Lecture 9 + Assignment 8 Flashcards

1
Q

Plasticity

A

ability of brain to change aspects of itself

  • response to experience or injury
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2
Q

Aplysia - sea slug

A

water enters gills - which extract oxygen - and exits siphon

head tentacles = tactile sensors

rhinospores = chemical sensors (like antennae)

  • gastropod invertebrate; coastal waters in California and Mexico

release ink from below mantle

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3
Q

Aplysia gill withdrawal reflex circuit

When siphon touched + sensitization

A

Axo-axonic synapse
- sensory neuron touching siphon skin
- directly synapses onto motor neuron
- sensory neuron touching tail skin
- synapses onto modulatory interneuron
= serotonergic
- synapses onto siphon SN

glutamate onto motor neuron, ACh to move gill muscles and pull them in

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4
Q

Serotonin role in aplysia

A

makes SN release more glutamate than normal during APs

= greater motor neuron EPSP
= more voltage-gated Ca channels stay open
= longer AP falling phase

serotonin=5HT

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5
Q

Eric Kandel

A
  • won Nobel prize for simple memory and learning in aplysia
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6
Q

Aplysia habituation

A

a progressive decrease in response to a repeated stimulus

stop responding to a harmless touch to siphon bc it’s a waste of energy

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7
Q

The scientific method

A
  1. Research question
  2. Hypotheses
  3. Predictions
  4. Data

then back to hypotheses

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8
Q

Sensitization in aplysia

A

a heightened response to an innocuous stimulus, caused by a previous noxious stimulus to the tail

shock then touch again
= sensitization

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9
Q

In-depth aplysia gill withdrawal reflex

Adenylyl cyclase mechanism too

A
  • Tail shock activates the tail sensory neuron
  • The modulatory interneuron releases serotonin onto the siphon sensory
    neuron’s axon terminal (axo-axonic synapse)
  • Tail sensory neuron (glutamatergic) excites the modulatory (facilitatory)
    interneuron
  • Inside the sensory axon terminal, the enzyme adenylyl cyclase converts ATP
    into cAMP
  • cAMP activates the enzyme protein kinase A
  • Protein kinase A phosphorylates (adds PO4 to) voltage-gated K+ channels
  • This reduces the probability that the K+ channels will open during AP
  • This prolongs the AP falling phase (depolarization of axon lasts longer)

Now siphon stimulation → prolonged action potential in siphon sensory axon terminal → more Ca++ entry than normal → more glutamate release
than normal → greater motor neuron response!

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10
Q

Tetanus

A

a high frequency (100 Hz) stimulation

can even have an effect hours after it’s done = long-term potentiation

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11
Q

LTP induction

A

When Ca enters the postsynaptic dendrite, LTP occurs at that location

2 conditions for Ca to enter:
1. The postsynaptic cell must be depolarized
2. Glutamate must be present

means Mg will pop out of the NMDA receptor channel and Ca can enter

First, glutamate is released by the presynaptic cell. When glutamate binds to the ionotropic NMDA receptor channels on the postsynaptic neuron’s dendritic spine it causes them to open. However, the channel is blocked by magnesium ions that are attracted to the negative cell interior but get stuck due to their size. All three of these mechanisms involve calcium ion entry into the postsynaptic dendrite which initiates LTP.

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12
Q

LTP specificity

A

Axon 1: strong stimulation
Axon 2: inactive

Ca++ enters the dendrite at synapse 1 only, because:
1. The postsynaptic cell is depolarized (everywhere)
2. Glutamate is present only at synapse 1

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13
Q

LTP associativity

A

Axon 1: strong stimulation
Axon 2: weak stimulation

Ca++ enters the dendrite at both synapses, because:
1. The postsynaptic cell is depolarized (everywhere), and
2. Glutamate is present at both synapses.

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14
Q

LTP cooperativity

A

Axon 1: weak stimulation
Axon 2: weak stimulation

Ca++ enters the dendrite at both synapses, because:
1. The postsynaptic cell is eventually depolarized (by the
joint action of both synapses), and
2. Glutamate is present at both synapses

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15
Q

2 possible mechanisms for LTP expression at dendritic spine

post-synaptic plasticity

A

ionotropic AMPA receptors (also respond to AMPA)
- permeable to K/Na

what calcium does once inside
1. Enhancement of existing AMPA receptor conductance
- activates enzyme Cam kinase II
- phos. AMPA receptors
- conformational change increases conductance

  1. Insertion of new AMPA receptors
    - cam kinase II causes insertion of more AMPA receptors
    = more sensitive to glutamate
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16
Q

Pyramidal cell synapses

A

at dendritic spines
- glutamatergic

17
Q

Memory categories

A

Declarative (explicit)
- daily episodes
- words and their meanings
- history

Nondeclarative (implicit)
not available to consciousness
- motor skills
- associations
- priming cues
- puzzle-solving skills
“how” I remember how

18
Q

Amnesia

A

retrograde
- loss of previously stored memories (things from the past)

anterograde
- inability to form new memories

19
Q

Hippocampus + memory

A
  • looks like a little seahorse
  • under temporal lobe
  • evolutionarily old (not neocortex)

IS involved in
- consolidation/acquisition of new explicit, LTMs

ISN’T involved in
- long term storage of explicit memories (just delivers them)
- consolidation or storage of implicit memories

20
Q

Patient HM

A

Henry Molaison

  • Temporal lobe epilepsy
  • Bilateral hippocampectomy

Anterograde amnesia
- Thought he was still 27

Also temporally graded retrograde amnesia (only just before the event)
- Loss of memory for events in the decade preceding surgery

Childhood memories in-tact, could acquire new implicit memories

21
Q

Hippocampus + declarative memory storage sites

A
  • hippo not final storage, just puts things there
  • hippo receives input from widespread areas of the cortex (direct and indirect)
  • sends outputs back out
22
Q

Explicit memory consolidation and storage model

A
  1. Cooperative LTP between 2 synapses onto hippo from cortex
    - due to simultaneous experience
  2. Non-simultaneous experience causes an associative LTP
    cortex -> hippo -> cortex
  3. Associative LTP in cortex
  4. Doesn’t need connection to hippo anymore

1-2 explicit hippo
3-4 implicit connections, cause explicit to weaken

ex. fragrance and sight

23
Q

Extracellular electrical stimulation - purpose

A
  • Excite neurons to stimulate APs by shocking an axon
  • Put a stimulating microelectrode with a negative charge (wire connected to voltage source) on the axon
  • Will make the inside positive relative to the outside
  • Depolarization causes an AP, voltage is difference of inside-outside
  • Will make voltage-gated sodium channels open

get APs moving away from the electrode

24
Q

Extracellular electrical stimulation - issue & solution

A

Might stimulate en passant axons (fibres of passage) of other cells
= can’t directly determine relationship between only 2 cells

Solution
Use glutamate photo-uncaging (focal photolysis)
Doesn’t stimulate axons of passage bc no glutamate receptors
Can selectively engage glutamate in only the nucleus of the cell we want

25
Q

Temporally graded retrograde amnesia

A
  • in first stages of memory consolidation, connection relies on the hippocampus

if incident occurs, might never get the chance to exist without the hippo as not yet consolidated

26
Q

Alzheimer’s - gen info

A
  • most common dementia
    5-10% of ppl over 65
    45% of ppl over 85

affects memory and attention, then language, thinking, personality

causes retro and antero amnesia

affects hippo and the rest of the cortex

27
Q

Alzheimer’s - plaques and tangles

A

Plaques
- extracellular amyloid proteins

Tangles
- intracellular cytoskeletal filaments of tau protein

both associated, don’t know if cause or effect

28
Q

Place vs. grid cells

A

Place cells
- in hippocampus
- fire when individual is in a particular location in a room
(not response to visual stimulus)

Grid cells
- entorhinal cortex (behind hippo)
- fire when you reach a particular region in a hexagonal region
- one cell fires to several places

probably inform eachother