Chapter 13: Memory

William James (1890) and Memory

there are 2 types:

1. primary which is current consciousness

2. secondary which is stored memories

Atkinson-Shiffrin “multi-store” model (1968)

The model describes how incoming information is processed through different stages: it enters sensory memory (lasting 0.5 seconds for visual, 3 seconds for auditory, and 10 seconds for tactile). Unattended information is lost, while attended information transfers to short-term memory. If short-term memory is rehearsed, it encodes into long-term memory; without rehearsal, it is lost. Information not frequently retrieved may revert to short-term memory or be lost over time from long-term memory.

Baddeley & Hitch (1974)

working memory is short term memory

How long is STM and LTM

STM is 10-30 secs (can be longer with rehersal)

LTM is more than 30 secs

Long-term memory and protein synthesis

Long-term memory requires protein synthesis, meaning that the formation of long-term memories needs the creation of new proteins. Short-term memory does not require this process.

Types of LTM

Instrumental Conditioning

associative a voluntary behavior and its outcome or consequence. In 1898 it was described as trial and error learning by Thorndike, but in the 1950s it was called operant conditioning by Skinner

Classical/Pavlovian Conditioning

associate an involuntary response and a stimulus. also called reflexive learning because the response measured is a reflex.

Thorndike’s Law of Effect in Instrumental Conditioning

the consequences of a response determine whether the tendency to perform is strengthened or weakened. If the response is followed by a satisfying event, it will be strewngthened. If its not, it’ll be weakened.

Engrams

the places in the brain activated during memory formation

Karl Lashley and Engrams (1930s)

Lashley was looking for engrams of memory in rat brains after they performed maze learning. he concluded that there were not specific lesions or cuts done to the cerebral cortex that produced a clear effect.

Law of Mass Action: the more damage you do to the brain the more you effect behavior

Where are classical conditioned memories stored?

Cerebellum

Model for classical conditioning the eye blink reflex in the rabbit

Model for instrumental conditioning the Skinner box

Dopamine and Reinforcement

Dopamine is released when an unexpected reward is received. the dopamine decreases when a reward is expected but doesn’t come.

Dopamine strengthens active circuits

Cajal (1894) on Neural Mechanisms of Learning

memory is stored as an anatomical change in the strength of neuronal connections

Hebb (1949) on Neural Mechanisms of Learning

If neuron A repeatedly helps make neuron B fire, the connection from A → B gets stronger.

Evidence comes from studies of the preforant path in the rabbit hippocampus

Bliss and Lomo (2973) Discovery on Long Term Potentiation (LTP)

They discovered that giving high‑frequency tetanic stimulation to hippocampal synapses causes a long‑lasting increase in EPSP strength (the EPSP slope stays elevated for minutes to hours). This showed that synapses can undergo persistent strengthening, suggesting a cellular basis for learning and memory. Their graph demonstrated stable baseline responses → tetanus → sudden, lasting potentiation.

What are the requirements and consequences for LTP?

LTP requires presynaptic activity plus strong postsynaptic depolarization, which opens NMDA receptors. This triggers long‑lasting synaptic strengthening, including enhanced neurotransmitter release from the presynaptic cell. LTP is synapse‑specific, occurring only at the active synapse.

What is associative LTP, and how does it relate to classical conditioning?

Associative LTP occurs when a weak synapse becomes strengthened because it is active at the same time as a strong synapse. The strong input depolarizes the postsynaptic neuron enough to allow the weak input’s NMDA receptors to open, causing LTP at the weak synapse. This explains classical conditioning: a neutral stimulus (tone) becomes associated with a reflex‑triggering stimulus (air puff) because their synapses are co‑active. LTP is also specific—only the synapses that were active during depolarization are strengthened, while inactive pathways remain unchanged.

Retrograde Amnesia

old memories lost

may spare really old memories like skills

Anterograde amnesia

no new memories

for declarative memory only

Hollywood Amnesia

Episodic only

Interference with memory formation

Interfering with maintenance rehearsal for STM or encoding from STM to LTM produces anterograde amnesia

interfering with LTM or retrieval (still there, just can’t get them) produces retrograde amnesia

6 major structures in Medial Temporal Lobe in regards to Memory

1. hippocampus

2. amygdala

3. limbic cortex: entorhinal, parahippocampal and perirhinal regions

HALEPP

H.M. Case Study

HM was a patient with severe epilepsy in 1953 who had a medial temporal lobectomy that left him with severe anterograde amnesia even though he had normal STM & IQ. and he had moderate retrograde amnesia; he remembered childhood but not things from week before

3 major damage points:

1. his parahippocampal cortex was gone

2. cerebellum shrank due to anti-epileptic drugs,

3. extensive damage to hippocampus and entorhinal cortex on both sides of the brain

N.A. and B.J. Case Study

NA experienced a fencing injury that produced lesion the mammillary bodies and left medial dorsal thalamus

BJ was from the UK and damaged just their mammillary bodies

they both experienced profound anterograde and milder retrograde amnesia for explicit (NOT implicit) memories.

they had normal STM and no damage to hippocampus

Clive Wearing Case Study

he got encephalitic which caused damage to large areas of both temporal lobes.

7-second memory; anterograde and retrograde amnesia

2 spared memories:

1. wife

2. conducting and playing music

K.C. Case Study

were in motorcycle accident that cause damage to both hippocampus’s and limbic cortexs and frontal and parietal cortex

retrograde and anterograde amnesia

• episodic memories mostly gone but could rmbr family

• still had semantic memory, and capable of some new semantic learning, possibly due to spared temporal cortex

4 conclusions made from Case Studies

1. hippocampus and medial temporal lobe is needed for episodic memories

2. hippocampus and medial temporal lobe not needed for STM or implicit learning

3. hippocampus essential for semantic memories

4. NA and BJ showed that other areas, the maxillary bodies and medial dorsal thalamus are also involved

5. implicit, episodic, and semantic memories involve different, but possibley overlapping, circuits.

Location of Episodic Memory

Episodic memories may not be stored in the hippocampus/MTL b/c

• people w damage to hippocampus remember older memories

• when people are tested on recalling older memories, both the HI and CC are needed

O’Keefe and Dostoevsky (1971) Morris Water Maze in Animals

recorded individual hippocampus cells as animals moved around enclosure. found that lesions in hippocampus disrupt learning of spatial memory tasks but not learning of a single path

suggests involvement of hippocampus in spatial learning and awareness

Most severe deficits in animal hippocampal function

required damage to limbic cortex and hippocampus

What is memory reconsolidation, and why does blocking protein synthesis during reconsolidation cause memory loss?

Reconsolidation is the process where a previously stored long‑term memory becomes unstable when recalled and must be restabilized to remain stored. Like initial consolidation, reconsolidation is protein‑synthesis dependent. When a memory is recalled, it enters a fragile “active memory” state; if protein synthesis is blocked during this window, the memory cannot be reconsolidated and may be weakened or erased. This shows that memories are not fixed—they can be modified or lost each time they are retrieved.