Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is declarative memory?

A

Memories of knowing that and what, facts and events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is non-declarative memory?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Who made the simple model of memory: Aplysia?

A

Kandel - said memory is extremely complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Aplysia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What did Kandel use to study Aplysia?

A

Used sea slugs to understand mechanims

(This is behavioural habituation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Please look at the diagram of the structure of the hippocampus

A

It is stained with nissl stain (stains for DNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the general structure of the hippocampus?

A

Has a characteristic structure of 2 interlocking C shapes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Does the hippocampus work alone?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What sort of cells are found in the CA regions of he entorihnal cortex?

A

Pyramid neurones

26
Q

What type of cells are found in the Dentate gyrus?

A

Granule cells

27
Q

Where does info enter the entorhinal cortex?

(You will defo need to refer to the diagram for this)

A

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
Q

Where do signals go once they have entered the entorhinal cotex?

A

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
Q

What is the mossy fibres pathway?

A

Where the granule cells (in the dendrite gyrus) project to CA3 region

30
Q

Once a signal has reached the CA3 region of the hippocampus where does it go?

A
  • From here the pyramidal cells in the CA3 region –> their axons project to the CA1 region & synapse there (called Schaffer Collaterals)
31
Q

What are Schaffer Collaterals?

A

The axons that project from the CA3 to the CA1 region of the hippocampus

32
Q

What happesn after the signal reaches the CA1 region of the hippocampus?

A

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
Q

How do we know that the order info travells around the hippocamus is correct?

A

If we stimulate it at one end we can record the response at the other end

34
Q

Give some examples of the hippocampal inputs and outputs?

A

Outputs:
- Cingulate gyrus
- Mammillary body
- Fornix column/body

Inputs:
- Parahippocampal gyrus

35
Q

What is long term potentiation?

A

The mechanism that allows us to form long term memories

36
Q

What does potentiate mean?

A

To strenthen

37
Q

What did Bliss and Limo (1973) do?

A
  • 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
Q

What did Bliss and Limo find during their experiment?

A
  • 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
Q

What did Bliss and Limo (1973) conclude from their experiment?

A

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
Q

What are the 2 requirements for forming LTPs?

A
  • Postsynaptic neurone must be strongly depolarised
  • Input specific
41
Q

Why must the postsynaptic neurone must be strongly depolarised to form an LTP?

A
  • Synapses msut be activated at sufficient frequencies to cause temporal summation
  • Enough synapses must be activated simultaneously to cause spatial summation = cooperativity
42
Q

Why are must LTPs be input specific?

A
  • 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
Q

What is the overall mechanism of LTP at a synapse?

A
  • 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
Q

Why is glutamate an important NT in LTP?

A
  • 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
Q

Why won’t NMDA receptors open when glutamate initially binds?

A
  • 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
Q

What effect does calcium have with LTP?

A

Increased intracellular Ca2+
Activates a range of kinases:
- Kinases = phosphorylation enzymes
- Protein kinase C (PKC)
- Ca2+ calmoduin dependent protein kinase II (CaMKII)

47
Q

What are the mechanisms of LTP: kinases?

A
  • Increased ionic conductance of AMPA receptors
  • Insertion of additional AMPA receptors
  • Synaptic structural changes
48
Q

What are the increased ionic conductance of AMPA receptors?

(Mechanisms of LTP)

A
  • Phosphorylation of existing postsynaptci receptors
  • PKC
  • CaMKII
49
Q

What are the insertion of AMPA receptors?

(Mechanisms of LTP)

A
  • Vesicle fuses w membrane
  • CaMKII
50
Q

What are synaptic structural changes?

(Mechanisms of LTP)

A
  • Postsynaptic dendritic spines bud and form new synaptic contacts
  • PKC activates CREB = alters gene expression & protein synthesis
51
Q

How long do LTP changes take in each of the below:

  • Glutamate
  • NMDA
  • Kinases
  • Structural
A
  • Glutamate = over milliseconds
  • NMDA = in seconds
  • Kinases = in minutes
  • Structural = in hours
52
Q

What evidence is there that LTP is linked to memory?

A
  • 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
Q

What does increased glutamate (in presynaptic) lead to?

A

(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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions