Neuroscience Final Flashcards

1
Q

How thick is the neuronal membrane?

A

5 nanometers

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2
Q

How large is a neuronal soma?

A

5-50 micrometers

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3
Q

Describe the scaffolding of a neuron?

A

Microtubules —tublin based molecules with diameters of 20 nanometers— are present everywhere except axon terminals. Neurofilaments (10 nm). Microfilaments —actin based molecules with diameters of 5 nm — are present throughout the membrane.

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4
Q

Describr the differences brtween the cytoplasm of axon terminal and axon

A

Axon terminals require lots of energy to send out neurotransmitters. As a result, they contain more mitochondria. They have no microtubules. There are more proteins. And there are synaptic vesicles.

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5
Q

Describe voltage gated sodium channels?

A

These channels open and close fast. They inactivate after closing to prevent back-flow from triggering another action potential.

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6
Q

Describe voltage-gated potassium channels

A

These open slow and shut slow. They do not inactivate. They open slow to allow for sodium channels to depolarize the cell before they depolarize it.

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7
Q

Which neurotransmitters do ionotropic receptors respond to?

A

Small molecule neurotransmitters

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8
Q

Which neurotransmitters do metabotropic receptors respond to?

A

Neuropeptides

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9
Q

GABA receptors

A

Gaba gated anion channels are inhibitory. The receptors also respond to modulators that enhance the function of GABA in its presence.

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10
Q

How do GPCRs work?

A

When a GPCR is activated, the gprotein splits into two parts which activate ion channels and enzymes

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11
Q

Describe signal amplification by GPCRs

A

G-protein stimulates a structure to convert ATP to CAMP. Increased CAMP levels activate protein kinases which add phosphate groups to AMPA receptors making them more conductive to sodium. It also causes the insertion of additional AMAPR.

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12
Q

Describe synaptic integration

A

Synapses receive thousands of EPSPs and IPSPs. Synaptic integration is the summation of these inputs within the postsynaptic cell. This process allows for complex computations

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13
Q

Describe long term potentiation?

A

Synapses that activate concurrently are strengthened. An inactive synapse will not be strengthened.

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14
Q

Describe AMPAR and NMDAR

A

Glutamatergic cation channels. NMDA id voltage gated. When there is sufficient depolarization, owing to current from AMPA receptors, NMDA opens. Ca2+ enters —if there is a high level within the cell, LTP takes place.

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15
Q

What happens when there is substantial Ca+ increase?

A

Kinases activate and add phosphate groups to AMPA receptors, making them more conducive to Na+. They also cause the insertion of additional AMPA receptors.

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16
Q

How can LTP activate “silent stnapses”

A

If the cell is sufficiently depolarized, then AMPA receptors will insert themselves in the cell membrane.

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17
Q

Describe long term changes during LTP

A

There are changes in gene expression that cause the growth of additional dendrites to form new synapses.

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18
Q

Describe the molecular mechanisms of LTD

A
  1. Moderate Ca2+ -> phosphorylates
  2. Remove phosphate groups from AMPAR and internalize AMPAR
19
Q

Protoplasmic astrocytes

A

Exist in the gray matter. Shorter, highly complex, arborized processes

20
Q

Fiborous astrocytes

A

Less complex, elongated processes. Exist in white matter

21
Q

Morphogenesis of astrocytes

A

Tiling feature: little to no overlap between processes. Astrocyte differentiation results in this tiling, as cells show decreasing overlap during development.

22
Q

How do astrocytes communicate with each other?

A

Gap junctions

23
Q

Potassium Spatial Buffering

A

Normal and pathological conditions increase extracellular potassium concentration. Astrocytes uptake potassium through reuptake channels and redistribute it to maintain concentration graduents.

24
Q

Astrocyte-neuron lactate shuttle hypothesis

A

The uptake of glutamate triggers glycolis which produces lactate for neurons. Possible mechanism for coupling lactate production with neuronal activity

25
Q

Astrocyte functions

A
  1. Synapse maturation and removal
  2. Neurotransmitter reuptake
  3. Metabolic support
  4. Potassium homeostasis
  5. Synaptogenesis
26
Q

How do astrocytes regulate neurons?

A

Ca+ dependent signaling

27
Q

Reactive astrocytes

A

Swollen shorter morphology during injurious conditions

28
Q

Changes in gene expression for reactive astrocytes

A

Gain new functions or loss homestatic ones

29
Q

Moderate resctivity

A

Swollen, shorter morphology. Tiling property retained.

30
Q

Severe reactivity

A

Glial scar tissue, overlap between processes

31
Q

Reactive astrocyte pros

A
  1. Growth factors
  2. Phagocytosis of debris
  3. Homeostatic support
32
Q

Reactive astrocyte cons

A
  1. Release of cytokines
  2. Oxidative stress
  3. Synaptic damage
33
Q

Type 1 Oligodendrocyte

A

Small rounded body, white and gray matter, many fine processes

34
Q

Type 2 Oligodendrocytes

A

Polygonal shape, fewer thicker processes, white matter

35
Q

Type 3

A

Bulky cell body, white matter, one to four processes

36
Q

Type four

A

Elongated cell body, white matter, attach to and envelop medium to large axons

37
Q

Myelin composition

A

Lipids, proteins, and water

38
Q

functions of oligodendrocytes

A
  1. Regulate expression of ion channels on nodes of ranvier
  2. Myelinatiom of axons
    3 maturation and maintenance of the node of ranvier
  3. Modulation of neuronal excitability and neurotransmitter release
  4. Metabolic support to axons and ion homeostatic maintenance
39
Q

Microglia origin

A

Progenitor cells in the yolk sac

40
Q

Resting microglia

A

Ramified morphology, found under physiological conditions

41
Q

Activated microglia

A

Swollen morphology, larger cell body and smaller processes. Present during development and pathological conditions

42
Q

Microglia delf renewel

A

During physiological conditions, microglia stay within a region of the brain. When there is a deficit of microglia, they self-renew by division.

43
Q

Synaptic pruning

A

A process during postnatal development in which synapses are eliminated

44
Q

Synaptic pruning

A

Microglia phagocytose inactive synapses using the complement system