week 11 Memory and Language Flashcards
Understand the concept of the Hebbian synapse and habituating and sensitization in Aplysia.
The concept of a Hebbian Synapse is that with use (learning), the structure of a synapse changes or the strength of it changes. ie the presynaptic neuron becomes better at affecting the post synaptic neuron. (via changes occurring in one/other/both neurons)
Aplysia are sea slugs with a very basic neural system, so studied in neuroscience.
Habituation=a repeated stimulus produces less of a response.eg in Aplysia initially a squirt of water causes mantle to draw in. After a few repeats, there is less neurotransmitter released by the presynaptic cell at the synapse, thus the motor neuron does not develop an ap and there is no retraction of the mantle.
Sensitization= exposure to strong stimuli means subsequent exposure to mild stimuli results in a heightened response. eg Strong stimulus to aplysia’s skin causes withdrawal. Later, light touch results in withdrawal.
Understand the concept of Long-term Potentiation and the underlying chemical mechanisms.
synapse between 2 neurons is becoming stronger. An explanation for how long term memories might form.
A. Specificity;around a cell some synapses have been very active, and others not. The very active synapses are strengthened.
B. Cooperativity; close to simultaneous stimulation by 2 or more axons produces more LTP (long term potentiation) than does repeated stimulation by 1 axon.
C; Associativity;pairing a weak input with a strong input enhances later response to the weak input. Pavlov’s conditioning might work this way.
CHEMICAL MECHANISM of LTP;one example is with Glutamate receptor varieties AMPA and NDMA.The NDMA receptor under normal circumstances has a magnesium ion sitting on it and thereby blocking it’s calcium channel. When more glutamate is being released by pre synaptic axons, sodium enters post synaptic cell and depolarises, thus the change inpolarity repels the magnesium away from the NDMA recpetor, allowing calcium to enter the cell. Calcium in the cell results in a series of events culminating in the release of a protein called creb. Creb enters the cell’s nucleusand regulates the expression of some genes. This altyeration of gene expression may last for years. This is an epigenetic change. This is how LTP works (there may be variations). In addition, the dendrites release brain derived neurotrophic factor which helps to maintain LTP. LTP may occur by increased responsiveness of AMPA receptors, new dendrite branches , and sometimes retrgrade neurotransmitter (released post synapse but acts pre-synapse) and or synapses etc. Once LTP is established, it is not reliant on NMDA receptors. Drugs which interfere with NMDA receptors impede new learning but do not affect what has already been learnt.
Long Term depression (not the illness) is where over time there is a decreased response of the synapse, the opposite of LTP.
During REM sleep, weak synapses are culled. During REM sleep, there is chaotic, unpatterned activity and so prior weak associations can be lost as no longer working together.
Distinguish between short- and long-term memory.
Short Term Memory(STM); events that have only just occurred. For most people, limit of 7 items.Short duration. Requires attention. Electrical neuronal activity. The concept these days has largely now shifted to “Working Memory”.
Long Term Memory (LTM); events from earlier. Possibly unlimited capacity?Potentially unlimited durability??Requires structural change (long term potentiation).
Many memories seem somewhere in between short and long term.
In time, episodic memory tends to become more like semantic memory as facts remain but context tends to be hazier.
What is Hebb’s explanation for the conversion of information from short-term storage to long-term storage? What is a reverberating circuit and what is its function? What does the term ‘consolidation’ refer to in this context?
suggested short term memories reverberate or keep re-exciting neurons in a loop until after sufficient time, are converted to long term memories via a process of consolidation (possibly new synapses or other long term change).
What is working memory? What are its components and what do they do?
“Working memory” is the memories currently having attention. Components include the Central Executive Pre frontal cortex which manages things), Phonological Loop (for auditory and language), Episodic Buffer (link between short term and long term memory) and Visuospatial Sketchpad (for images and spatial connections).
What is amnesia? Distinguish between retrograde and anterograde types.
Amnesia= inability to recall memories. May be very mild, may be very specific, may be quite widespread.
Anterograde Amnesia-reduced memory for events after brain damage/incident. Tends to be more severe than retrograde. ie difficulty forming new memories esp long term ones.
Retrograde amnesia; reduced memory for events before brain damage/incident. Often more psychological aetiology than trauma/dz.
Global amnesia is a combination of retrograde and anterograde. Most people with a brain injury have global.
Understand clinical evidence (from patient HM) that the hippocampus is important in memory formation. In your answer consider the differences between retrograde vs anterograde memory deficits.
Hippocampus very important for working memory and explicit memory and spatial memory. Hippocampus is involved in consolidation (short term becomes long term memory). Theorised hippocampus might somehow work as a kind of “index system” for long term memory. It seems more important for long term memory of a few years and less important for long term memory of decades.
Patient HM had damage bilaterally to medial temporal cortex, hippocampi and possibly thalamus post surgery for intractable epilepsy. HM’s signs included emotional placidity, severe anterograde amnesia and retrograde amnesia. Personality and intellect remained the same.
Compare HM’s declarative memory to his procedural memory, and his implicit memory to his explicit. How were these different aspects of memory tested? What do the results suggest?
Procedural memory better. Able to get better at “drawing the star in the mirror” task but had not remembered that he had done the task the previous day/s.
Implicit memory better than explicit. Wary of shaking someone’s hand who had previously concealed a thumbtack in their handshake, but did not remember meeting them before.Poor at forming new memories, able to form limited semantic memories (facts) ie learnt a few famous names after his surgery.
His working memory was normal. Severe anterograde amnesia for declarative memory. Severe episodic memory loss including most from before surgery.
(note that declarative memory=explicit memory). (procedural memory is a type of implicit memory)
Although the hippocampus is important for memory formation, it is not entirely clear what role it plays. This is possibly because the hippocampus contributes in numerous ways to memory and behavior. HM’s performance suggests that the hippocampus is important for storing long-term memories but that, once stored, these memories are consolidated somewhere else (in the cortex, especially in the frontal lobe) and accessed from there (There is evidence that this consolidation process occurs during sleep). There is also evidence that the hippocampus is specialized for storing declarative information; that it is important for spatial memory (and cognitive ‘map- building’); and that it is critical for contextual learning. After reading this section of the text you should be able to comment on some of the evidence consistent with each of these putative roles for the hippocampus.
Hippocampal damage impairs performance in animals on “delayed matching to sample task” and “delayed nonmatching to sample task”.
Where hippocampal-damaged rats managed to learn things, their learning showed to difference with context changes.
Rats with damaged hippocampi forget which maze arm they have explored. Hippocampal damaged rat can slowly learn where platform is in Morris water maze, but is disorientated if start position is altered.
What is Korsakoff’s syndrome? What are its main symptoms? What is its primary chemical cause (and relate this cause to chronic alcoholism)?
Usually from chronic excessive alcohol consumption with a poor diet. Vitamin B1 deficiency. Amnesia, confusion,confabulation,apathy. Thiamine deficiency (vit b1) causes neuronal shrinkage.
Which brain region is implicated in Korsakoff’s syndrome? Note that anterograde and retrograde amnesia co-occur in this syndrome.
Damage to Mammilary bodies and Dorsomedial thalamus.
What are the symptoms that characterize Alzheimer’s disease? Is procedural memory disrupted to the same extent as declarative memory?
Memory fluctuates (ie part of issue may be lack of alertness/arousal). Progresses over time. Latter stages of confusion, depression, hallucinations,delusions, insomnia and lack of appetite. Initially are quite good with procedural memory and patchy with declarative/episodic memory.
Understand evidence of a genetic component to Alzheimer’s disease. What are amyloid deposits and what role do they appear to play in the disease? The cortex and hippocampus appear to be particularly susceptible.
As those with Down’s Syndrome (3 x chromosome 21) who survive into middle age tend to develop early onset alzheimers (early onset alzheimers=develop before age 60), found some genes linked to early onset form. However late onset form is far more usual (affecting 5% between age 56 and 74 and higher percentage in olders) and whilst there are multiple genes involved it seems genes are only a weak aspect, and of those, some are epigenetic in nature.
In the early onset form, genes involved seem to cause increased amyloid-beta to accumulate. This damages axons and dendrites and they form plaques damaging cerebral cortex and hippocampus. But this is not clear cut, as many with older onset azheimers have no amyloid and many olders with amyloid have no alzheimers. Some believe the problem is increased level of Tau protein. When there is much amyloid, this causes phosphate groups to bind to tau which disrupts its usual ability to bind in axons so it lodges in cell bodies and dendrites. Damaged alzheimer brain areas seem to correlate better with where there are areas of tau as opposed to amyloid. Tau forms tangles which form from degeneration of neurons.
Be familiar with the role of the striatum in memory.
Striatum=caudate nucleus and putamen (part of basal ganglia). Important for Probalistic learning (learning to guess fairly accurately what is most likely, by considering multiple clues).
Parkinsons have impairment to striatum.(do not acquire non verbal habits)
Note also that most parts of the brain contribute somehow to memory eg amygdala for fear memories, parietal lobes for associations between memories.
Be familiar with the concept of Semantic Dementia.
Mainly damage to Temporal Lobe (anterior temporal cortex). Often is a forgetting of the colours of common fruits or appearance of various animals etc.
