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Fundamentals of neuroscience > Hippocampal systems & memory (systems) > Flashcards

Hippocampal systems & memory (systems) Flashcards

1
Q

What is short term memory?

A

Can be held for a short amount of time

Forgotten by the end of the day

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2
Q

What is declarative memory?

A

Memories of knowing that and what, facts and events

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3
Q

What is non-declarative memory?

A

How to do memory –> skills & habits able to perform

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4
Q

Who made the simple model of memory: Aplysia?

A

Kandel - said memory is extremely complex

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5
Q

What is Aplysia?

A

Simple model that displays non-associateive learning - don’t associate a respone

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6
Q

What are Aplysia like and how did Kandel use this?

A

Have large, identifiable neurones that form identifiable circuits

Allowed Kandel to gain insights into the molecular mechanisms of memory

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7
Q

What did Kandel use to study Aplysia?

A

Used sea slugs to understand mechanims

(This is behavioural habituation)

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8
Q

What did Kandel study in sea slugs & how did he do this?

A

Habituation was studied

The withdrawal reflex was studied using a gentle stimulus

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9
Q

What did Kandel find in his study on sea slugs?

A

Response declined to the stimulus over time (there is a graph showing a decline in response)

Happens when slug realises that it is not a threat, can go away for a while and come back –> it will still remember this

(This is behavioural habituation)

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10
Q

What did Kandel use to study habituation via electrophysiology?

A

He used an abdominal ganglion

He looked at the cellular mechanisms going on, the neurones are very easy to record from

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11
Q

What was Kandal’s method of studying habituation in abdominal ganglion cells?

A
  • Simple pathway as it has a sensory neurone, brings in the info to stimulate the motor neurone to contract & withdraw the gill
  • He stuck an electrode in the cell of both sensory (pre) & motor (post) neurone, can manipulate both pathways
  • Projections on the left diagram are connecting to other ganglion as they don’t have a brain
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12
Q

What did Kandal record in the pre and postsynaptic neurones in his study?

A

Pre = sensory, post = motor

He recorded the change in membrane potential in the motor neurone

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13
Q

What were the conclusions of Kandal’s study on habituation (electro one)?

A

Single AP will not trigger AP in motor neurone, this is excitatory postsynaptic potential

Change in membrane potentials get smaller (unlike in presynaptic), this shows less gill response = suggests during habituation there is something that reduces the AP

(In simple terms = when stimulated the sensory neurone still identifies the stimulus & a reaction happens, but in the motor neurone (going to effector) the response lessesns = habituation)

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14
Q

What happens to synapses during habituation?

A

Normal synapse = leads to AP

During habituation there was a reduction in response from Ca2+ channels to the stiumulus - less Ca entering axon terminal = LESS AP so SMALLER RESPONSE!!

(Diminished EPSP)

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15
Q

How did the HM case help us to understand the hippocampus?

A

HM suffered from epilepsy - had bilateral removal of the hippocampus by Schofield –> removed epilepsy but could no longer form new memories

Helped us to understand hippocampus is important in forming new memories

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16
Q

Where is the hippocampus located?

A

Found in the temporal lobe, looking at the left side to the top (please refer to the diagram of where it is found)

Found deep in the temporal lobe = subcortical structure (below the cortex) –> hard to acces can cause damage getting to it

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17
Q

What is the structure of the hippocampus?

A
  • Is bi-lateral = spans both hemispheres
  • Essentially sheets of cells that are folded into each other
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18
Q

Please look at the diagram of the structure of the hippocampus

A

It is stained with nissl stain (stains for DNA)

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19
Q

What is the general structure of the hippocampus?

A

Has a characteristic structure of 2 interlocking C shapes

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20
Q

What are the 2 C shapes in the hippocampus called & what surrounds these?

A

Smaller one = Dentate gyrus

Larger one = known as the CA region - can be divided into CA3 & CA1

Overlaying area of cortex = entorhinal cortex

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21
Q

Does the hippocampus work alone?

A

Although it looks isolated, it doesnt work alone - does have one way circuitry

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22
Q

What is the long tail of the hippocampus calld & used for?

A

Called the fornix, has a major output of the hippocampus

23
Q

What is the fornix (tail) made up of?

A

It is a white matter tract (like corpus callous)

White matter is myelinated axons - they’re projecting to different parts of the brain

24
Q

Where in particular does the fornix (tail) branch to?

A

Branch to mamillary body on the left side at the end of the hippocampus

Mamillary plays a key role in the limbic system

25
What sort of cells are found in the CA regions of he entorihnal cortex?
Pyramid neurones
26
What type of cells are found in the Dentate gyrus?
Granule cells
27
Where does info enter the entorhinal cortex? (You will defo need to refer to the diagram for this)
Info comes in from layer 2 of the entorhinal cortex - have some pyramid cells These have their body in the cortex & their axons project into the hippocampus via the preforant pathway
28
Where do signals go once they have entered the entorhinal cotex?
Once they have entered onto the preforant pathway: - They synapse w the dendrites of granule cells in the dendrite gyrus - Their axons project out of this region into the CA3 region where they synapse w pyramidal cells, this pathway is called the mossy fibres pathway
29
What is the mossy fibres pathway?
Where the granule cells (in the dendrite gyrus) project to CA3 region
30
Once a signal has reached the CA3 region of the hippocampus where does it go?
- From here the pyramidal cells in the CA3 region --> their axons project to the CA1 region & synapse there (called Schaffer Collaterals)
31
What are Schaffer Collaterals?
The axons that project from the CA3 to the CA1 region of the hippocampus
32
What happesn after the signal reaches the CA1 region of the hippocampus?
In the CA1 region we have the cell bodies of the pyramidal cells which recieve inputs --> their axons project to layer 5 of the entorhinal cortex
33
How do we know that the order info travells around the hippocamus is correct?
If we stimulate it at one end we can record the response at the other end
34
Give some examples of the hippocampal inputs and outputs?
Outputs: - Cingulate gyrus - Mammillary body - Fornix column/body Inputs: - Parahippocampal gyrus
35
What is long term potentiation?
The mechanism that allows us to form long term memories
36
What does potentiate mean?
To strenthen
37
What did Bliss and Limo (1973) do?
- Looked at rabbit hippocampus, using the one way system - They stimulated the Schaffer collateral pathway, they are the neurones that project from the CA3 to CA1 - They recorded the response from the cell bodies in the CA1 region
38
What did Bliss and Limo find during their experiment?
- Just stimulating once doesn't mean you are likely to get a single response in the CA1 region so they looked at the grade potentials (EPSPs) - Found low freq = low output, small EPSP - High freq, lots one after another = bigger response in the CA1 region, response was long lasting - Go back to small stimulus would still produce large response --> has essentially remembered the stimulus, STRENGTHENED SYNAPSE
39
What did Bliss and Limo (1973) conclude from their experiment?
Even tho the test was not doen in vitro the results suggested this would still happen when in vivo Showed the strengthening of a synapse to a repsonse was possible
40
What are the 2 requirements for forming LTPs?
- Postsynaptic neurone must be strongly depolarised - Input specific
41
Why must the postsynaptic neurone must be strongly depolarised to form an LTP?
- Synapses msut be activated at sufficient frequencies to cause temporal summation - Enough synapses must be activated simultaneously to cause spatial summation = cooperativity
42
Why are must LTPs be input specific?
- Oly synaptic inputs that recieved tetanic stimulus show a strengthened response - Other inputs onto the same neurone that did not recieve tetanus do not show modified response
43
What is the overall mechanism of LTP at a synapse?
- Presynaptic is about glutamate, neurones release this into the synapse & it binds to glutamatergic receptors - In particular ionotropic receptors, binding causes opening & influx of ions into postsynaptic neurone - During LTP we get signalling cascade of Ca2+ ions & activation of range of proteins - leads to changes in strengthening of the synapse & changes in gene expression
44
Why is glutamate an important NT in LTP?
- Release of glutamate from pre can bind to ionotropic receptors & NMDA receptors - Binding causes opening of AMPA channel, sodium can enter post - causes depolarisation in membrane
45
Why won't NMDA receptors open when glutamate initially binds?
- They don't initially open as they have a magnesium block --> needs high level of depolarisation for it to open, binding of glutamate alone isn't enough for the channel to open fully - Occurs via sodium entering from AMPA receptors - this alone isn't enough, we need a bigger stimulus, these combined is enough so the magnesium ions are released from the NMDA receptors & calcium passes through NOT sodium - Increases conc of intracellular calcium = cascade od Na+/Ca+ & therefore LTP happens
46
What effect does calcium have with LTP?
Increased intracellular Ca2+ Activates a range of kinases: - Kinases = phosphorylation enzymes - Protein kinase C (PKC) - Ca2+ calmoduin dependent protein kinase II (CaMKII)
47
What are the mechanisms of LTP: kinases?
- Increased ionic conductance of AMPA receptors - Insertion of additional AMPA receptors - Synaptic structural changes
48
What are the increased ionic conductance of AMPA receptors? (Mechanisms of LTP)
- Phosphorylation of existing postsynaptci receptors - PKC - CaMKII
49
What are the insertion of AMPA receptors? (Mechanisms of LTP)
- Vesicle fuses w membrane - CaMKII
50
What are synaptic structural changes? (Mechanisms of LTP)
- Postsynaptic dendritic spines bud and form new synaptic contacts - PKC activates CREB = alters gene expression & protein synthesis
51
How long do LTP changes take in each of the below: - Glutamate - NMDA - Kinases - Structural
- Glutamate = over milliseconds - NMDA = in seconds - Kinases = in minutes - Structural = in hours
52
What evidence is there that LTP is linked to memory?
- Knock out NMDA receptor (in CA1) = unable to form memories, found in animal studies - Calcium removed (stopped kinases) = receptors still work but no memoreis formed - Knock out CaMKII & shows deficits in LTP & memory in mice
53
What does increased glutamate (in presynaptic) lead to?
(These are all w chain of events which follow on from each other:) - Increased AMPAR activation = larger EPSP - NMDAR activation - Increased Ca2+ - Activation of kinases (PCK & CaMKII) Branches off ot these 3: - AMPAR phosphorylation - AMPAR insertion - New dendritic spines

Fundamentals of neuroscience (38 decks)

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