Chapter 9 - the physical basis of memory formation

State the Hebb Rule

"Neurons that fire together, wire together"

Summarise the statistics of Australians affected in Alzheimer's disease

- 100,000 Australians effected - 1 in 25 over 60 - 1 in 8 over 80 - No simple diagnostic test - really only know for sure when post-mortem conducted - Symptoms are different for each person further complicating diagnosis

Briefly explain how amnesia can occur

- Brain trauma - damage inflicted through injury interferes with functioning. E.g. Brain injury, stroke, drug abuse etc - Neurodegenerative disease - decline in structure and function of neurons. E.g. Alzheimer's disease

Summarise the key brain structures that are damaged in Alzheimer's disease

- Degeneration of neurons in the brain (neurons become damaged, brain tissue shrinks and eventually dies) - Presence of amyloid plaques (proteins forming on axon terminals) - Amyloid is not usually found in the brain and is highly toxic to brain cells - Build-up of neurofibrillary tangles (proteins within neurons) - A massive lack of acetylcholine (an important neurotransmitter) - Usually begins in the hippocampus and other areas of the temporal lobe - Spreads to the frontal lobe - especially the pre-frontal cortex - Spreads to other areas of the brain

State the explanations of memory decline over the lifespan

- Loss of confidence - Lack of motivation - Depends on the kind of measure of retrieval used than with their age - Slowing of the central nervous system functioning (neurons in the brain decline in speed of processing) - Cognitive slowing - being unable to mentally processes information with the speed and efficiently that they once did. This has been attributed to a reduction in the size of the frontal lobes as one age.

Summarise the memory decline over the lifespan

- Memory decline is not an inevitable consequence of ageing - Most people show only minor decline in some areas of memory and can remain as mentally sharp as when they were young - Is NOT dementia - May be linked to loss of confidence and motivation rather than memory loss - Can be improved (even reversed) with training and confidence boosting

Summarise the memory processes affected during Alzheimer's disease

- Memory loss, confusion, poor judgement, disorientation, impaired attention - As disease progresses - mood and personality changes, loss of physical functioning (eg. talk, walk, control bladder etc.) - Initially, impaired declarative memory- eg. Events and names - Severe decline in episodic memory -eg. can't recall what happened yesterday - Severe decline in semantic memory -can't recall well learned facts - eg. times tables - Severe decline in procedural memory - eg can't tie shoelaces - Severe decline in working memory/short term memory - Trouble recognising close family and friends - Anterograde and retrograde amnesia - Loss of ability to learn new tasks

Briefly explain what occurs in neurons and the cells in Alzheimer's disease.

- Neurodegenerative disease that causes wide spread cell death - Post-mortems reveal deposits of plaque along the damaged synapses and tangles of brain fibres - These plaques and tangles effect neural transmission

Summarise the memory processes affected during memory decline over the lifespan

- Some decline in episodic memory - No decline in semantic memory - No decline in procedural memory - Some decline in working/short term memory: - Takes longer to retrieve declarative memories • Takes longer to process information • Reaction times increase • Divided attention more difficult • Difficulty ignoring distractions • Recognition tasks unaffected but recall tasks impaired • Problem solving can take longer • Decreased performance on complex cognitive tasks

Summarise examples and effects of neurotransmitters

Acetylcholine- Memory, learning, muscle movement Dopamine - Voluntary movement, emotional arousal, memory and learning Serotonin - Regulates sleep, regulates mood, controls eating, memory and learning Glutamate - Memory formation, learning Gamma Aminobutyric acid (gaba) - Slows down neuron activity, reduces anxiety

Summarise neurotransmitters

Are any chemical released by a neuron that alters activity in other neurons. They may also excite the next neuron, inhibit the next neuron.

Summarise the neuron functions

Axon - Carries information from the cell body to the terminal buttons Dendrites- Receive information from other neurons Soma - Cell body. Controls the maintenance and metabolism of the neuron Synapse - The junction between two neurons Neurotransmitter - Chemicals released by the terminal buttons that travel across the synapse and communicate with the next neuron.

What evidence did the case of H.M find?

Case provided evidence that the hippocampus and temporal lobes are involved in formation of new long-term memories, but are not storage sites for memories. In particular, the hippocampal area has an important role in formation of declarative explicit memories but not procedural implicit memories. No effect on STM demonstrates STM is a separate memory system to LTM and that the temporal lobe is not involved in STM.

Briefly summarise Kandel's experiment

He placed slight onto the sea slug with a pairing of touching it with a glass rod. Soon after the slug learned to withdraw its gills when a light was shone which suggest the slug formed a long term memory. It was dissected and found that extra serotonin was released and the neuron has physically changed with new dendrites formed.

Briefly explain dementia

It includes: - Large group of neurodegenerative diseases - Loss of mental capacity - Loss of memory - interfering severely with the ability to function independently -Develops progressively

Summarise Alzheimer's disease

It includes: - Most common form of dementia - Gradual, severe memory loss, confusion, impaired attention, thinking, depression. - Causes decline in all aspects of cognitive function (not just memory) - Involves anterograde and retrograde amnesia. - Affects both hippocampus and frontal cortex.

Summarise Korsakoff's syndrome

It is caused by chronic alcoholism and a Bad diet with lack of thiamine (vitamin B). Sometimes confabulate in which they make up stories to fill in the gaps in memory.

Summarise the role of the hippocampus in the formation of memory.

It is important for formation of declarative memories (consolidation). It transfers declarative information to other relevant parts of the brain for long term storage. If the hippocampus is destroyed, no new memories can be formed.

Summarise the role of the amygdala in the formation of memory

It is involved in the consolidation of emotional information in memory, especially fear. It plays a role in activating the hippocampus, therefore enhancing consolidation of declarative memory. Seizures involving the amygdala involve intense fear and damage leaves a person unable to learn a fear response through classical conditioning.

Define amnesia

Loss of memory, partial or complete, temporary or permanent

Summarise the neural basis of memory

Memories are not stored in one specific brain location. Memories are stored throughout the brain and linked together by neuron circuits. Specific brain parts crucial to memory include the temporal lobe and the hippocampus.

Summarise Anterograde amnesia

People with anterograde amnesia can't make new Long Term memories and they cannot retain memories prior to trauma. Also they cannot transfer information from STM to LTM and it includes damage to the temporal lobe and hippocampus.

Summarise the consolidation theory of memory formation

Physiological changes in brain cells occur when something is being learned and during a period of time immediately after the learning process has been completed. If memory is disrupted during the period of consolidation memory loss will occur as neural changes do not happen. It can be disrupted by head injury, amount of attention given, anxiety, disease, drug use, ECT. This process takes about 30 minutes (can be years sometimes!). Hippocampus and Medial Temporal Lobe involved and is aided by REM sleep.

Summarise the case of Henry.M

Portions of his medial (middle) temporal lobes were removed to control severe epilepsy. STM and intellectual capacity remained normal. He could no longer form long term memories after the operation. Could learn and store procedural memories but not declarative memories. Also the medial temporal lobe is 4cm underneath the temporal lobe.

Summarise the role of the neuron in memory formation

Research has shown that memory is formed due to biochemical changes in the synapses in response to different neurotransmitters (eg. acetylcholine, serotonin). New memories (either short or long term) are NOT stored in individual synapses but in the pattern of thousands of new interrelated connections. We know that there is a molecular basis to memory formation, what we do not know is exactly how thousands of these new connections hold our memories.

Summarise the neuron changes

Synapse strength can increase in 3 ways: - Release extra neurotransmitter (change in function). Increase number of receptor sites (change in structure). Growth of new synapses (change in structure). These changes mean the pathway or circuit can communicate more easily. - STM - only an increase in neurotransmitter - LTM - all structural and functional changes

Summarise retrograde amnesia

They can't remember old information and events before the injury is lost. Can lose minutes or years and usually temporary and caused by a blow to the head. Older memories return first and memories of events immediately preceding the injury are permanently lost.