Quiz 2 Preparation Flashcards

1
Q

T/F: The neurotransmitter that a neuron releases is not always fixed.

A

True

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2
Q

What determines the neurotransmitter that the neuron releases?

A

transcription factor programs– otherwise neuron will default to it’s hardwired fate

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3
Q

What can change neurotransmitter identity once the neurotransmitter is determined by TFP’s?

A

experience and target innervation

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4
Q

Neurotransmitter identity is plastic

A

Changes through rewiring and connectivity

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5
Q

Is a neuron’s neurotransmitter phenotype fixed or flexible?

A

It is hardwired but can change based on experience and target derived signals

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6
Q

T/F: Sympathetic neurons are initially specified with a
Noradrenergic transmitter phenotype (start with a noradrenergic fate). Most of these neurons will retain this transmitter phenotype.

A

True

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7
Q

For Neural crest differentiation, what are the first and second this that give rise to sensory neurons?

A

1) Ngn2 + FoxS1 = sensory precursor
2) Ngn1 = sensory neuron

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8
Q

What transcription factors turn a sensory neuron into nociceptive neuron?

A

Runx1 and TrkA

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9
Q

What transcription factors turn a sensory neuron into proprioceptive neuron?

A

Runx3 and TrkC

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10
Q

How do neural crest cells differentiate?

A

They give rise to sympathetic and sensory neurons. Sensory neurons are fixed, while sympathetic neurons can change their fate.

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11
Q

If a gland secretes IL-6 cytokine, it transforms a ______ neurons fate to _______ (instead of noradrenergic)

A

1) sympathetic
2) cholinergic

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12
Q

How do peripheral targets influence neuronal fate?

A

Secreted signals like IL-6 can change neurotransmitter phenotype, especially in sympathetic neurons.

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13
Q

T/F: In CNS, neurotransmitter phenotype is less fixed compared to the periphery.

A

FALSE– more fixed

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14
Q

bHLH? (transcription factors)

A

Basic Helix-Loop-Helix

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15
Q

What are examples of bHLH?

A

Neurogenin and Mash1

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16
Q

bHLH TF are expressed in what cells?

A

neuroepithelial cells (not in mature neurons)

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17
Q

What does it mean for these TFs to be expressed in neuroepithelial cells?

A

CNS neurotransmitter identity is largely determined before differentiation, migration, and final specification.

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18
Q

Is neurotransmitter phenotype in the CNS is flexible like in the periphery

A

No, CNS neurotransmitter identity is more “hardwired” due to early transcription factor expression before differentiation.

19
Q

Neurogenin 1 and 2 give rise to what neuroepithelial cells in the cerebral cortex?

20
Q

Mash1 give rise to what neuroepithelial cells in the cerebral cortex?

21
Q

What is the concept of apoptosis?

A

When over half of all neurons born during development die due to programmed cell death

22
Q

Why does apoptosis occur?

A

The brain overproduces neurons, and only those that establish proper connections survive.

23
Q

What does apoptosis ensure with this process?

A

This ensures efficiency: neurons must compete for survival signals, eliminating excess cells that don’t form proper connections.

24
Q

Why do so many neurons die during development

A

Neurons are overproduced, and competition for survival factors determines which ones live. This ensures efficiency and proper wiring.

24
Q

T/F: Motor neurons (MNs) depend on muscle targets for survival.

25
Q

When adding an extra limb bud to a chick embryo, the area that received the additional
limb bud from transplantation
exhibited less neuronal death than the
control side! What does this mean and what does this prove?

A

Adding an extra limb bud to a chick embryo → More motor neurons survive.
Removing a limb bud → More motor neurons die.

Trophic signals from muscles prevent motor neuron death.

26
Q

How do muscle targets influence motor neuron survival?

A

Muscle-derived signals provide essential survival factors. More muscle tissue = more motor neuron survival.

27
Q

What does blocking muscle activity do?

A

Increases MN survivalW

28
Q

What is Curare and what does it prevent?

A
  • a drug that blocks acetylcholine receptors in muscles
  • prevents normal synaptic activity → rescues many neurons from dying
29
Q

T/F: Synaptic activity normally triggers localized release of a pro-death signal from muscle, which kills about 25% of motor neurons.

30
Q

How does synaptic activity affects motor neuron survival?

A

Active muscles release signals that contribute to MN death. Blocking muscle activity (e.g., with curare) rescues more MNs.

31
Q

What are the three major neurotrophins?

A

NGF (Nerve Growth Factor)
BDNF (Brain-Derived Neurotrophic Factor)
NT-3 (Neurotrophin-3)

32
Q

What is the neurotrophic factor hypothesis?

A

Neurons must compete for survival factors

33
Q

What are neurotrophins?

A

Small proteins secreted by target tissues that prevent apoptosis in neurons.

34
Q

Key Experiment!!

A

Injecting NGF into an embryo → More neurons survive.
Blocking NGF → More neurons die.

This confirms that NGF is a critical survival signal.

35
Q

Why do neurons die despite being “healthy”?

A

They lack enough neurotrophic factors, leading to apoptosis.

36
Q

Two Main Neurotrophin Receptors

A

Trk Receptors → Promote survival.
p75 Receptor → Promotes cell death (binds all neurotrophins with low affinity).

37
Q

Survival depends on receptor activation”

A

If Trk is activated, neurons live.

If p75 is activated, neurons die.

38
Q

How do neurotrophins influence survival?

A

Neurotrophins bind Trk receptors for survival, but if they bind p75 receptors, neurons undergo apoptosis.

39
Q

What is the binding of NGF to TrkA activates survival pathways?

A

FRS2 → Ras Pathway → Promotes differentiation.

PI3-K Pathway → Promotes survival.

40
Q

What are the Cell Death (Apoptosis) Pathways?

A

Extrinsic Pathway: Activation of death receptors on the cell surface.

Intrinsic Pathway: Mitochondria release signals to activate caspases, leading to apoptosis.

41
Q

What are caspases?

A

Key executioners.

Caspase-9 (initiator) is inhibited by PI3-K.
Caspase-3 (executioner) completes cell death.

42
Q

How does NGF prevent apoptosis?

A

NGF binds TrkA, activating PI3-K signaling, which inhibits caspase-9 and prevents apoptosis.