lecture 8

Question 1

what did Lashley’s (1927) studies of the localisation of memory find

Answer 1

looking for an engram: physical manifestation of memory in the brain
lesioned different percentages of the cortex, and then counted the number of errors the rat made in running through a maze to find food

Question 2

what is the case of patient HM

Scoville & Milner, 1957

Answer 2

HM had severe, medically intractable epilepsy so underwent Scoville’s radical and experimental operation that surgically excised the medial temporal lobes, bilaterally.
damage also extended to the areas surrounding the hippocampus, including the amygdala
His post-operative IQ was above average (even improved slightly), and his perception, reasoning, abstract thinking, and motivation appeared normal. He could also engage in sophisticated conversations although he spoke in monotone.
But H.M. acquired a severe and persistent amnesia,

Question 3

how global was HM’s amnesia?

typical pattern of medial temporal lobe amnesia

Answer 3

anterograde amnesia (no new memories)
retrograde amnesia with a temporal gradient (more memory loss of recent events)
for both semantic and episodic memories
no new declarative memories
no new long term memories
intact short term memory and non-declarative memory

Question 4

what is Korsakoff Syndrome (Sanders & Warrington, 1971)

Answer 4

Alcohol induced amnestic memory syndrome - common
Thiamine deficiency (vitamin B1), which affects the brain and nervous system, associated with excessive alcohol intake.
Anterograde amnesia and sometimes retrograde amnesia too.
Korsakoff’s patients typically lack insight into their condition, yet are likely to confabulate.
Prognosis is very poor.
Damage to diencephalon, especially to mamillary bodies and the thalamus.
Can extend to frontal lobe (symptoms of FL lesions include confabulation)

Question 5

what is Alzheimer’s Disease

Answer 5

Amyloid plaques - clumps of protein fragments that accumulate outside neurons
Neurofibrillary (tau) tangles - twisted strands of another protein that form inside neurons
Seen first in the Transentorhinal region on the border of the perirhinal cortex
Hippocampus sees the greatest cell death and atrophy
Proceeds to spread to other brain areas
Extends to medial temporal lobe and other regions of the brain
Most common form of dementia in elderly population: 7% people over 65 40% people over 80
‘Recent’ memory affected initially; ‘remote’ memory affected at later stages.
Progressive decline in cognitive function.
Life span 3-20 years (8 on average)

Question 6

what is the delay-biron circuit

Answer 6

hippocampus, entorhinal cortex, retrosplenial cortex, fornix, cingulate gyrus, anterior thalamus, mammillo-thalamic tract, mammillary bodies
damahe to any one of these areas is proposed to produce amnesia

Question 7

what is the taxonomy of memory

Answer 7

short term memory
long-term memory - declarative and non declarative
declarative memory - episodic and semantic
non-declarative memory - procedural, perceptual represenation system, classic conditioning, non-associative learning

Question 8

what is consolidation theory?

the standard model

Answer 8

accounts for the gradient of retrograde amnesia
information is initially registered in widespread areas of the sensory neocortex
this is bound into a memory trace in a short term synaptic consolidation process
longer term systems consolidation depends on the hippocampus for storage and retrieval
the contribution of the hippocampus diminishes with time until the neocortex alone is capable of sustaining the permanent memory trace

Question 9

what are the potential challenges to consolidation theory

Answer 9

can’t determine how steep the gradient of retrograde amnesia is - could be almost a flat line
unclear how long consolidation takes, rodent studies would indicate the process takes seconds, while HM’s gradient seems to slop back 17 years
a decade long process seems incredulous as no mechanism can account for this variability

Question 10

what are the differences between the standard model and multiple trace theory on the role of the hippocampus

Answer 10

standard model: hippocampus plays a temporary role in the retrieval of semantic and autobiographical memory.. the neocortex plays a more permanent role in long term consolidation of these memories

multiple trace theory: hippocampus plays a role in the retrieval of autobiographical memories for the whole of a person’s life

Question 11

what is multiple trace theory (Nadel & Moscovitch, 1997)

Answer 11

Hippocampus plays a role in the retrieval of autobiographical memories for the whole of a person’s life
Each retrieval produces new traces
Old memories have been retrieved more than recent memories on average and so survive
Traumatic memories thought about lots produce lots of traces
No gradient - damage to entire hippocampus removes all traces
Greater explanatory power

Question 12

what is the difference between the standard model and multiple trace theory on spared remote memory following partial hippocampal damage

Answer 12

Standard model: attributed to completed consolidation
Multiple trace model: attributed to the fact that older memories have been retrieved more time and enough of these distributed may survive the subtotal lesion to support the memory,

Question 13

what is the difference between the standard model and multiple trace theory on localisation of episodic and semantic memory

Answer 13

Standard model: hippocampus required for consolidation of both
Multiple trace model: dissociations, with autobiographical memories more severely affected than standard semantic memories after hippocampal lesions

Question 14

what is the difference between the standard model and multiple trace theory on gradients to retrograde amnesia

Answer 14

Standard model: always gradients that can span decades such that consolidation processes must take decades to complete.
Multiple trace model: point to instances of flat or absent gradients, especially after complete hippocampal lesions. Account for this as evidence that in the total absence of the hippocampus, no traces can remain to support autobiographical memory retrieval.

Question 15

what is non declarative memory

Answer 15

Implicit LTM; can be broken down into procedural memory, perceptual representation systems, classical conditioning and non-associative learning.

Question 16

what is habituation

Answer 16

non-associative learning, the simplest form of nondeclarative memory
learning to ignore a large number of innocus stimuli
behavioural responses reinstaed by novel stimuli
Observed in aplysia to stimuli not relevant to survival
Stimulation of syphon produces withdrawal reflex - repetition habituates this response - can be reinstated with time gap
Able to target individual sensory/ motor neurons to identify how each contributes to the habituation behaviour and then identify neuronal circuitry associated with the habituation behavior

Question 17

synaptic transmission

Answer 17

action potential in presynaptic terminal opens Ca2+ channels
Ca2+ entry causes vesical fusion and transmitter release
transmitter molecules bind to excitatory receptors, receptor channels open and Na+ enters the postsynaptic cell

Question 18

modification in the strength of synapses stores learning and memory

Answer 18

with novel stimulaiton, the sensory neuron excites the interneuron and motor neuron strongly. the converging sensory and interneuron inputs on the motor neuron lead to fast withdrawl.
repeated stimulation results in habituaiton of withdrawl. The sensory neuron still produced excitatory postsynaptic potentials in the interneuron and motor neuron but they are weak - synaptic depression.

this is due to the modificationi of the presynaptic terminal
fewer packets of neurotransmitters are released by each action potential
this is due to fewer transmitter vesicles docked at release sites and fewer vesicles fusing with membranes

longer term habituation is due to inactivation of connections and structural changes such as fewer boutons

homosynaptic

Question 19

what is sensitisaiton

Answer 19

non-associative learning, a more complex form of non-declarative memory
noxious stimuli sensitise us to non-noxious stimuli

results from increase in synaptic strength such that the animal expresses an altered response to a stimulus following repeated presentation of that same stimulus

heterosynaptic facilitation

serotonin neurotransmitters bind to metabotrpic receptors
activity transmitted via the G-protein and the andeylyl-cyclase enzyme leads to cAMP activation in the sensory neuron

cAMP activates protein kinase A which acts on target proteins to enhance vesicle mobiliation and release and close K+ channels - prolonging action potentials

Long-term alterations due to regulation of protein synthesis and growth

Question 20

post-synaptic receptors

Answer 20

Ionotropic:
control transmitter-gated ion channels
when neurotransmitters bind (eg glutamate) a conformational change occurs to open channel
fast acting, short-lived effect
Metabotropic
do not have ion channels
activate second messenger systems (i.e. they engage the cells metabolism)
extracellular signal is brought into cell and is amplified and prolonged.
cAMP is not unique to neurons, rather memory has co-opted an existing efficient 2nd messenger system

Question 21

mechanisms of long-term sensitisaiotn in aplysia

Answer 21

Regulation of protein synthesis and growth
Short term alterations due to transmitter vesicle mobilisation and release (presynaptic facilitation).
Whereas more long-term alterations are achieved through regulation of protein synthesis and growth.
Cyclic AMP-response element binding protein (CREB) plays regulatory roles in these structural changes; CREB activates genes in the neuron’s nucleus that initiate new synaptic growth.

Question 22

what is pavlovian conditioning

Answer 22

associative learning
CS-US
learn about temporal contiguity and contigency

due to activity dependent enhancement of transmitter release

presynaptic component:
If action potentials in sensory neuron (CS) have opened Ca2+ channels then Ca2+ binds to calmodulin.
Makes adenylyl cyclase more effective in catalysing cAMP production.
Leads to PKA activation and ultimately more neurotransmitter release
So a serotonin signal (US) should also arrive via interneuron shortly afterwards
Action potential → Ca2+ release → calmodium → adenylyl cyclase → cAMP → PKA → serotonin

postsynaptic component
A train of action potentials produced by pairing CS and US substantially depolarizes motor-neuron and unplugs Mg2+ block in NMDA receptor channels;
Ca2+ flows in and activates a series of steps, one of which is believed to be a signal back to sensory neuron telling it to release more neurotransmitter.

Question 23

what is eye blink classical conditioning

Answer 23

n implicit learning task because EBCC can occur even when the subject is not aware that learning is occurring.
Studies in rabbits have shown that the cerebellum (and not the hippocampus) is essential for learning and retention of EBCC.
HM not impaired at EBCC (Woodruff-Pak, 1993)

Question 24

perceptual priming in HM

Answer 24

Performance of HM on a pattern priming task demonstrated intact visual pattern priming in the absence of visual pattern memory
No recollection of this

Question 25

perceptual learning

Answer 25

Repeated exposure to a certain type of stimuli improves ability to perceive fine detail and discriminate
Physiological changes underlie this e.g Expanded representations of digits
Somatosensory cortex of owl monkeys (Recanzone et al., 1992 and Gilbert et al., 2001)
Expansion of representation in sensorimotor cortex of the reading finger in human braille readers (Pascual-Leone & Torres, 1993).

Question 26

procedural learning in hm

Answer 26

Mirror task (hand-eye coordination)
Improvement with practise - but no recollection

Intact perceptuo-motor skill learning in amnesic patients
amnesic patients also faster with practice but they remain unaware of what they learnt
Sequence learning
This is impaired in PD and cerebellar degeneration patients