The Biopsychology of
Learning and Memory

Chapter 13

Early Proposal

u   Pavlov – learning (such as classical conditioning) strengthens the connections between the involved brain areas

u   If this is the case, disrupting these connections should impair the learned response


Early Research

u    Karl Lashley – attempted to locate memory “engrams” in rats’ cortex by studying the effects of cortical cuts or lesions

u    Law  of equipotentiality – all areas of cortex seemed to be equally important to the performance of the learned response – no single critical “memory area”

u    Law of mass action – degree of impairment was correlated with amount of cortex removed, not the region of the cortex removed

u    Lashley was probably misinterpreting his results


Lashley’s Cuts in Rat Cortex


Successful Location of An Engram?

u   Richard Thompson found a nucleus in the cerebellum (LIP – lateral interpositus) essential for the conditioned eyeblink response of rabbits

   Neurons active during this learning

   Inactivating these neurons disrupts conditioning

   These neurons also appear to be active in humans during eyeblink conditioning


Hebb’s theory of memory “consolidation”

u   Hebb distinguished between STM & LTM

u   Proposed STM mediated by temporary activity in “reverberating circuits”

u   LTM depends on structural changes

u   Increased connectivity resulting from repeated activation of the same synapses caused the “consolidation” of LTMs


Retrograde Amnesia
by ECS or Other Traumas

u   Recent memories most susceptible to disruption

u   Rats given ECS 10 secs to 10 mins after learning showed decreased memory for task. ECS 1-3 hrs after learning had no effect.

u   Humans receiving ECT show decreased recall of TV shows from last 1-3 years, no impairment of memory of shows from 4-17 years ago.


Retrograde vs. Anterograde Loss


Prefrontal Cortex & Working Memory

u   Animals or people with prefrontal damage are impaired on delayed response tasks

u   Monitoring brain activity reveals that the prefrontal area is active during the delay

u   Different cells in the prefrontal region seem to represent temporary memories of               different locations or stimuli


Delayed Response Task


Piecing Together the Human Memory System From Case Reports

Different Aspects of Memory

u   Declarative memory – memories we can state in words

u   Procedural memories – motor skill memories

u   Explicit memory – conscious intentional  recollection

u   Implicit memories – memories evidenced by improved/altered performance without conscious recollection


The Sad Case of H. M.

u    Focal epilepsy uncontrolled by medication

u    Had bilateral medial temporal lobectomy

u    Epilepsy improved but memory impaired

u    Severe anterograde amnesia for declarative memories. STM normal but once HM is distracted, those memories are lost.

u    Some retrograde amnesia for things within the 2-3 years before surgery, but older memories and IQ intact


Quote from H.M. (Milner, 1970)

u    Right now, I'm wondering: Have I done or said anything amiss?  You see, at this moment everything looks clear to me, but what happened just before? That's what worries me. It's like waking from a dream; I just don't remember.


H.M. continued

u   H.M. has shown evidence of the formation of new procedural & implicit memories

u   Finger maze, mirror tracing, rotary pursuit, classical conditioning


Mirror-Drawing Task


Clive W.

u   Suffered damage to hippocampus and frontal cortex during a bout of encephalitis (this is the case that starts the chapter)

u   Extreme anterograde amnesia similar to H.M.’s  although his old LTM s are fine


Amnesia Due to Diencephalon (Thalamus/Hypothalamus) Damage

u   Korsakoff’s Syndrome - serious anterograde & retrograde amnesia but once again implicit memories are better preserved. Tendency to confabulate.

u   Due to thiamine deficiency which impairs the supply  of energy (glucose) to the brain

u   Widespread loss of neurons, most concentrated damage in mammillary bodies & DM thalamus


Alzheimer’s Disease

u    Several pathological changes in brain

    Production of abnormal amyloid protein which damages neurons, causing  distinctive tangles & plaques of neural debris

    Neuron loss heaviest in association cortex areas, medial temporal lobes, and basal forebrain (nucleus basalis of Meynert)

    dramatic decline in cholinergic (Ach) activity in the forebrain

u    Runs in families; genes on at least 4 different chromosomes have been linked to AD (21, 14, 1, 19)

u    Progressive decline in almost all aspects of memory & cognitive abilities


Memory Role of Other Areas

u   Frontal lobe - memory for temporal order

u   Amygdala - emotional significance

u   Cerebellum & Basal Ganglia - implicit, procedural memories

u   Long-term memories seem to be stored in the secondary & association cortex areas involved in the original stimulus perception