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Neuroscience > EAA & Excitotoxity > Flashcards

EAA & Excitotoxity Flashcards

1
Q
  • Derived from α-ketoglutarate

* Metabolic and transmitter pool strictly separated.

A

Glutamate

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2
Q

• Often co-localized with glutamate

• Serves as neurotransmitter on its
own in visual cortex and
pyramidal cells.

• Metabolic and transmitter pool strictly separated.

A

Aspartate

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3
Q

EAA Location

A

Widely distributed throughout CNS

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4
Q

EAA receptors?

A
  • Both ionotropic and metabotropic receptors

* Several kinds of each

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5
Q

Ionotropic Receptor:
The NMDA Receptor
• ? is an exogenous agent that activates these receptors.

  • Glutamate, aspartate, etc… all activate them in the body.
  • When activated, the channel allows influx of ?

• Has multiple modulatory sites
- ? binding site

A
  • NMDA
  • calcium
  • GLYCINE
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6
Q

NMDA Receptor
• is a required co-agonist, but it alone cannot open the channel
• Both EAA and ? must be present for the channel to open.

A

GLYCINE binding site

  • glycine
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7
Q

NMDA Receptor
• Within the channel itself
• Blocks the channel at resting membrane potential

A

Magnesium (Mg++) binding site

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8
Q

NMDA Receptor

  • Prevents ? influx when the channel opens
  • Makes the NMDA receptor both ligand- and voltage-gated.
A

Magnesium (Mg++) binding site

  • calcium
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9
Q

The NMDA Receptor
• Horse tranquilizer
• Blocks channel

A

PCP binding site

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10
Q

2 main types of non-NMDA receptor

A
  • AMPA

- Kainate

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11
Q

Also ionotropic – but primarily a Na influx

A

non-NMDA receptors

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12
Q
  • Exogenous agent ? activated
  • Glutamate/Aspartate are the endogenous ligands
  • Modulatory sites as well.
  • Sodium influx when open
A

AMPA

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13
Q

AMPA

  • ? bind to a site on the extracellular face of the protein
  • reduce the amount of sodium that enters
A

Benzodiazepines

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14
Q

? Receptors

- Sodium comes in and a little calcium as well

A

Kainate Receptors

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15
Q

Activation of the ? receptors produces a typical excitatory post- synaptic potential (epsp) with a relatively short onset and duration.

A

Non-NMDA

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16
Q

While activation of the ? receptors produces a “long” latency epsp with a long duration.

A

NMDA

17
Q

Why does the epsp produced by activation of NMDA
receptors have a longer latency and longer duration than a
typical epsp?

A
  • Blocked by magnesium and prevents calcium
  • Get magnesium away from channel by depolarizing the cell
  • So the delay is the time it took to get magnesium out of the way
  • Takes long because its a calcium influx
18
Q

Functions of Non-NMDA receptors

A
  • Primary sensory afferents
  • Upper motoneurons
  • Too many to name
19
Q

Functions of NMDA receptors

A
  • Critical in short- and long-term memory formation

* Synaptic plasticity in many forms

20
Q

Metabotropic Receptor

  • 3 groups
    1. Group 1: ? coupled
    2. Group 2 & 3: ? coupled
A
  • Gq

- Gi

21
Q

Metabotropic Receptor
Functions
- Pre-synaptic:
-Post-synaptic:

A 
• Pre-synaptic:  control NT release
• Post-synaptic:
- Learning 
- Memory 
- Motor systems
22
Q

Functions and where of NO?

A

• Memory

  • Long-term potentiation
  • In hippocampus & cerebellum
  • Elsewhere

• Cardiovascular and respiratory control
- Pons and medulla

23
Q

Downsides of NO

A
  • Vary unstable – half-life is about 5 seconds.
  • Leads to production of free radicals.
  • In high concentrations – toxic to neurons
24
Q

The uptake of the EAA is dependent on secondary active transport of ?

A

Na+

25
Q

Excitotoxicity
• “Substantial evidence” for involvement in: ?

• “Strong evidence” for involvement in ?.

A

• “Substantial evidence” for involvement in:

  • Strokes
  • Global hypoxia or anoxia
  • Traumatic injury to brain - Hypoglycemia

• epilepsy

26
Q

What are the 4 consequences of high intracellular calcium?

A
  1. Increase in Phospholipase A
    activity.
  2. Activation of μ-calpain (a proteolytic enzyme)
  3. Activation of calcineurin
  4. Activation of the apoptotic pathway
27
Q

Consequences of high intracellular calcium:

  1. Increase in Phospholipase A activity.
    - Acts on membrane to release ?
    - Physical damage to the membrane with high activation!!
A
  • Arachidonic Acid
28
Q

Consequences of high intracellular calcium:

  1. Increase in Phospholipase A activity.

• Arachidonic acid becomes another messenger and leads to:

  • ? release from ER &
    mitochondria
  • ? – ER stops
    making proteins
  • ? activation
  • ? dysfunction
A
  • Ca++
  • Unfolded protein
    response ***
  • eIF2α-kinase
  • Mitochondrial
29
Q

Consequences of high intracellular calcium:

  1. Activation of μ-calpain (a proteolytic enzyme)
    - Proteolysis of structural proteins, including ?.
  • Proteoloysis of other enzymes, proteins,
    including ? (further disruption of protein
    synthesis).
  • Leads to ?
A
  • spectrin
  • eIF4G
  • Leads to metabolic and
    structural impairment of neurons. ***
30
Q

Consequences of high intracellular calcium:

  1. Activation of calcineurin
    • Excess production of ? via activation of ?.
A
  • Nitric Oxide (NO)

- nitric oxide synthase (NOS)

31
Q

Consequences of high intracellular calcium:

  1. Activation of the apoptotic pathway

• A consequence of the
previous steps, in particular the release of calcium from intracellular stores.

• Mitochondrial release of
enzymes, including ?

  • Activation of ?
  • ? is pro-apoptotic.
A
  • caspase 9
  • Caspase 3
  • Caspase 3
32
Q

Reperfusion

  • What happens to oxygen?
A

Free Radicals

33
Q

Reperfusion

  • Kinases take ATP and convert it into?
A
  • ADP and PO4
34
Q

Reperfusion

  • Phosphorylation of ? leads to a FURTHER decrease in protein synthesis & FURTHER activates ?, which FURTHER INCREASES ? signaling.
A
  • eIF2α kinase
  • caspase 3
  • apoptotic
35
Q

Acetylcholine

- Function and location?

A

Location
- Brainstem –> Arousal

  • Basal Ganglia- Striatum –> motor control
36
Q

Ionotropic Receptor

  • NT : Acetylcholine
  • Agonist: ?
  • Modulator: X
  • Ion: ?
A
  • Agonist: Nicotine and Acetylcholine

- Ion: Na+ and a little calcium because the channel has 5 subunits

37
Q

Metabotropic Receptors
- Agonists: ?

  • G-protein coupled: ?
  • General Effects: ?
A
  • Agonists: Muscarine/Ach
  • G-protein coupled: M1, 3, 5 coupled to a Gq protein (IP3 and diacylglycerol and calcium release)
  • General Effects: M2 and 4 = connected to Gi (inhibitory- decreases adenylate cyclase)

Neuroscience (14 decks)

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