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Neurobiology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is the CLARITY method?

A

The brain is suspended in gel to make it transparent. Any fluorescent antibodies that were added then glow. Thus, you can see whole 3D structures in the brain.

Dead tissue.
Non-humans because of technology limitations. Assesses structural information.

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2
Q

What is the computed tomography (CT) method?

A

Different X-rays take structural pictures of the brain in different planes and then a computer comes back with a whole image.

Alive, whole organism.
Mostly done on humans because of technology limitations.
Assesses structural information.

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3
Q

What is the magnetic resonance imaging (MRI) method?

A

Measures the magnetic resonance of H+ as water is transported throughout the brain and changes. Comes up with a structural picture.

Alive, whole organism.
Mostly done on humans.
Assess structural information.

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4
Q

In what ways is MRI better than CT?

A

More high-resolution images. Does not use X-rays which can be dangerous.

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5
Q

What is Positron Emission Tomography (PET)?

A

Uses radioactive labeled substances and can label different parts of the brain based on blood flow and metabolism of that area.

Living whole organisms.
Done on humans.
Examines activity.

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6
Q

What is functional magnetic resonance imaging (fMRI)?

A

Measures the magnetic resonance of HbO and changes when it gives off an O. Thus, can detect which brain area is getting more O2 and thus blood flow.

Living whole organisms.
Done on humans.
Examines activity.

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7
Q

What are Nissl stains?

A

They stain for the soma of nuclei. They don’t have high resolution but you can count all the neurons in a given area because all the neurons are stained.

Dead tissue.
Done in humans and non-humans.
Examines structure.

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8
Q

What are Golgi stains?

A

They stain some neurons but in high resolution, getting all the neurites as well.

Dead tissue.
Done in humans and non-humans.
Examines structure.

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9
Q

What are microarrays?

A

Typically DNA microarrays, there is a plate with a bunch of different labeled DNA. If the RNA or DNA from the sample is complementary to the DNA then it will glow and you know the match.

The sample must start alive to get the sample.
Done on humans and non-humans.
Measures gene expression activity.

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10
Q

What are transgenic mice?

A

They are mice that have been genetically altered. These can include knockout mice.

A genetic test.
Only done in non-humans.
Manipulates the brain to do something.

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11
Q

What are Cre/LOX mice?

A

Like GAL4/UAS, but this system cuts out genes that are surrounded by LOX sequences. Can target gene knockout to different tissues.

A genetic test.
Only done in non-humans.
Manipulates the brain to do something.

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12
Q

What is GAL4/UAS?

A

A very versatile genetic system to overexpress or knockout different genes in different tissues.

A genetic test.
Only done in non-humans.
Manipulates the brain to do something.

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13
Q

What are artificial membranes?

A

They are a model system to test for permeability of different substances and how Vm can change as a result.

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14
Q

What is the difference between intracellular recording and extracellular recording?

A

Both record Vm. Intracellular recording has the electrode on the inside while extracellular recording has the electrode on the outside.

Done to living tissue.
Done in humans and non-humans.
Examines activity.

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15
Q

What is optogenetics?

A

Expressing light-sensitive channels in the brain to manipulate brain activity. The channels are typically excitatory or inhibitory light-sensitive ion channels.

A genetic test.
Only done in non-humans.
Manipulates the brain to do something.

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16
Q

What is the difference between voltage clamping and patch clamping?

A

Voltage clamping is less specific and it just records Vm at the membrane. Patch clamping is more specific and it isolates a piece of membrane and can analyze the structure of proteins there at different voltages.

Done to living tissue.
Done in non-humans.
Examines activity.

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17
Q

What is 3DEM?

A

3D Electron Microscopy. Assesses the structure of different areas at a very high resolution.

Dead tissue.
Only done in non-humans because of technology limitations at the moment.
Assesses structure.

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18
Q

What is immunohistochemistry?

A

Immunohistochemistry adds different labeled molecules and then their location is visualized under a microscope. BrdU stains DNA while proteins have a system of 2 antibodies where the secondary antibody has the fluorescent tag.

Can start in alive or dead tissue. Depends on the test.
Done to humans and non-humans.
Examines activity.

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19
Q

Fluorescence in situ hybridization (FISH)

A

Uses a complementary RNA strand for the target RNA..

Done in dead tissue.
Done to humans and non-humans.
Examines activity.

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20
Q

What is MEG?

A

Like EEG but with magnets. Keeps a higher temporal resolution but has a better spatial resolution than EEG.

Living, whole organisms.
Done to humans.
Assesses activity.

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21
Q

What is EEG?

A

Assess electrical signals. Has a high temporal resolution but not a great spatial resolution.

Living, whole organisms.
Done to humans.
Assesses activity.

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22
Q

What is microiontophoresis?

A

Assesses the postsynaptic response of a NT. NT is placed in the cleft as the Vm response is recorded.

Alive tissue.
Must do while in alive tissue but can be done to humans and non-humans.
Manipulates the brain to do something.

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23
Q

What is the ligand-binding method?

A

Assesses the effect a receptor has before the real NT ligand is found. Uses different drug ligands to see what the effect in the cell is.

Alive tissue.
Must do while in alive tissue but can be done to humans and non-humans.
Manipulates the brain to do something.

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24
Q

What are neuropharmacological analyses?

A

Assesses the effects of different drugs on the nervous system. Can also distinguish receptor structure and receptor subtypes.

Alive tissue.
Done in humans and non-humans.
Manipulates the brain to do something.

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25
Q

What is CRISPR?

A

A genetic method that can alter genes.

Alive tissue.
Only done in non-humans.
Manipulates the brain to do something.

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26
Q

How are primary antibodies for immunohistochemistry made?

A

They are made by injecting the antigen into an animal and the animal makes antibodies for the antigen.

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27
Q

What are microelectrodes/ECog?

A

They are like miniEEGs in the brain. Can be done in humans but they are very invasive. Done in living whole organisms. Examines activity.

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28
Q

What are IEGs?

A

Immediate early genes. These can be stained with immunohistochemistry. Shows which neurons were active before the subject died.

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29
Q

What is declarative memory?

A

It is focused in the hippocampus and is mostly semantic and episodic memory.

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30
Q

What is semantic memory?

A

Memory of facts.

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31
Q

What is episodic memory?

A

Memory of stories/events from life.

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32
Q

What is working memory?

A

Working memory is located in many places, one of them being the prefrontal cortex.
The memory is not being consolidated yet and the neurons have to stay active for the memory to stay on the mind.

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33
Q

What is habituation?

A

Responding less to signal as the brain learns it doesn’t mean anything.

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34
Q

How was habituation tested in Aplysia?

A

Continuing to touch the siphon until the gill reflex decreased.

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35
Q

What is a molecular mechanism for habituation?

A

Inactivating Ca2+ channels.

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36
Q

What is sensitization?

A

A stronger response to a stimulus than normal.

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37
Q

How was sensitization tested in Aplysia?

A

Shocking the tail, and then touching the siphon.

Shocking the tail makes the siphon neuron more sensitive.

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38
Q

What is a molecular mechanism for sensitization?

A

Serotonin → G protein → adenylyl cyclase activated → cAMP → PKA → K+ channels locked for longer. This leads to a higher Ca2+ influx.

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39
Q

What is classical conditioning?

A

Pairing stimuli together so that a response happens to the now conditioned stimulus.

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40
Q

What is the conditioned stimulus?

A

The stimulus that is the new one being associated with the US.

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41
Q

What is the unconditioned stimulus?

A

The stimulus that evokes a response without any association.

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42
Q

What is the conditioned response?

A

The response to the CS after pairing.

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43
Q

What is the unconditioned response?

A

The response to US.

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44
Q

In classical conditioning training, which stimulus is presented first, CS or US?

A

CS.

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45
Q

How was classical conditioning tested in Aplysia?

A

Touching the siphon, shocking the tail, and then touching the siphon.

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46
Q

Which leads to a stronger response: Sensitization or classical conditioning?

A

Classical conditioning.

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47
Q

What is a molecular mechanism for classical conditioning?

A

One molecular mechanism for this is that there is more cAMP and PKA production and activation of calcium-calmodulin which is an enhancer for adenylyl cyclase and a longer-term protein.
The G protein is still vital to adenylyl cyclase’s activation so serotonin release is needed during pairing training.

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48
Q

What is instrumental/operant conditioning?

A

Learning a behavior in response to reward and punishment.

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49
Q

What is procedural memory?

A

Habit and muscle memory.

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50
Q

Where does procedural memory consolidated?

A

In motor areas of the brain such as the cerebellum and basal ganglia.

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51
Q

What are the main functions of the hippocampus?

A

The pairing of arbitrary ideas
Transivity
Consolidation
Spatial memory

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52
Q

Does all consolidation happen in the hippocampus?

A

No. The hippocampus does a lot of declarative memory consolidation but nondeclarative memory consolidation and memories related to specific sensory modalities take place in different parts of the brain.

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53
Q

What are engrams? Why are they useful?

A

A net of connected neurons who all uniquely contribute to holding a memory. A threshold of activation must be reached for the memory to be retrieved.
They are useful because instead of one neuron holding a memory, you spread your eggs among many baskets by letting multiple neurons hold the memory.

54
Q

What is the standard model of memory?

A

Memory is consolidated in the hippocampus.

The engram moves from the hippocampus to the neocortex and has no more connections to the hippocampus.

55
Q

What is the multiple trace model of memory?

A

Memory is consolidated in the hippocampus.
The engram moves the hippocampus to the neocortex but still has connections to the hippocampus.
Thus, the hippocampus can reopen the memory and refresh it with new stimuli information and connections.

56
Q

What did bird studies say about retrieval in the hippocampus?

A

The hippocampus has a weaker retrieval function compared to consolidation.
When birds need to make memories of where they hid seeds (like during the fall), they have big hippocampuses.
When birds need to retrieve the seeds and the memories of where the seeds are hidden, they have small hippocampuses and don’t need it to be active.

57
Q

What are place cells?

A

Spatial memory cells that activate for one particular familiar location.

58
Q

What are grid cells?

A

Spatial memory cells that activate at particular intervals for both familiar and unfamiliar locations.

59
Q

What are Jennifer Aniston cells?

A

This was a study that found that people had a particular hippocampal neuron that activated for particular familiar celebrities.

It showed that the hippocampus might store specific memories.

This cell also activated at different perspectives of Jennifer Aniston and even just her name written out.

60
Q

Who was Karl Lashley? What did he find?

A

Karl Lashley used rodents and cut different parts of the top of their cortex to see if it produced deficits in remembering how to go through a maze.
The problem with his study is that he only cut the top of the cortex and the task he chose for the mice to remember may have been testing different facets of memory.

61
Q

Who was Wilder Penfield? What did he find?

A

He found that shocking the medial temporal lobe had people talking about what seemed like memories.
He did get a great sample size.
The problem with his study is that the people were under a lot of drugs to be conscious during this, he has no way to verify if what people were telling him were actual memories or hallucinations, and epileptics do not have typical brains.

62
Q

Who was Brenda Milner? What did she find?

A

Brenda Milner only had a sample size of 1 but she extensively studied H.M.
She determined that declarative memory was focused in the hippocampus was non-declarative memory was not in the hippocampus.
The hippocampus is key for consolidating memories.
The problem with H.M. was that he was such a rare and severe case.

63
Q

What is the Morris water maze?

A

Can be used for spatial memory for rats.
Habit learning occurs if the rat is placed in the same location each time.
Spatial memory is learned so that the rat knows where to go each time despite being dropped in a new location.

64
Q

What is the radial arm assay?

A

Can be used for multiple assays.
At a basic level, it tests for hippocampus function because the rat has to remember what arms it has gone down and which arms it hasn’t gone down yet.
Ex: The Win-stay task measures habit memory.
The rats learn that where the light is, food is.

65
Q

What is the delayed non-matching sample (DNMS) assay?

A

The subject must pick the stimulus they haven’t seen before.
This assures that working and habit memory is not being used.
Tests for declarative memory.

66
Q

What is the seed retrieval with lidocaine assay?

A

During experiments where the hippocampal function was blocked either during hiding or retrieval, the bird made many more errors in retrieving the seeds when the hippocampal function was disrupted during hiding.

67
Q

What is the Wisconsin card sorting test?

A

Tests working memory in what the rules of sorting the categories are.
People with prefrontal lesions, an area associated with working memory, do not do well on this assay.

68
Q

How are MRIs used to test memory?

A

Used in humans to test the size of the hippocampus.

69
Q

How are fMRIs used for memory assays?

A

Used in humans to see what parts of the brain are active during different activities.
Ex: During a spatial memory task, is the hippocampus lighting up?

70
Q

What is the weather prediction test?

A

Used to test habit learning.
People are presented with cards with different types of symbols of numbers of symbols.
The rules are very complicated but there are rules.
People are able to learn the habit and implicitly know the rules which present as a gut feeling for whether the correct prediction will be sunny or rainy.
Declarative memory amnesiacs do well on this test.

71
Q

How are Jennifer Aniston cells different than expected?

A

Since they are single cells that are activating to this one specific stimulus, they don’t seem to be engrams.
Also, it is thought that consolidated memories move outside of the hippocampus but these memories are still in the hippocampus.

72
Q

What did H.M. teach us?

A

Memory systems are separate.
Declarative is separate from nondeclarative.
Short-term memory and long-term memory are distinct.
Working memory is separate.
The hippocampus is key for consolidating memories.

73
Q

In the multiple trace model for memory, what is a possible function for the connections to the hippocampus?

A

They may be there so the hippocampus can reopen the memory, update it, and make more connections.

74
Q

What is the difference between learning and memory?

A

Learning=acquistion of new knowledge and skills.

Memory=retention of new knowledge and skills learned.

75
Q

What is transient global amnesia?

A

Transient global amnesia=memory spell where working memory is fine but they have anterograde amnesia when the person recovers they have a memory gap by retrograde amnesia.
It may be caused by brief cerebral ischemia or loss of blood flow to the brain.

76
Q

What is the difference between retrograde and anterograde amnesia?

A

Anterograde means you lose the ability to form new memories.
Retrograde means you lose the ability to retrieve old memories.

77
Q

What makes Aplysia a great model organism for learning and memory?

A

Simple. Large neurons with distinctive shapes and invariant placement.
The neurons can also survive outside the body for a few hours.

78
Q

What are 4 learning rules?

A

More repetition=longer/better learning.
Relearning is easier than learning something for the first time.
Learning a new thing can disrupt the consolidation of something else you learned right before.
Electric shocks disrupt consolidation.

79
Q

What are some similarities between place cells and specific memory cells (Jennifer Aniston cells)?

A

Both activate for a particular thing.

Both don’t last forever.

80
Q

What roles do the hippocampus and basal ganglia play in habit learning?

A

The hippocampus can help learn hard rules first (like learning fingerings on an instrument) but then the striatum can help learn the routine of where fingers go so that you don’t really have to consciously recall it.

81
Q

What are the main two parts for vision plasticity?

A

Ocular columns and binocular vision.

82
Q

What are ocular columns?

A

Ocular columns=neurons that heavily receive input from one eye.

83
Q

Compare and contrast the ocular columns connections during and after the critical period.

A

During the critical period, each column does have connections to the contralateral eye but it is weaker and these connections disappear after the critical period.
So, during the critical period if one eye is covered, then there is no competition anymore for the contralateral eye and it can take over the column.

84
Q

What is binocular vision?

A

Binocular vision requires input from both eyes and for the eyes to work together.
Binocular vision allows people to be able to gauge distance.

85
Q

What would happen if it alternated which eye was covered for a day?

A

Ocular columns - fine
Each eye is able to practice on its own and build connections.
Binocular vision - not working
The eyes don’t have time to practice together.

86
Q

What would happen if you alternated between covering both eyes for a day and then not covering the eyes?

A

Ocular columns - fine
Both eyes have time to practice.

Binocular vision - fine
Both eyes have time to practice together.

87
Q

What would happen if you covered one day every day for a few months?

A

Ocular columns - not fine
The uncovered eye will take over the covered eye’s ocular column.

Binocular vision - not working
The eyes don’t have time to practice together.

88
Q

What would happen if you covered both eyes for the entire critical period?

A

Ocular columns - not working
The ocular columns would not have developed at all.

Binocular vision - not working
This area never got any signal and is now most likely being used for something else.

89
Q

Explain the reason for eye patch treatment in humans:

A

Used for people who have lazy or weaker eyes.
People put an eye patch over their strong eye for a few hours every day to allow their weak eye some time to practice on its own. The weak eye is able to strengthen its connections and can eventually be as strong as the nonlazy eye.

90
Q

What is the trisynaptic pathway in the hippocampus?

A

Entorhinal cortex (also called granule cells) → perforant path → dentate gyrus (granule cells) → mossy fibers → CA3 (pyramidal cells):
→ Schaffer collateral → CA1 (pyramidal cells) → entorhinal cortex
→ fornix.
This may come back to the entorhinal cortex.

91
Q

What does the trisynaptic pathway of the hippocampus do?

A

The trisynaptic pathway repeats information.
Because it loops, new information can override old information or if old information is strong enough, new information will not be consolidated.

92
Q

What is LTP?

A

Long-term potentiation (LTP) is an artificial learning-like system known in the hippocampus.

93
Q

How does LTP affect synaptic firing rate?

A

It increases the rate of synaptic firing and strengthens synapses.

94
Q

Do you want LTPs to be specific or nonspecific?

A

Specific.

You don’t want LTPs that are nonspecific because then you are not remembering what you want to remember.

95
Q

What is an NMDA receptor?

A

NMDA is a voltage-gated and ligand-gated channel.
Glutamate is the ligand used for the ligand gate.
It is a Ca2+ channel.

96
Q

What is an AMPA receptor?

A

A sodium channel that is ligand-gated by glutamate.

97
Q

What is Hebbian learning?

A

Neurons that fire together, wire together.
If you use a connection it gets stronger.
If you don’t use a connection, it gets weaker.

98
Q

What are some structural pieces that indicate stronger synapses?

A 
Heavier cerebral cortex
Larger cell bodies
More dendritic branching
More spines
Places where synaptic contact happens. 
Leads to a larger postsynaptic spot. 
Larger synaptic contacts
99
Q

What are the general steps of LTP?

A

In LTP, the membrane is depolarized enough that NMDA receptors are activated.
Ca2+ comes into the cell, depolarizes it more, and starts signal transduction pathways that activate CaMKII and PKA that lead to AMPA phosphorylation and insertion.
AMPA phosphorylation leads to the AMPA receptors being open for longer.
AMPA insertion means there are more places glutamate (AMPA’s ligand) can bind to.

100
Q

How is BDNF involved with LTP?

A

Brain-derived neurotrophic factor (BDNF) is also activated during LTP.
It helps keep the cells happy and can trigger the growth of the synapse.

101
Q

How are retrograde signals involved with LTP?

A

Retrograde signals can trigger LTPs by causing an increase in glutamate neurotransmitter release.

102
Q

AMPAkines are marketed as memory-enhancing drugs. What could these drugs be doing and would it do as it is marketed to do?

A

AMPAkines could phosphorylate them or act as agonists enough to depolarize the membrane enough to activate NMDA receptors.
With activated NMDA, LTP will occur.
These drugs will enhance memory but the drugs are not specific.
Thus they will lead to seizures, overstimulation, and feeling of being overwhelmed.

103
Q

How will the synapse adjust to someone taking AMPAkines?

A

With the extra signal that the system doesn’t want, homeostasis will kick in and decrease the amount of glutamate that is released.
Thus, it will try to lower the synaptic signal.
This can have negative effects once someone stops taking an AMPAkine because now their memory may be worse before their homeostasis readjusts because now there are releasing less glutamate than they were before taking the drug.

104
Q

What is LTD and how does it affect synaptic firing rate?

A

Long-term depression (LTD) happens when the synaptic firing rate decreases. This leads to the synapse getting weaker.

105
Q

Why is LTD important for memory?

A

LTD is not all about forgetting. It also forms a memory of what something is not.
Thus, it prevents certain stimuli from activating unrelated memories.

106
Q

What is the molecular mechanism for LTD?

A

LTDs lead to the activation of phosphatases and fewer AMPA receptors inserted into the membrane.

107
Q

What are CREs and CREBs?

A

Certain genes have cAMP response elements (CREs).
These bind to regulatory elements of certain genes and are a loading dock for cAMP response element-binding proteins (CREBs).
CREBs are transcription factors.

108
Q

What are two kinases that cAMP activates?

A

PKA + MAPK.

109
Q

What is needed for long-term memory? How is this process started?

A

Protein synthesis.

It is started by kinases being activated for long enough.

110
Q

What does PKA + CREB1 do for long-term memory?

A

PKA phosphorylates CREB1 which activates gene expression and is associated with long-term memory.

111
Q

What does MAPK + CREB2 do for long-term memory?

A

MAPK phosphorylates CREB2 and removes it from the CREs.

CREB2 normally blocks CREB1 and prevents transcription which is negatively associated with long-term memory formation.

112
Q

What would happen if PKA functioned better than normal?

A

More CREB1 phosphorylated → better formation of long-term memories.

113
Q

What would happen if PKA did not function in its role with CREB1?

A

Less CREB1 phosphorylated → less formation of long-term memories.

114
Q

What would happen if MAPK functioned better than normal?

A

More CREB2 phosphorylated → better formation of long-term memories.

115
Q

What would happen if MAPK did not function in its role with CREB2?

A

Less CREB2 phosphorylated → less formation of long-term memories.

116
Q

What genes does CREB1 express?

A

CREB1 is a transcription factor that leads to the expression of late proteins and ubiquitin hydrolase.

117
Q

What do late proteins do for long-term memory?

A

Late proteins lead to long-term memory formation.

118
Q

What does ubiquitin hydrolase do?

A

Ubiquitin hydrolase leads to breaking off ubiquitin from PKA. Ubiquitin targets proteins for degradation so removing them leads to better long-term memory formation.

119
Q

What is synaptic tagging?

A

Synaptic tagging is when the synapses have a tag to snatch newly synthesized proteins and direct them into the correct synapse.

120
Q

What is a tetanus?

A

Tetanus=string of electrical signals to depolarize the cell repeatedly.

121
Q

What should happen to maze learning if LTP is inhibited?

A

Lack of memory formation.

122
Q

What should happen to maze learning if a tetanus is provided?

A

While LTP will occur, tetanus is not specific. So, memory will actually be worse.

123
Q

What is the advantage of fruit flies for memory experiments?

A 
Small 
Can learn
Genetics
Quick generation time
Easy maintenance
124
Q

What are the disadvantages of fruit flies for memory experiments?

A

Different neural system.
Don’t have the same brain areas vertebrates do.
Tiny neurons.

125
Q

In a mutant, how can you break up sensitization and classical conditioning?

A

Changing Ca-calmodulin activity.

126
Q

In a mutant how can you separate short-term and long-term memory?

A

By MAPK activity, CREB-1, or CREB-2 activity.

127
Q

What would inhibiting all proteins do for memory formation?

A

Inhibiting all proteins means that memory is not formed.

128
Q

What are ways to break up the intense emotional connections to some memories?

A

Propranolol is a 𝛽 blocker that turns off the emotional system.
This leads to remaking the memory without the emotional part.
MDMA (Molly and ecstasy) and other psychedelics can really relax people and disconnect the emotional part of the memory.

129
Q

Who was N.A. and what did they tell us about memory?

A

N.A. was the victim of a fencing foil accident and their diencephalic structures were damaged. This is part of the fornix for the hippocampus and as a result, they had similar (but not as severe) memory loss to H.M.

130
Q

How is CaMKII involved in memory formation and how does it stay active?

A

CAMKII phosphorylates proteins like AMPA and can make them more active leading to an LTP.
After an LTP, CAMKII doesn’t close all the way can it can keep itself activated by phosphorylating itself.

131
Q

How does ZIP zap memories?

A

It inhibits PKM𝜁 long enough that its targets become dephosphorylating and the LTP is disrupted.
Without LTP, the memory weakens.

Neurobiology (5 decks)

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