Intro to Brain and Behaviour - Learning, Memory and Amnesia (Chp 11)

Learning

how experiences change the brain

Memory

how the experiences that change the brain are stored and reactivated

Capacity of short term memory

• 7 seconds ± 2

• reheasing gets it into long term memory

Amnesia

any pathological loss of memory

Retrograde amnesia

• unable to recall memories from before a disease or injury

• backward acting

Anterograde amnesia

• unable to form new memories

• forward acting

Case of HM

• medial portions of temporal lobes were removed as a treatment for severe epilepsy

• seizures were reduced

• memory deficits were instrumental

• mild retrograde and severe anterograde amnesia

Tests used to assess HM anterograde memory deficits

• digit span - could repeat digits as long as the time between learning the digits and having to repeat them was short

• block tapping - he demonstrated amnesia was not limited to one part of his brain

• mirror drawing - improved but not aware of improvement

• incomplete pictures

• pavlovian conditioning

Major findings of HMs case

1. the medial temporal lobes play an important role in memory

   • memory may not be disrupted throughout the brain

   • individual brain structure each may have their own function in memory

2. bilateral medial temporal lobectomy took away HMs ability to form certain kinds of long term memories without disrupting performance on tests for short term memory

   • theres different storage for short term, long term and remote memory

3. memory may exist but not be recalled

   • two catgories of long term memory were created - explicit and implicit

Remote memory

memory for expeirences in the distant past

Two types of long term memory

1. explicit

2. implicit

Explicit long term memory

• conscious long term memories

• transferable - by telling others

• two types

  1. semantic

  2. episodic

Semantic memory

general information - words and basic facts

Episodic memory

events that one has experienced - what you did on your birthday, what you did this morning

hard to assess - doctors dont know what you have done in your life

Implicit long term memories

• unconscious memories

Medial temporal lobe amnesia

• severe antergrade amnesia and moderate retrohgrade amnesia for explicit memories

• semantic memory may function while epidosic memory does not

  • able to learn facts but do not remember doing so

• preserved intellectual functioning

• implicit long term memories - unconsciously aware

Why do we have an unconscious memory and a conscious memory

• evolution

• provides flexibility in thinking

• able to use more of brain

Global cerebral ischemia

• interruption of blood supply to brain

• damage in hippocampus and memory

• medial temporal lobe amnesia

• more widescale damage

Cerebral ischemia on hippocampus

• damage do the hippocmpaus alone can produce amnesia

• specifically damage to the CA1 pyramidal cell layer of the hippocampus

  

Transient global amnesia

• sudden onset in the absence of any obvious cause in otherwise normal adults

• episode of confusion - amnesia is short

• may be caused by stroke

• abnormalities in CA1 of hippocampus

• clear after a bit

Amnestic disorders

• korakoffs

• alzhimers

Korsakoff syndrome

• Disorder of memory

• most common in alcoholics, malntrituion, thiamine deficiency

Korsakoff syndrome - symptoms

• amnesia

• confusion

• personality changes

• physical problems

• conflabulation - saying something not true but believing its true

Damage in Korsakoff syndrome

• lesions in medial dicephalon - medial thalamus and medial hypothalamus

• damage in hippocampus and cerebellum

other difficulties or damage

• sensory and motor problems

• liver complications

• gastointestional difficulties

• heart disorders

damage not caused by one structure and is likely a combination of many structures

Amnesia in Korsakoff syndrome

comparable to medial temporal lobe amnesia in early stages

1. anterograde amnesia for explicit epsodic memories

2. in later stages - reterograde amnesia all the way to childhood

damage in medial diencephalic nuclei, mediodoral nuclie of thalamas

disease is progressive - this complicates thing, both anterograde and retrograde continue to get worse

Progression of amnesia in alzheimers disease

individual can have a shrivelled brain but still have cognitive functioning

focus on pre-dementia stage

• major anterograde and retrogade deficits in tests of explicit memory

• deficits in short term memory and implicit memory

  • verbal and perceptual info

• low levels of acetylcholine - degeneration of the basal forebrain

• implicit sensorimotor memory is still intact

Damage of neurons with alzhimers

• protiens in axons start to fold and lose structure - creates neurobibrillary tangles

• build up of beta amyloid plaques

  • glymphatic system usually gets rid of this during sleep

• begins in the medial temporal lobes - causes memory impairment

• moves to medial, prefrontal then occipital

Why does damage happen with alzheimers

• decreased acetylcholine

  • due to basal forebrain degeneration

  • degeneration is this area causes amnesia and attentional deficits

• damage is diffuse - resulting amnesia is a consequence of decrease acetylecholine and brain damage

Process of amnesia with TBI

1. A blow to the head produces coma

2. When the victim regains consciousness there is a period of confusion

3. When the period of confusion ends, the victim has retrograde amnesia for events that occurred during the period just before the blow and anterograde amnesia  for events that occurred during the period of confusion

Postraumatic amnesia

• amount of amnesia after injury - correlates to how badly the brain was injured

• period of anterograde amnesia suggests a temporary failure of memory consolidation

Coma

• pathological state of unconsciousness

• follows a blow to the head

• can last seconds, mins or weeks

• period of confusion when consciousness is regained

• longer coma = more severe amnesia

• islands of memory

Islands of memory

surviving meories for isolated events that occurred during period for which other memories have been wiped out

Memory consolidation

Process that strengthens older memories, making then more stable and resistant to disruption over time

injuries can disrupt memory consoldidation - this is why when we have a brain injury, there is associated memory loss

Affects of TBI on memory consolidation

• affects retrograde amnesia - more recent memories are more likely to be affected

• shows the gradient of retrograde amnesia - older memories are less likely to be affected

Hebbs theory of memory consolidation

• memories are initally stores in short term memory through neural activity circulating in closed circuits

• if the circuit is disrupted, the neural activity is interrupted

• this prevents the consolidation of memories into long term storage

• the disruption or failure to convert memory causes structural changes in synapses

Electroconvulsive shock

• inducing seizure like effects in the brain

• shock disrupts ongoing neural activity which can erase recent memories that have not undergone consolidation

• helps researcher understand how long memory consolidation takes

• used with severe depression

Current view of memory consolidation

• memory consolidation may continue for a long time

• memories become more resistant to disruption as they are repeatedly recalled and integrated into new contexts

Hippocampus and memory consolidation

• standard consolidation theory - dual trace theory

  • memories are intially stored in the hippocampus but are later tranfered to more stable cortical regions

  • over time memories become more resistant to dissruption as they are recelled and reactivated

  • this process turns memories into semantic memories (factual knwoledge)

  • they rely less on the hippocampus and more on cortical areas

What is the process of reconsolidation

• memory is retrieved from long term storage and its enters a labile state

• memories can be updated, modified or even disrupted when they are retrieved

• susceptibility to posttraumati amnesia increased when memories are in the unstable state

Object recognition deficits and medial temporal lobectomy oberservations

• removal of rhinal cortex - object recognition deficits

• removal of hippocampus - no effects on object recognition

• removal of amygdala - no effect on object recognition

• removal does not necessarily predict object recognition yet ichemic damage to CA1 leads to severe impairments

Object recognition deficits and medial temporal lobectomy conclusions

• ischemia induced hyperactivity in CA1 pyramidal cells of hippocampus damage neurons outside the hippocampus

• damage is hard to detect but is responsibile to severe object recognition deficits

Object recognition vs spatial memory

• rhinal cortex plays critical role in object recognition

• hippocampus plays crucial role in spatial memory - navigating through a maze

Place cells

• hippocampal neurons

• neurons that are activated when individual is in a particular location

• spatial orientation - they create a mental map of environment

Grid cells

• how place cells obtain their spatial info

• repeating pattern of hexagons to “tile” a surface of environment

• help calculate distances and directions

Jennifer aniston neurons - concept cells

• medial temporal lobe neurons that respond to specific concepts or ideas

• highly selective and specific

• respond consistently

• may respond to related concepts

Engram cells

• always changing as a result of experience

• when activated or inhibited, the retreval of oriinal experience is triggered or suppressed

• store and restore memories

Where are memories stored

diffusely in the brain so they can survive destrution of a single structure and be more resistant

Five key brain areas for memory

1. inferotemporal cortex

2. amygdala

3. prefrontal cortex

4. cerebellum

5. striatum

Inferotemporal cortex role in memory

• visual perception of objects - changes in activity seen with visual recall

• active during the retention of an experience

• complex visual functions

• storing visual input

Amygdala role in memory

• emotion learning

• memory for emotiona signifcance of experiences

• strengthens emotional memories stored in other structures

• reason why emotion provoking events are remembered better

• lesion in area can lead to lack of fear

Prefrontal cortex role in memory

• temporal order of events and working memory

• damage leads to problems with tasks involving a series of responses

• deficits in this area produce antergrade and retrogade deficits in memory

• different parts of this structure may mediate different types of working memory

  • may stores episodic memory

Cerebellum role in memory

• storage of memories of sensorimotor skills through neuroplastic responses

  • eye blink

  • working memory

• can be conditioned

Striatum role in memory

• sensorimotor tasks

• stores memories for consistent relationships between stimuli and responses

  • associations between stimuli and response

  • memories that develop over many trials

Long term potentiation

• hebb theory

• plays role in learning and memory

• process by which synaptic connections between neurons become stronger with more frequent activation

• electrophysioloigcal phenomenon

• occurs mainly in CA1- CA4 field of hippcampus

Key properties of LTP

1. can last a long time (weeks) - once it occurs, the enhanced strength remains

2. co occurrence of activity - there much be activity in both neurons

3. strong consistent signals

Evidence of LTP

1. can be elicited by low levels of stimulation that mimic normal neural activity

2. most prominant in structures of learning and memory

3. learning can produce LTP like changes in the hippocampus

4. many drugs that influence learning and memory also influence LTP

5. disruption of LTP impairs memory performance

6. memories can be induced by LTP

7. LTP occurs at specific synapses that have been shown to participate in learning and memory

LTP in learning and memory mechanisms

• key phsyiological emchanism behind learning and memory

• when neurons communicate more efficiently due to LTP, learning is cocuring a synaptic level

• neurons that fire together, wire together

• process

  1. induction - learning

  2. maintenance - memory

  3. expression - recall

Induction of LTP process - learning

1. frequent and strong APs depolarize cell, this causes magnesium block in NMDA receptor to move out of the way

2. glutamate binds to the receptor and opens calcium channels

3. the influx of calcium ions activate protein kinases

4. protein kinases strengthen the synapse between neurons by adding more receptors (more ampa receptors) and enhancing existing receptors

5. this creates a stronger synapse that is more sensitive to glutamate, more likely to make a strong connection and to be activated later

LTP with conditioned and unconditioned stimulus

• LTP records the conditional sitmulus and the unconditional stimulus

• when events happen together, the connection becomes stronger

• learning of associations - stronger connection between neurons

• long lasting changes in glutamate levels

Maintenance and expression of LTP - storage and recall

many ways in which storage and recall is maintained by LTP, neurons are always adapting in their structure in response to learning, this is esstential for storage and recall

• specific changes in neuron

• long term maintainance

Specific changes in neuron - LTP influence

• changes in the neuron are highly specific - explains why we don’t have amazing memory about everything

• dendritic spines act as isolated compartments that are strengthened by influx of calcium

• nitric oxide over sees pre and post synaptic changes, it acts as a messager and diffuses Ca back into presynaptic membrane

Long term maintenance - LTP influence

structural changes require the production of new proteins and can include

• more or larger synapses

• bigger or more dendritic spines

• changes to the shapes of membranes

these changes ensure long term maintainance of the strong connection

Complexities of LTP

theres still a lot to learn