Exam 2 Flashcards

1
Q

Why are mitochondria in every part of the neuron?

A

Because each area of the neuron, especially the axon terminal, has a high energy demand.

Also, every part has the Na+/K+ pump, which takes a lot of energy (about 70% of the energy in the neuron goes to this).

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2
Q

What problems made the neuron hard to study?

A

Consistency, size, color.

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3
Q

What was the consistency problem of studying brains and how was it solved?

A

The consistency problem was that fresh brains are like jello and very easy to damage. This has been partly solved by the use of fixatives like formaldehyde. It’s not perfect as it takes a long time for the fixative to get everywhere, but it has allowed brains to be studied without damaging them.

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4
Q

What was the size problem of studying brains and how was it solved?

A

The size problem was that neurons are very hard to see. They couldn’t be seen at all until the light microscope, and couldn’t be studied in some detail (ex: the nature of connections between neurons) until the invention of the electron microscope.

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5
Q

What was the color problem of studying brains and how was it solved?

A

Neurons are all the same color. There are many connections so without some way to remove some of the input, none of it makes sense. The invention of selective stains like the Golgi stain alleviated this problem.

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6
Q

What was the beef between Golgi and Cajal?

A

Golgi believed in the reticular theory that neurons are physically created and make a net.

Cajal believed that neurons still followed the cell theory with neurons, saying that each neuron is its own discrete fundamental group. He believed in the physically synaptic gap between each neuron.

Whether neurons were physically connected or not wasn’t known for sure until the invention of the electron microscope in the 1950s.

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7
Q

What doesn’t make sense between proportions in the brain?

A

Brains of animals like macaws and rats are very tightly packed. However, the brains of primates are not tightly packed.

So, in humans the telencephalon makes up a huge portion of our brain (82%), it only contains 19% of the brain’s neurons.

There are also different proportions of glia in each part of the brain and we don’t yet know why.

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8
Q

What is the role of astrocytes?

A

Regulate extracellular fluid, physical support for neurons by filling in gaps.

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9
Q

What is the purpose of myelinating glia?

A

To provide insulation for axons so that they leak less. This leads to faster signaling.

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10
Q

Which myelinating glia is in the CNS and which is in the PNS?

A

Oligodendrocytes are in the CNS.

Schwann cells are in the PNS.

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11
Q

What are olfactory ensheathing cells?

A

Myelinating glia in the olfactory tract.

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12
Q

What are microglia?

A

They are the immune system of the neuron. They are phagocytes.

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13
Q

Do the concentrations of ions inside and outside the membrane ever change?

A

No. Though ions will “rush out” or “rush in”, it’s like throwing sand into the ocean and won’t make an overall impact. Plus, ion pumps like the Na+/K+ will keep concentrations the same.

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14
Q

What is Eion?

A

This is the equilibrium potential. This is the membrane potential needed for the electrical charge to have the exact same force as diffusion but in the opposite way.

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15
Q

What is a neuron’s resting potential?

A

-70 mV.

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16
Q

What is the Eion for K+?

A

-80 mV.

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17
Q

What is the Eion for Na+?

A

58 mV.

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18
Q

What is the Eion for Cl-?

A

-65 mV.

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19
Q

What is the Eion for Ca2+?

A

123 mV.

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20
Q

What kinds of gated channels are there?

A
Voltage-gated
Transmitter-gated/ligand-gated
Light-gated
Temperature-gated
Pressure-gated
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21
Q

What is a leak channel?

A

An ion channel that is always open.

There are many K+ leak channels.

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22
Q

What is the difference between microtubules, neurofilaments, and microfilaments?

A

Microtubules are the biggest cytoskeletal filaments made out of tubulin.

Neurofilaments are intermediate filaments.

Microfilaments are the smallest cytoskeletal filaments made out of actin.

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23
Q

What are ependymal cells?

A

Fluid-filled ventricles that direct cell migration.

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24
Q

What’s the difference between an ion channel and an ion pump?

A

Ion channels are passive facilitative diffusions paths for ions.
Ion pumps use ATP to pump ions against the membrane against their concentration gradient.

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25
Q

What is electrical conductance?

A

Ease of movement (bigger number = easier)

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26
Q

What is electrical current?

A

Amount of movement

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27
Q

What is electrical potential?

A

The force exerted due to charge difference in two areas

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28
Q

What is electrical resistance?

A

Ease of movement (bigger number = harder)

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29
Q

What is the difference between the Nernst equation and the Goldman-Katz equation?

A

The Nernst equation finds the equilibrium potential for a single ion.
The Goldman equation finds the equilibrium potential taking into account multiple ions, their concentrations, and their permeabilities.

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30
Q

Why is K+ concentration the most important to regulate?

A

Potassium is the only ion that has a higher concentration inside the cell than outside. If too much potassium lies extracellularly then K+ won’t be able to go down its concentration gradient from outside to inside. Then, hyperpolarization won’t occur.

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31
Q

What is the difference between the smooth ER connected to the rough ER and the smooth ER that is not connected to the rough ER?

A

Connected SER helps folds proteins that extend beyond the membrane.

Unconnected SER aids in the production of lipids and regulates the concentration of intracellular ions like calcium.

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32
Q

Quickly describe the mitochondria structure:

A

Outer membrane
Matrix fluid
Cristae (inner membrane)

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33
Q

What are axon collaterals?

A

Branches off the axon.

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34
Q

What are recurrent collaterals?

A

Axon branches that return to the cell it originated from.

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35
Q

What is axoplasmic transport?

A

Movement of materials down the axon.

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36
Q

How does axoplasmic transport work?

A

Materials are enclosed in vesicles and are connected to motor proteins that “walk” down the cytoskeleton.

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37
Q

What is anterograde transport?

A

Axoplasmic transport from the soma to the terminal.

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38
Q

What is retrograde transport?

A

Axoplasmic transport from the terminal to the soma.

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39
Q

What is the importance of dendritic spines?

A

They are thought to have some connection to learning and memory. They are stimulated by particular types of synaptic transmission. Some people with intellectual disabilities have fewer dendritic spines.

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40
Q

What are interneurons?

A

Neurons that only form connections with other neurons.

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41
Q

What are Projection neurons/Golgi Type I neurons?

A

Neurons that extend from one part of the brain into a different part of the brain.

Stellate cells (they are star-shaped).

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42
Q

What are local circuit neurons/Golgi Type II neurons? And what types of cells typically are these?

A

Neurons that have short axons that do not extend beyond the vicinity of the cell body.

Pyramidal cells.

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43
Q

What is a cathode?

A

Negative terminal.

Attracts cations.

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44
Q

What is an anode?

A

Positive terminal.

Attracts anions.

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45
Q

What is ionic driving force?

A

Difference between the real membrane potential and the equilibrium potential.
Vm-Eion.

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46
Q

What is the absolute refractory period and when does it occur?

A

The time that another action potential cannot be generated. This is when the globular protein lock is on the Na+ voltage-gated channel. Happens during the start of repolarization.

The purpose is to prevent depolarization of earlier areas the signal was. Prevents backward signaling.

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47
Q

What is the relative refractory period and when does it occur?

A

The Na+ channels are closed but unlocked. This occurs during the undershoot. The membrane is negative but the channels can open again if there is a strong enough depolarizing force. But, since it is during the undershoot, this is harder to reach.

Allows for variability in action potential frequency. Different frequencies can communicate how important that information is.

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48
Q

What is optogenetics?

A

Expressing genes in neurons where ion channels open in response to light.

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49
Q

Why do action potentials not last for very long?

A

Because the Na+ channels are only open for about a millisecond.

50
Q

What is deinactivation?

A

When the globular protein lock of the Na+ channel leaves the pore so that the channel can be opened again.

51
Q

Why does K+ not immediately leave the cell during depolarization?

A

Because the K+ channels delay in opening. They take about a millisecond to open.

52
Q

What are Nodes of Ranvier?

A

Breaks in the myelin that allow for the action potential to be refreshed.

53
Q

What is depolarization?

A

Moving the Vm towards 0.

54
Q

How does the Vm return to resting potential after the undershoot? What is fighting against this?

A

Permeability to other ions (Na+ leak and Cl- channels) allows the Vm to go back to the resting potential.

Things that fight against the Vm becoming more positive in the undershoot:
Na+/K+ pump pumping out more + ions than bringing in + ions.
Na+ diffusing away from the location.

55
Q

What is step 1 of the action potential?

A

Step 1 of the action potential is the resting potential.
There are some Na+ leak channels, way more K+ leak channels and the Na+/K+ pump is working in the background.
Because the membrane is permeable to other ions besides potassium EK is not reached and the Vm is at -70 mV.

56
Q

What is step 1.5 of the action potential?

A

Step 1 ½ of the action potential is where it is heading towards the threshold.
Because of Na+ diffusing to this location because of an earlier action potential from somewhere else, the cell becomes more depolarized.

57
Q

What is step 2 of the action potential?

A

Step 2 is the rising phase.
Na+ flows into the cell as the Na+ voltage-gated channel opens.
K+ leak channels are still open and flowing even more as the Vm is going in the opposite direction that K+ wants it to be.
This is why the Vm doesn’t hit ENa.

58
Q

What is step 3 of the action potential?

A

Step 3 is the repolarization phase.
K+ voltage-gated channels are open after a time delay.
Now Vm heads towards EK.
K+ leak channels are still opening and joining the effort with K+ voltage-gated channels to get the Vm closer to EK.
The Na+ voltage-gated channels now have their globular protein time lock inactivating them.

59
Q

What is step 4 of the action potential?

A

Step 4 is the undershoot.
More K+ left and now the Vm is below the resting potential.
The voltage-gated K+ channel was open and thus Vm is near EK.
Na+ voltage-gated channels are now deactivated, but now they are closed.
The K+ voltage-gated channel closes.
Now, with K+ outflow less, the permeability of other ions has a greater influence and repolarizes the neuron back to resting potential.

60
Q

What is step 5 of the action potential?

A

Return to the threshold.

61
Q

What would happen if there was no absolute refractory period?

A

Then the signal would go backward and the neuron would just be repeating the same action potential until it dies.

62
Q

What would happen if there was no relative refractory period?

A

Less variability in neuronal signaling. Harder to pick out which information is more important.

63
Q

How does the Na+ voltage-gated channel open and close?

A

The extracellular gate opens and closes by voltage.
The intracellular gate closes and opens based on time.
Note: The intracellular gate closes 1 ms about the extracellular gate has opened.

64
Q

How does the K+ voltage-gated channel open and close?

A

It opens and closes based on voltage but after its voltage trigger point is reached, it is delayed in opening by 1 ms.

65
Q

What is saltatory conduction?

A

Saltatory conduction is the idea of the action potential jumping from node to Ranvier to node of Ranvier.
That is because, in a normal myelinated cell, the action potential can only get refreshed at the nodes of Ranvier.

66
Q

What goes wrong in MS?

A

MS is an autoimmune disease against myelinating cells.
Without these cells, there is less insulation for axons.
Thus, there is a higher chance for depolarization signal to leak out of the axon.
This can mess up signaling.

67
Q

What is the expected Eion when there is a positive ion with a high concentration in the cell?

A

The equilibrium potential must then be negative because the cell wants to flow outside the cell. But if the cell is negative enough, the negative charge will attract the positive ions to stay in the cell.
This is like K+.

68
Q

What is the expected Eion when there is a negative ion with a high concentration outside the cell?

A

Diffusion will force the ion to move inside the cell.
The Eion must be negative because enough of a negative charge will repel the incoming negative ions.
Like Cl-.

69
Q

What is the expected Eion when there is a positive ion with a high concentration outside the cell?

A

Diffusion will force the ion to move inside the cell.
Eion must be + then because a positive interior will repel the incoming positive ions.
Like Na+ and Ca2+.

70
Q

What is the expected Eion when there is a negative ion with a high concentration inside the cell?

A

Diffusion will force ions outside of the cell.

Eion will be + because a strong enough positive charge will attract the ion to stay inside the cell.

71
Q

Why can ions never reach their Eion?

A

They can’t reach it because the membrane is permeable to other ions as well. Thus, the resulting Vm is an average of their Eions (and concentrations) taking their membrane permeability (and thus their influence on Vm) into account.

72
Q

What are electrical synapses?

A

Gap junctions between neurons made of connexons.

73
Q

What are the advantages of electrical synapses?

A

Faster
Less error in sending.
More confident that the signal will be sent.
Bidirectional signaling.
Each cell can influence the other.
Simpler. Don’t need to worry about vesicle exocytosis, etc.
Less energy is needed.
Don’t need to build synaptic architecture or neurotransmitters.

74
Q

What are the disadvantages of electrical synapses?

A
Less variety in responses. 
EPSP and IPSP. 
A few small molecules can be passed between cells. 
Less flexible. 
Less regulation.
75
Q

What are chemical synapses?

A

The connection between the axon terminal of a presynaptic cell and a postsynaptic cell.

76
Q

What are the advantages of chemical synapses?

A

Wide variety of responses.
Many different types of receptors can be stimulated.
Most individual chemical synapses have 1 type of neurotransmitters, but overall, there are a vast variety of responses.
Me: I guess this is the biggest advantage.
Bidirectional signaling.
Retrograde signaling.
More regulation
Ex: Homeostasis.
Because of bidirectional signaling.

77
Q

What are the disadvantages of chemical synapses?

A

Higher error rate due to having a larger gap between the cells.

78
Q

Which neurotransmitters are used for fast synaptic transmission?

A

Amino acids and amines because they are always present in the synaptic terminal or can be easily made.

79
Q

Which neurotransmitters are used for slow synaptic transmissions?

A

Peptides because they have to be made in the cell body and have to travel down the axon to get to the axon terminal.

80
Q

What is Dale’s principle?

A

1 type of neurotransmitter per neuron.

81
Q

Which neurotransmitters do not Dale’s principles?

A

Peptide neurotransmitters. They are used for slow transmission and the synapse can run out of them. So, for the neuron to always have something to fire, neurons that have a peptide neurotransmitter will also have 1 amino acid or amine neurotransmitter.

82
Q

What does Ca2+ influx do to the synapse?

A

Ca2+ influxes because of depolarization of the axon terminal. They help bind vesicle SNARE proteins to SNARE proteins in the membrane. Thus, Ca2+ facilitates vesicle exocytosis.

83
Q

What are EPSPs and what ion channels can cause them?

A

Excitatory signals.
They vote for Vm to head to the threshold.
Na+ channels and Cl- channels (when the Vm is below -63 mV) cause EPSPs.

84
Q

What are IPSPs and what ion channels can cause them?

A

Inhibitory signals.
They vote for the Vm to head farther away from the threshold.
K+ channels and Cl- channels (when the Vm is above -63 mV) cause IPSPs.

85
Q

What is temporal summation?

A

Temporal summation=signals coming from one synapse.

Ex: One site voting again and again.

86
Q

What is spatial summation?

A

Spatial summation=signals coming from multiple synapses.

87
Q

What type of summation is present at NMJs and why?

A

Temporal summation because 1 motoneuron innervates a postsynaptic muscle cell.

88
Q

Why do axoaxonic synapses have more influence over axodendritic synapses?

A

Because they don’t have to fight for summation. They are one voice that can push for an IPSP or EPSP.

89
Q

Why is NMJ signaling so reliable?

A

The motor endplate contains multiple shallow folds filled with receptors.
The presynaptic active zones line up directly above the motor endplate folds.
The fold allows for greater SA:V.
While the cleft is still there the NMJ has evolved to make sure the most receptors are activated.

90
Q

What neurotransmitters are not in vesicles?

A

Peptides.

They are secretory granules.

91
Q

Why do peptide neurotransmitters need higher Ca2+ concentrations to fire?

A

Because their secretory vesicles tend to be farther away from Ca2+ influx sites.

92
Q

What are transmitter-gated ion channels?

A

Transmitter-gated ion channels bind to neurotransmitters and as a result, open an ion channel. That is their one job.

93
Q

What are GPCRs?

A

G-protein coupled receptors.
Their binding to a neurotransmitter triggers a host of different signal transduction pathways. Some may lead to ion channels opening while others can lead to different transcription of genes.

94
Q

What are autoreceptors?

A

Autoreceptors are receptors on the presynaptic neuron that are sensitive to neurotransmitters. These receptors allow the presynaptic cell to know what it is sending and act as a safety value to regulate neurotransmitter transmission to make sure it stays at the appropriate levels.

95
Q

What are the 3 ways neurotransmitters are removed from the synaptic cleft?

A

Enzymatic removal.
Uptake- by the presynaptic neuron or glia.
Diffusion

96
Q

Why are dendrites not myelinated?

A

More opportunity for synaptic connection.

Dendrites are not for sending action potentials, they are collecting summating signals.

97
Q

Why do dendrites typically not have action potentials?

A

Not myelinated so the signal will leak easier out of the cell.
There is a host of warring signals (EPSPs and IPSPs) so it is much harder to start an action potential.
They don’t have voltage-gated channels.

98
Q

What is the advantage of dendrites being tapered?

A

Wider axons make the message easier to travel.

99
Q

Where on the dendrite would certain ion channels be worthless?

A

Cl- on the ends of the dendrite.
Cl- helps modify the signal to bring it closer to rest.
Thus, they have the strongest influence after the signal has happened.

100
Q

What are the general steps for synaptic transmission?

A

The action potential travels down to the synapse.
Voltage-gated Ca2+ channels open because of the depolarization of the synapse.
Ca2+ influx - Ca2+ attaches to the SNARE proteins.
Vesicle exocytosis
Neurotransmitters attach to postsynaptic receptors.
Postsynaptic signal
Neurotransmitter clean up and degradation.
–Enzymatic destruction
–Reuptake
–By the presynapse or glial cells.
–Diffusion
Retrograde signal
Some are autoreceptors.
By how much they are being activated, the presynaptic cell can tell how much neurotransmitter is left in the cleft.

101
Q

Why is cleaning up neurotransmitters from the synaptic cleft important?

A

Neurotransmitters need to be cleaned up so that they don’t keep binding to receptors and making the signal longer than intended.
Can lead to desensitization or unintended extra signaling.

102
Q

Why does reuptake not increase signaling?

A

Increasing reuptake does not increase signaling because it won’t impact the number of neurotransmitters the presynaptic cell has (especially for amino acids and amines).

103
Q

What is postsynaptic density?

A

Protein density just above and inside the postsynaptic cell.
Contains neurotransmitter receptors that change intercellular signals to intracellular signals.

104
Q

What are axodendritic synapses?

A

Postsynaptic membrane is a dendrite.

105
Q

What are axospinous synapses?

A

Postsynaptic membrane is on a spiny dendrite.

106
Q

What are dendrodenritic synapses?

A

Dendrities that form synapses with each other.

Only occurs in specialized neurons.

107
Q

What are axosomatic synapses?

A

Postsynaptic membrane is a cell body.

108
Q

What are axoaxonic synapses?

A

Postsynaptic membrane is on another axon.

109
Q

What are the two types of SNARE proteins in synapses?

A

Vesicles have v-SNARES
The outer membrane has t-SNARES.
T is for target membrane.
V and T SNARES bind very tightly to each other.

110
Q

What is synaptic integration?

A

Multiple synaptic signals combining in one postsynaptic neuron.
The neuron collects all of these and sends out 1 output.

111
Q

What is the subventricular zone (SVZ)?

A

This zone is on the outside of the ventricles.

The inside of the neural tube becomes the ventricles so the SVZ is outside the neural tube.

112
Q

What is the subgranular zone (SGZ)?

A

Neurogenesis location in the hippocampus.

113
Q

What are radial glial cells?

A

Radial glial cells are the pluripotent stem cells of the brain that can divide into neurons and glia.

114
Q

How do radial glial cells not deplete themselves?

A

One daughter cell of a radial glial cell stays a radial glial cell while the other becomes a neuroblast that will divide into a mature neuron or glia.

115
Q

Why are neuroblasts not an accurate measure of whether there is neurogenesis or not?

A

Because neuroblasts do not mature until they reach their final location. Thus, there may be identifiable neuroblasts but it may be unknown whether they are actually surviving long enough to mature.

116
Q

How do neuroblasts migrate?

A

Neuroblasts migrate using the scaffolding provided by radial glial cells.

117
Q

What are some known locations of neurogenesis in non-human animals?

A

It is known that in mice and rats that their olfactory bulb, hippocampus, and even their striatum and neocortex continue neurogenesis into adulthood.

118
Q

Does neurogenesis occur in humans?

A

It is contested. It may happen in the hippocampus.

The problem is that the good tests we use in mice are unethical to do to a large healthy sample size of humans.

119
Q

What is BrdU?

A

A carcinogen who uridine acts like uracil and binds to adenine in DNA. Thus any new daughter cells will be labeled with BrdU.

120
Q

What is the clinical significance if neurogenesis can be found or manipulated?

A

Therapeutic drugs
Brain tissue replacement.
Spinal cord repair
Tumors

121
Q

How do neurons start differentiating?

A

Neuronal cells start differentiating by extending neurites.