it relates to memory?

Show that blocking LTP prevents memory formation, shows that reversal of LTP produces forgetting, show that learning leads to LTP-like changes, show that producing LTP creates false memories or masks existing memories

Does LTP blocking prevents memory formation, and how do we know?

LTP activation depends on the NMDA subtype glutamate receptor → high dosages of NMDA antagonist AP5 (blocks receptors) inhibits LTP → when LTP is blocked/inhibited, performance in a spatial memory test (Morris water maze) decreases significantly → shows that inhibiting LTP inhibits formation of memories (Davis et al 1992)

Does reversing LTP induce forgetting, and how do we know?

LTP maintenance can be prevented using zeta-inhibitory peptides (ZIP) → animals injected with ZIP are more likely to forget when they touched something that shocked them (degraded associated inputs) → indicates the memory is lost and they forget that if they do something they’ll be shocked → indicates that reversing LTP induces forgetting (Pastalkova et al 2006)

Does learning lead to LTP-like changes, and how do we know?

LTP is a model of neuroplasticity, so if you learn something through repeated exposure (practice), structural changes should be observed → basically, yes, we know that repeated stimuli exposure during learning changes the brain as seen in many neuroimaging studies

Does producing LTP create false memories or mask existing memories, and how do we know?

In the short of it, we can’t actually know, because testing this is almost impossible and often unethical

Who is Karl Lashley and what was his theory of mass action?

An American psychologist who coined the theory of ‘mass action’ - all the sites of the cortex worked to get it, so site-specific lesions may or may not alter memory, but because memory is distributed throughout the cortex, if the lesions are large enough, they disturb memory.

How did the HM case study contradict Lashley’s findings?

HM underwent temporal lobectomy (1953 at age 27), removing his temporal pole, hippocampus, and adjacent cortex. This was observed to cause severe anterograde amnesia as well as retrograde amnesia for the two years leading up to surgery. His short term memory and remote (ie. before 2 years) remained intact. He was able to improve performance on tasks, even if he did not remember practicing them. This indicates that the cortex in and of itself is not the only site or dominant site responsible for mediating memory, and that functions of memory may be localised primarily to the hippocampus and temporal lobes

HM’s deficits showed that…?

Intelligence can be dissociated from memory (IQ improved), declarative and procedural memories are distinct, the hippocampus is involved in memory consolidation