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Neuroscience > Exam 2 - Chapter 2 and 3 > Flashcards

Exam 2 - Chapter 2 and 3 Flashcards

1
Q

What is a synapse?

A

functional connection between two neuronal cells

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2
Q

Where are interneuronal synapses anatomically located? How does this relate to their classification (axodendritic, axosomatic, etc.). Which type is most common? Which is least common?

A
  • interneuronal synapses are the synapses btwn two neurons
  • classification determines what type of cell the pre and postsynaptic cells are (axodendritic = pre cell is axon and post cell is dendrite)
  • most common is axodendritic
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3
Q

How can synapses be detected and localized histologically?

A
  • some areas of synapses are more dense in electrons, which will appear darker in EM
  • these areas have more proteins
  • in presyn cell - there are a lot of proteins that are related to the release of NTs
  • in postsyn cell - there are a lot of proteins that are related to the receiving of NTs
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4
Q

What are dendritic spines? What is their role in synapse formation? How are they involved in neuroplasticity?

A
  • specialized structures that receive specific types of synaptic input
  • most common in areas of plasticity - which is the ability to change
  • they can change their structure and size, which is the process that also occurs in processes involving plasticity in the brain like learning and memory
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5
Q

What are neuronal growth cones, and how are they organized?

A
  • dynamic structure that forms while neurons are developing
  • important in areas of plasticity
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6
Q

What is their anatomy (growth cones), and what cytoskeletal structures to they contain?

A
  • look like webbed fingers
    • finges are filopodium - elongated filamentous shapes
    • webbing are lamellipodium - sheet like structures that connect the filopodium
  • microtubules and microfilaments are involved in the structure (microfilaments are the most abundant)
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7
Q

What is the function of growth cones?

A
  • extend filopodium in order to create changes in their cytoskeleton, allowing the neuron to grow with it
  • treadmilling - minus end (closer to nucleus) moves towards the plus end (distal end of filopodium) with the help of actin, allowing the plus end to extend
  • important in neuronal growth and regeneration
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8
Q

What specific example of axon guidance/growth cones did we discuss in lecture?

A
  • optic chiasm - visual system
  • optic nerves from the retina project with growth cones, and cross over to the contralateral side of the optic chiasm
  • some remain on the same side (ipsilateral), but extracellular matrix factors provide cues to determine which side they grow to
    • repulsive - grows away from this cue
    • attractive - grows towards this cue
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9
Q

What is Wallerian Degeneration? Which neurite is involved, and what part degenerates?

A
  • when the axon begins to break down when disconnected from the soma (axonal transport is interrupted)
  • usually due to injury
    • site distal to injury breaks down, because the proteins can no longer be transported to it, but the proximal site will eventually form growth cones
  • Augustus Volney Waller
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10
Q

Why is axonal transport so important for neuron function?

A
  • due to axon not being able to produce its own proteins, it has to receive proteins from the soma in order to continue functioning
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11
Q

What cytoskeletal structures are involved in transport?

A
  • microtubules
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12
Q

What are the different types of transport (anterograde/retrograde and fast/slow). How are they different?

A
  • Fast transport - 1000 mm per day, material is enclosed in vesicles and then transported down microtubules, fueled by ATP
    • anterograde transport - fast transport, soma to axon terminal, done by protein kinesin
    • retrograde - mainly fast transport, axon terminal to soma, done by protein dynein
  • Slow transport - 10 mm per day, a lot of starting and stopping in order to drop off cargo at different points of the microtubules
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13
Q

What are the two major motor proteins that drive axonal transport? Which is used for which type of transport?

A
  • kinesin is in charge of anterograde
  • dynein is in charge of retrograde - also present in cilia
  • attach to microtubules
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14
Q

What is tract/circuit tracing?

A
  • injection of biological markers into the nervous system, and then seeing how they are transported into the neurons/what type of transportation is used
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15
Q

Explain the method for tract tracing we discussed in class. How does this technique relate to axon transport mechanisms?

A
  • injection of HRP, which is a viral protein
  • taken up by neurons, and is transported via retrograde transport to the cell body
  • retrograde tracing specifically
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16
Q

What are the two major histological markers associated AHZ with that can be identified postmortem?

A
  • neurofibrillary tangles - tau, a microtubule stabilizing protein, forms abnormal clumps that interfere with the cytoskeleton’s microtubules
  • amyloid plaques - extracellular deposits of beta amyloid, derived from abnormal proteolysis of amyloid precursor protein
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17
Q

Where are these proteins found in the tissue? Are they intracellular or extracellular proteins?

A
  • NFTs are intracellular
  • Plaques are extrecellular
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18
Q

How are each of these abnormal proteins formed (NFTs and plaques)?

A
  • beta amyloid - comes from the amyloid precursor protein. Too much is produced when there is a lot of beta and gamma sekretase (enzymes that cut out beta amyloid from APP)
  • tau - becomes hyperphosphorylated (too many Ps from ATP is transferred onto it), becomes misfolded and gets detached from microtubules, and begin to form insoluble clumps called GTOs, which clump together to form PHFs, which then clump together to form NFTs
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19
Q

What is the biological consequence of tau becoming hyperphosphorylated?

A

plaques cause the death of nearby neurons

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20
Q

What are paired helical fragments (PHF)? Where are they found?

A
  • large helical molecules that are formed by clumps of GTOs
  • clump together for form NFTs
  • found in the brain
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21
Q

Chronic traumatic encephalopathy, in what way is it similar to Alzheimer’s disease? How is it different?

A
  • progressive and fatal brain disease
  • also diagnosed post mortem by looking at brain sections
  • also have plaques and tangles
  • main risk for AD is age, but for CTE the main risk is chronic head injuries
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22
Q

Which promising new Alzheimer’s therapy did we discuss? What type of therapy is this, and how does it appear to work?

A
  • antibody based immunotherapy that mainly targets the plaques
  • antibodies attach to plaques in hope that the immune system will target them
  • all drugs typically end in -mab
    • monoclonal antibodies
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23
Q

What brain imaging method was used to study the effects of this treatment in the study we discussed?

A

PET scans

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24
Q

What is the history of this treatment in terms of human clinical trials and review by the FDA?

A
  • aducanumab was the first successful type of this treatment, moved to phase 3 clinical trial, and after being discontinued, results were gone over again and the trials began again
  • got FDA approval, named the drug Aduhelm
  • Recently, there has been congressional inquiry into it over the prices and marketing, despite this, FDA granted accelerated approval for Aduhelm and Lequembi
  • drug produced by a diff company, Donanemab was also given FDA approval
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25
Q

What are PNN’s? Where are they found, and what is their biochemical composition?

A
  • found in extracellular matrix, mainly surrounding the soma and dendrites
  • made of proteoglycans (proteins and sugars, mainly composed of GAG chondroitin sulfate)
  • very common in connective tissue and in the nervous system in areas of plasticity, mainly in CNS
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26
Q

What roles are PNNs thought to have in the nervous system?

A
  • regulate plasticity by inhibiting it
  • prevent neurons from expanding
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27
Q

What potential therapies are being investigated that relate to PNNs?

A
  • helping pts with PTSD and drug addiction by potentially erasing their memories, by breaking down PNNs to encourage plasticity
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28
Q

What are some related experiments carried out in animal models that we discussed relating to PNNs?

A
  • Try to erase fear memories in rats – 1st they established a fear memory through pavlovian conditioning, then injected chondroitinase ABC (ChABC) into the amygdala (the area in charge of fear) that breaks down chondroitin sulfates, which in turn breaks down PNNs, thus restoring plasticity, and found that the rat no longer had a fear response
  • Try to erase drug memories in mice – established conditioned place preference in mice and found that if they injected ChABC into the amygdala of mice, they no longer exhibited drug seeking behaviors
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29
Q

What are 4 major types of glial cells in the CNS? What are major functions of each that we discussed?

A
  • Astrocytes - helps create and regulate the BBB, provide structural and metabolic support
  • Oligodendrocytes - create myelin sheaths in CNS, only connect to neurons
  • Ependymal - line the inside of ventricles, aid in the secretion, filtration, and circulation of CSF
  • Microglia - come from monocytes, phagocytic cells that take in and break down materials/cells (immune response, also important in taking up debris from injury)
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30
Q

Which cells myelinate neurons in the CNS and PNS?

A
  • CNS - oligodendrocytes
  • PNS - schwann cells
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31
Q

What are nodes of ranvier?

A
  • gaps in the myelin sheath
32
Q

How are myelinated axons different from non-myelinated axons? What is the function of myelin?

A

Myelin allows the electrical impulses to propagate faster than unmyelinated

33
Q

What are the two major diseases of myelination that we discussed in class?

A
  • Multiple sclerosis - Autoimmune disorder that only affects oligodendrocytes, periods of flare ups when the immune system attacks the oligodendrocytes
    - Creates inflammation and scar tissue (sporadic plaques), interrupts with nerve transmission
    • Lots of motor affects
  • Guillain barre – autoimmune disorder in which the immune system is attacking the myelin in the PNS, and the satellite cells
    • Usually caused by viral infections and sometimes vaccination complications
    • Often affects the nerves in the legs, but in the most severe cases, it can affect the phrenic nerve (controls breathing)
    • Possibly related to COVID
34
Q

Which of the two myelination diseases affects the CNS? The PNS?

A
  • MS is only in the CNS
  • GBS is only in the PNS
35
Q

What are NG2 cells? What other names do these cells have, and what types of cells can they differentiate into? What properties do they have that currently make them of special interest to some neuroscientists?

A
  • glial cells in the CNS made of NG2 (glycoprotein), a.k.a. oligodendrocyte progenitor cells or polydendroyte
  • have pluripotency, which means that they can be coaxed to differentiate into diff types of glial cells
    • mainly oligodendrocytes and astrocytes
    • could be coaxed into replenishing some of the damaged neurons in the CNS after an injury
36
Q

How many types of glial cells are found in the PNS? What are they and what do they do?

A
  • satellite - only found in ganglia, provide metabolic support to the glia
  • schwann - create myelin sheaths in the PNS
37
Q

Response to neural injury, CNS vs PNS In which (CNS or PNS) is successful axon regeneration more likely? Why is that?

A
  • regen is much more likely in PNS because it is more permissive, CNS in nonpermissive
  • Glial scar forms and microglia move very slowly to remove debris
38
Q

What is in the glial scar?

A
  • cells attempt at walling off the injury
  • astrocytes - differentiate into reactive astrocytes that release chondroitin sulfate proteoglycans (same thing PNNs are made of), which inhibits neural growth cones
  • oligodendrocytes - produce many inhibitory factors like MAG, OMgp, and Amino-Nogo, to regenerative growth cones
39
Q

What are the two major types of chemical factors we discussed that inhibit axon regeneration in the CNS?

A
  • repulsive factors - cause growth in the opp. direction
  • motor proteins in the myosin - cause growth cone to collapse
40
Q

What are the 2 major factors that drive diffusion of ions (charged atoms) across the cell membrane?

A
  • particles always move from areas of high concentration to areas of low concentration
  • particles have kinetic energy, so are always moving, so at any given point they could make contact with an ion channel on the membrane
41
Q

What is meant by net diffusion?

A
  • total amount of diffusion occurring/total movement of a molecule
42
Q

What is required for ions to diffuse across a cell membrane?

A
  • charged ion cannot cross
  • channel is required
43
Q

What do ion channels possess that allow them to be selective for particular ions?

A
  • have diff subunits that determine the properties of the channels, like their kinetics and leakiness, threshold of activation, and size
  • also have filters called pore loops
  • have channels that are specific for an ion channel
44
Q

What is the mechanism for K+ channel selectivity that we discussed? Which mutation lead to the first sequencing of a K+ channel?

A
  • have negatively charged carbonyl groups that strip the sphere of hydration away from K+
  • a mutation in a gene in drosophila flies that caused them to shake, and in another gene called Eferagogo, that had the same effect
  • there are also some potassium channels that are not gated, so the membrane is much more permeable to potassium
45
Q

What causes the unequal distributions of ions inside and outside of a cell?

A
  • Leaky channels, molecules are constantly leaking through their specific channels
  • Passive diffusion from membrane transport
  • Cells are using energy to create these gradients, because once they are formed, they function like batteries that cells can then harvest energy from to discharge In the form of electrical impulses like action potentials
46
Q

What specific types of membrane transporters maintain these ion gradients? Does these require energy?

A
  • Ion pumps – mainly use ATP, and when ATP attaches to it, one of the phosphates is used to change the shape of the configuration, causing one side to open-Na/K pump specifically is an example of this
    • Is also electrogenic, because it generates a small membrane potential
  • Yes, because they are moving ions against the gradient
  • Diff from channels because it has binding sites for the ions that they are moving
47
Q

What is the difference between active and passive transport?

A
  • Active transport requires energy, EX is pumps
    • Energy comes from ATP
    • Moving against the gradient
  • Passive transport does not require energy, EX is channels
    • Energy comes from the gradient
    • Move with the gradient
48
Q

What is the difference between electrical and chemical gradients?

A
  • Electrical gradients begin to form once molecules cross to one side more than the other, causing that side to become either more negative or positive than the other
  • Chemical gradients is when a molecule will flow to areas of lower concentration
49
Q

What direction do Na, K, Cl and Ca move usually?

A
  • K is usually moving out of the cell
  • Na, Ca and Cl are usually moving into the cell
50
Q

What is the membrane potential? How is it represented/abbreviated? In what units is membrane potential measured? Most of the membrane potential results from what process? What contributes the remaining 5% of the membrane potential?

A
  • Membrane potential (mV) is the measure of the voltage of a membrane
  • Potential is measure in millivolts
  • 95% of membrane potential is contributed by passive diffusion
  • 5% of membrane potential is contributed by active pumping
51
Q

What is the equilibrium potential for an ion (Eion)? How is this value calculated? What does this value mean? What is the name of the equation used to calculate this value? Who is this equation named after?

A
  • Equilibrium potential is the membrane potential that exactly opposes net diffusion of an ion across the cell membrane, also called electromotive force or Nernst potential
  • Calculated for individual ions, measure in mV
  • (Walter) Nernst equation is used to calculate this – only takes into account one ion, and free permeability
52
Q

Nernst equation

A
  • Eion – RT/ZF ln([ion]o/[ion]I)
  • R – gas constant - doesn’t ever change
  • T- abs temp – measure in Kelvins, so will be around 310 K, cannot be negative
  • Z – ion valence – the charge of the ion, can be pos or neg
  • F – faraday constant - doesn’t ever change
  • Ln – natural log
  • [ion] - concentration of the ion
  • O – outside
  • I – inside
  • Can also use (+/-)61 log ([ion]o-[ion]I)
  • the number that you get is the value at which the molecule will change the direction of its current
53
Q

How is resting potential (Em or Vm) measured? How is Vm different from Eion? What ion is Vm most sensitive to?

A
  • Can’t use Nernst equation bc it only accounts for a single ion
  • Instead you use the Goldman equation – takes into account multiple ions and passive diffusion
  • P - permeability constant
  • does not include Z
  • most sensitive to K+
54
Q

How does changing the extracellular concentration of K+ change Vm? What are some physiological repercussions of this that we discussed in class?

A

Changing the extracellular concentration of K can alter the membrane potential of cells (depolarize), altering the function of nerve and muscle cells – disrupts the electrical potentials of these cells, depolarizing these membrane potentials past threshold, permanently deactivating Sodium channels – can lead to things like seizures

55
Q

Which glial mechanism is used to help regulate extracellular concentrations of K+?

A
  • Astrocytes buffer K that begin to accumulate outside of the membrane, which occurs whenever the voltage gated potassium channels open when the cell is repolarizing
  • Spatial buffering – spread large accumulations of K+ with their projections/processes, have potassium uptake mechanisms that allow them to take up K+, and then spread it elsewhere in the cell
56
Q

Voltage

A

Voltage – difference in electrical charge btwn 2 points – measured in mV

 For cells – diff in charge across membrane (ECF/ICF) 

 Named after Alessandro Volta 

 Goldman equation measures this
57
Q

Current

A

Current – flow of charge (ions) across membrane – measure in amps

 Directly proportional to voltage, if voltage increases, then so does current, without voltage, there is no current  

 Can flow in different directions – either across the membrane or along it  

 Im and Ia
58
Q

Resistance

A

Resistance – opposition/resistance of membrane to current flow – measured in Ohms

 Increased resistance decreases the current 

 Rm and Ra 

      Rm – membrane resistance – resistance across the membrane 

      Ra – axial resistance – resistance along the membrane
59
Q

Conductance

A

opposite of resistance, aids in the flow of current

measured in mhos or siemens

60
Q

What are the two different versions of Ohm’s law? Why are they equivalent?

A

V=IR or I=gV

 V – voltage – volts, V 

  I – current – amperes/amps, A 

  R- resistance - ohms 

 G – conductance – mhos or siemens, S  = to 1/R

Equal because conductance is the reciprocal of resistance

61
Q

What are the different types of current modeled for an axon? What is the difference between Im and Ia?

A

Im is the current across the membrane (membrane current) – EX is sodium channels, sodium moving into the cell, potassium channels letting potassium flow out of the cell

Ia is the current alongside the membrane (axial current) - action potential propagating along the cell

62
Q

What is the difference between inward and outward current? How is this affected by the charge of the ion? What types of current describe the following: Na+ influx, K+ efflux, Cl- influx.

A

Current flow across the membrane is indicated by two conventions: inward and outward current

Inward current is the positive flow of ions into the cell, indicated by Ii (EX: Na and calcium)

Outward current is the flow of positive ions out of the cell, indicated by Io (EX: K+)

 Chloride technically flows into the cell, but is still an example of this, because it is a negatively charged ion
63
Q

What is membrane capacitance? Why does the plasma membrane function as a capacitor?

A

Storage of charge across barrier – measure in farads, F

Cm – membrane capacitance

Requires two conducting media that are separated by a thin barrier – also called a separator

  EX: plasma membrane  

      Leaky capacitor, have ion channels that resemble holes in the membrane  

      Have lipids that are weak conductors, but good insulators – which makes it a good capacitor, b/c it has lipids that function as insulators between two good conducting media, the ECF and ICF
64
Q

What are the different experimental methods used perform intracellular recordings of cells? What is the difference between using a sharp microelectrode and patch clamping?

A

Intracellular is when at least one electrode is inside the cell, making contact with the cytoplasm and one reference electrode is outside of the cell

Sharp microelectrode – one electrode that is filled with an electrolyte solution that has a very thin and sharp tip is used to impale the cell and make contact with the cytoplasm

Patch clamping – sharp electrode is not used, instead, a fire polished and blunt electrode is used

65
Q

What are the 2 different methods of patch clamping we discussed?

A

Whole cell patch clamping – suction is used to tear a hole in the membrane, and the blunt tip can then be inserted through the hole – similar to sharp electrode method

On cell patch clamp - Form a seal on the membrane without breaking it, such that you have one or more ion channels within the patch you are recording from

 Can record currents from singular ion channels if the tip is small enough
66
Q

What are the different recording configurations used in experimental measurements? What configuration allows the experimenter to measure voltage? Which allows measurement of current? What configurations allow the experimenter to manipulate these parameters?

A

Current clamp – inject a current into a cell, after which you can record the voltage

  used to study membrane potentials

Voltage clamp – manipulate voltage and hold it at a specific level

 Camp cell at holding potential  

  Step to command potential  

 Used to study ionic currents, and measure inward and outward current
67
Q

Depolarizing, Repolarizing, Hyperpolarizing

A
  • Depolarization - Membrane potential becomes less negative/more positive – always approaching 0
  • Repolarization - Membrane potential becomes more negative/less positive
  • Hyperpolarization - Membrane potential goes more negative than –70 mV
68
Q

What are graded potentials? What is major difference btwn graded potentials and action potentials that we discussed in class?

A

Graded potentials are variable/graded in amplitude, in which the amplitude of the membrane potential is proportional to the amplitude of the stimulus

Action potentials are all or none

69
Q

Which are graded vs all-or-none? What does this actually refer to, specifically?

A

APs are said to be all or none, membrane has to reach a specific voltage in order to be triggered

Graded are variable

70
Q

Which is decremental vs regenerative? What do these words mean?

A

Graded are decremental - Voltage change does not get regenerated, continues to diminish

APs are regenerative - Have a mechanism that actively regenerate the voltage change through positive feedback

71
Q

Which is bidirectional vs unidirectional? What is the context to this? Are there exceptions?

A

APs are unidirectional, and propagate away from the soma

Graded are bidirectional, depolarization occurs in both directions

72
Q

Which is passive vs active? In what way?

A

APs are actively conducted, which means that they do not lose amplitude

Graded are passive – aka electrotonic conduction

  Amplitude passively diminishes/dissipates the farther it goes from the site of cytostimulation
73
Q

What is the term for passive conduction of graded potentials?

A

Electrotonic conduction

74
Q

What is the shape of a graded potential waveform? Why does it have that shape?

A

B – shows how the voltage would change if it was a pure capacitor, which is only how the membrane acts initially

A – a shows what would happen if it was a pure resistor

C – the combination of A and B, what happens after the voltage change

Has a curved shape because the membrane has both capacitive and resistive properties – true for both the depolarization and repolarization phases

75
Q

How does the membrane have both resistive and capacitive properties? What does this mean?

A

Neither perfect capacitors or perfect resistors, has properties of both

76
Q

What is the formal definition of the time constant? Can you illustrate this graphically?

A

How rapidly/how much time it takes the membrane to change based on the stimulus

= to membrane resistance x membrane capacitance ( t = Rm x Cm)

Increase in either of these will result in an increase in the time constant

Indicated by T

Neuroscience (5 decks)

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