neu 335 exam 3

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70 Terms

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What is explicit memory?

A type of memory that requires you to consciously recall events

e.g. recalling the year of the American Revolution

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What is implicit memory?

A type of memory where no conscious retrieval of information is required

e.g. brushing your teeth

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Semantic memory

The type of long-term memory associated with recalling facts

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Working memory

Type of short-term explicit memory associated with temporally holding information

e.g. remembering a verification code

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Habituation

A type of implicit memory where you get used to a stimulus (can be short term or long term)

e.g. habituating to your smelly roommate after a few minutes of him arriving from the gym

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<p>Which cell is a better candidate for a working memory cell?</p>

Which cell is a better candidate for a working memory cell?

The 2nd cell because it is very active during the delay period of the Delay-Response task when there is no visual stimulus —> suggesting that the cells are processing where the plate could be

<p>The 2nd cell because it is very active during the delay period of the Delay-Response task when there is no visual stimulus —&gt; suggesting that the cells are processing where the plate could be</p>
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<p>With respect to this image, describe what goes on during the delay period of the delay-cue task?</p>

With respect to this image, describe what goes on during the delay period of the delay-cue task?

Neurons engage in a feedback excitation loop after the primate is exposed to the visual stimuli —> the loop persists during delay and is amplified during the choice phase

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Which part of the brain did patient HM’s brain was damaged?

medial temporal lobe

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Retrograde Amensia

a type of memory loss where one can’t recall what happened some time before a traumatic event

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Anterograde Amnesia

A type of memory loss where one can’t form new memories after a traumatic event

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Did patient HM suffer from anterograde or retrograde amnesia?

He suffered from both, though it was a mild form of retrograde amnesia and a very severe form of anterograde amnesia

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Is the medial temporal lobe involved in the formation of long-term or short-term explicit memories?

Long term explicit memories

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Describe the structure of the morris water maze?

A small pool of shallow water containing a hidden platform. This experimental design is used for training spatial memory.

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What are the effects of a bilateral lesion on the medial temporal lobe on brief working memory and long-term memory?

working memory unaffected but long term memory disrupted

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Compare the performance of a trial 1 and trial 10 of a mouse in a Morris water maze after they suffer a hippocampal lesion.

The performance is about the same

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What are place cells?

cells in the hippocampus that fire when an animal enters a specific place in their environment

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what is a place field?

the specific region in space that an animal can stand in and the place cell fires

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<p>T/F a place cell can have different place fields in different environments?</p>

T/F a place cell can have different place fields in different environments?

True

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what type of cells function as the “where” component of episodic memory?

place cells

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Describe the development of place cells during spatial memory training?

After several trials, place cells can form excitatory connections with each other so they can stimulate subsequent place cellsW

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What is a grid cell?

  • Cells in the entorhinal cortex that fire when an animal is in ANY of its place fields

  • Don’t provide a direct representation of where an animal is in space

  • Presynaptic to place cells


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<p>How can you identify the location of an animal using grid cells and place cells?</p>

How can you identify the location of an animal using grid cells and place cells?

Since grid cells are presynaptic to place cells, place cells sum all grid cell inputs and fire only when the rat is at a specific location

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describe classical (pavlovian) conditioning

Prior to conditioning:

  • An unconditioned stimulus (e.g. food bowl) —> unconditioned response (e.g. salivating, which is untrained)

After conditioning:

  • conditioned stimulus (e.g. metronome click) —> conditioned response (e.g salivating, which is now a trained response)


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What type of response is the conditioned salivating by pavlov’s dog?

implicit reseponse bc it dosn’t require any conscious recollection that the bell is associated with food

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T/F operant conditioning is a type of implicit memory?

T

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Describe the structure of fear conditioning?

Initially, there’s a tone (neutral stim) played while a foot shock (US) electrifies that mouse, causing it to freeze (UR). Over time, just playing the tone (CS) is enough to freeze (CR) the mouse.

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<p>Which of the following examples would exemplify stronger conditioning?</p>

Which of the following examples would exemplify stronger conditioning?

Example 1 because the shock is always aligned with the tone

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What is extinction wrt to fear conditioning?

Extinction is when the tone is playd without a foot shock and over time the mouse is less likely to freeze

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<p>What is the difference in fear conditioning between mice with hippocampal lesions and amygdala lesions <strong>before </strong>fear conditioning training?</p>

What is the difference in fear conditioning between mice with hippocampal lesions and amygdala lesions before fear conditioning training?

Damaging the hippocampus has a small effect on fear conditioning while damage to the amygdala prevents the mouse from learning the association

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What does the GAL4 line represent?

GAL4 is the gene that determines in which cells another particular gene is expressed in.

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What does the UAS line represent?

A gene that determined “WHAT” gene will be expressed.
e.g. if GAL4 only expressed in optic lobes, and UAS paired with GFP, GFP will be expressed in the optical lobes

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What is the similarity between the Morris water maze + the experimental design of the Ofstad et al. 2011 paper?

  • Like the mice, the flies in Ofstad et al. also needed to find a specific spot in their experimental structure

  • flies also use visual cues to ID where they are

  • both protocols measure how fast an animal can get to the spot


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In Ofstad et al. what happens after the flies find the cool spot?

After the flies find the cool spot, the arena rotates, which displaces the cool spot and the LED visual cues → forcing the flies to find the cool spot again

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What evidence did the paper provide for showing that the flies are learning to quickly find the cool spot?

Flies take less time to find the spot with each subsequent sub-trial

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<p>Which figure clarifies that the flies are NOT just walking faster to the next school spot?</p>

Which figure clarifies that the flies are NOT just walking faster to the next school spot?

Figure 2D shows walking speed throughout each trial is the same

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Define Direction Index and why it improves over trials?

Direction Index is the ratio between flies moving in the right direction toward the cool tiles over number of flies moving in the opposite direction of the cool tile

Over time, the flies rmr where the cool tile is at so mor of them start moving in the right direction

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What research question were the Ofstrad et al 2011. researchers trying to answer?

Trying to answer if flies can learn spatial locations using visual cues + which brain regions required?

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What did the researchers in Ostad et al find about the Ellipsoid body?

Silencing EB neurons impair visual place learning, and only that one.

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What did the researchers in Ostad et al find about the Mushroom body?

Silencing MB neurons did NOT impair visual place learning, but are important for olfactory learning

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What is the MAIN finding of the Ofstad et al paper?

Flies can retain visual place memories for up to 2 hours.

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In terms of time, how do short term and long term habituation differ?

short term = seconds to minutes

long term = hours to years

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<p>Describe the gill reflex neural circuit in aplysia?</p>

Describe the gill reflex neural circuit in aplysia?

Siphon stimulated → sensory neuron detects mechanical stimulus → excite motor neuron → cause gill retraction

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Describe habituation at the cellular level

During habituation, there’s a decrease in NT release from sensory neurons to MN → decrease in NT release from MN to gill → decrease gill withdrawal

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Is the aplysia gill circuit an example of short term or long term habituation?

short term

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<p>which of these 2 images represent long term habituation on the aplysia circuit?</p>

which of these 2 images represent long term habituation on the aplysia circuit?

the 2nd one because it shows limited activation of the MN

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<p>which of these 2 images represent long term habituation on the aplysia circuit?</p>

which of these 2 images represent long term habituation on the aplysia circuit?

The 2nd image because in long term habituation there is a decrease in synapses from sensory neuron to MN

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What is the relationship between more noxious stimuli in sensitization and ill withdrawal in aplysia

More noxious stimuli done multiple times per day create more long term sensitization

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The difference between sensitization and classical conditioning?

Sensitization:

  • strengthen response to the same stimuli

Classical conditioning:

  • create new behavioral response to previously neutral stimuli



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<p>What happens at the molecular level with sensitization?</p>

What happens at the molecular level with sensitization?

More NT release from sensory neuron → MN

More NT release from MN → gill

increased gill retraction

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<p>What causes the increase in NT release from sensory neuron to MN in  SHORT TERM <strong>sensitization</strong></p>

What causes the increase in NT release from sensory neuron to MN in SHORT TERM sensitization

the tail shock stimulus activates a modulatory serotonin neuron, which synapses onto the axon terminal of sensory neuron → release serotonin (5-HT) onto terminal of sensory neuron → greater cAMP production in terminal of sensory neuron → greater levels of PKA → greater Glutamate release onto MN

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How does PKA increase glutamate release?

PKA phosphorylates K+ channels in terminal of sensory neuron → K+ Channels close → prolongs AP because less (+) leaving cell → more time for Ca2+ to enter terminal of sensory neuron → greater Glutamate release

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Is only increasing NT release related to short term or long term sensitization?

short term sensitization is associated with greater NT release at ONE synapse

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Describe long-term sensitization

during long term sensitization, an abundance of PKA travels to the nucleus → transcriptional changes → growth of new synapses from sensory neuron to MN

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<p>why does the right image result in long term sensitization?</p>

why does the right image result in long term sensitization?

because the amount of serotonin added is great, mimicking greater shock frequency

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<p>why does the smaller addition of serotonin also cause long-term sensitization in the right neurons?</p>

why does the smaller addition of serotonin also cause long-term sensitization in the right neurons?

the serotonin stimulation of left synapse leads to the expression of synaptic growth proteins in the nucleus of the sensory neuron. These proteins are shared by both synapses, also causing long-term sensitization changes in the right synapse

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<p>are these images examples of short term or long term habituation/sensitization?</p>

are these images examples of short term or long term habituation/sensitization?

left: long term habituation due to lower # of synapses on MN

right: long term sensitization due to higher # of synapses onto MN

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Describe the direct and indirect circuit of the hippocampus

Direct: EC (main input) → CA1 (main output cells) → other cortical parts of brain

Indirect: EC (main input) → denudate gyrus (granule cells) → CA1 → CA3

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circuit of Schaffer colateral patwhways?

CA3 → CA1

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<p>Which type of receptor does the CA3 glutamate bind onto?</p>

Which type of receptor does the CA3 glutamate bind onto?

CA1 AMPARs → Na+ flow into the cell → CA1 neuron undergoes EPSP

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What 4 things are NMDARs coincidence detectors of?

  • glutamate release from presynaptic membrane

  • "AMPAfication" of postsynaptic membrane

  • depolarization of postsynaptic membrane

  • Mg2+ dislodged from NMDA receptors in postsynaptic membrane

  • open when both pre and post cells active




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Describe initiation of LTP?

Strong stimulation releases glutamate, activating AMPA receptors and depolarizing the postsynaptic neuron. This removes the Mg²⁺ block from NMDA receptors, allowing Ca²⁺ and Na+ to enter + cause large EPSP

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explain how NMDARs → AMPAfication?

Ca2+ via enter post cell via NMDARs and activate kinases (PKC or CaMKII), which phosphorylate AMPARs and cause them to add onto the membrane

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<p>describe what’s going on here</p>

describe what’s going on here

neuron B receives a large stimulus, causing a large EPSP in the post cell that ends up spreading to the synapse between neuron A and the dendrite. HOWEVER, no glutamate is released by A

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<p>how can this occur if no neuron is strongly activated?</p>

how can this occur if no neuron is strongly activated?

each synapse is weakly activated, which can lead to LTP at all synapses

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<p>According to this image, what can cause late LTP?</p>

According to this image, what can cause late LTP?

more frequent tetanus → long term LTP

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what is the main cause of late LTP?

prolonged Ca2+ influx into post cell caused by repeated tetanus stim

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<p>Describe the late LTP signaling pathway?</p>

Describe the late LTP signaling pathway?

Prolong Ca2+ signaling due to repeated tetanus stim → activation of adenyl cyclase → greater cAMP → greater activation of PKA → greater activation MAP kinase → expression CREB-1 → newly made synaptic growth proteins

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Early LTP v Late LTP?

AMPAfication vs synthesis of synaptic growth proteins

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What is the main driver of LTD

weak stimulation → weak glutamate release → weak activataion of NMDARs —> small influx of Ca2+ into post cell → activate phosphatases → removing AMPARs from membrane