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HOM > Neurons (Cahill Stuff) > Flashcards

Neurons (Cahill Stuff) Flashcards

1
Q

What is the Davson- Danielli model

A

That cell membranes had a 3 layered structure: protein, bilayer, protein
Based on electron micrograph a

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2
Q

What happened in 1966

A

Branton used freeze-fracturing to split cell membranes and proteins were seen through the fracture plain

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3
Q

Experimental evidence for fluid mosaic model

A

Distinctly Labelled mouse and human proteins were combined in a hybrid cell, the surface proteins became intermingled

(Frye and Edidin, 1970)

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4
Q

What are the two main kinds of non covalent interactions in the fluid mosaic model

A

Hydrophobic and hydrophilic

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5
Q

What does the value of the potential difference across a membrane reflect

A

The concentration of unbalanced charge

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6
Q

Is the inside of a cell more or less negative

A

Inside is more negative

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7
Q

How does a cell membrane act as a variable resistor

A

It contains channels that allow a flux of ions under specific conditions

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8
Q

How is electrical potential across a membrane measured

A

A micro electrode is inserted within the neuron (usually in the soma) and a second is placed in the extra cellular fluid

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9
Q

By Whom and when was the ionic basis of resting potentials put forward

What was he aware of

A

Bernstein, 1902

That intracellular K> extra cellular
And that the membrane was more permeable to K than any other ion

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10
Q

What is the equilibrium potential

A

A balance between concentration gradient and charge gradient

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11
Q

What can’t electrodes do that means the Nernst equation is needed

A

Can’t tell us which ions account for the charge recorded

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12
Q

What are the assumptions in the Nernst equation

A

For a single ion
Completely permeable membrane to that ion
Ion in equilibrium

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13
Q

What is the Nernst equation

A

E=RT
-— x ln([ref]/[test])
zF

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14
Q

Does reference= out or in

A

Out

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15
Q

What is Nernst equation simplified to at room temperature and at body temperature

A

58xlog([out]/[in])

Body: 61.5log([out]/[in])

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16
Q

How did Hodgkin and Horowicz realise other ions contribute to the potential

A

At high [K] the results agreed with the Nernst equation but at lower concentrations, the results deviated

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17
Q

Give the Goldman Hodgkin Katz equation

A

RT Pk[out]+PNa[out]+PCl[in]. — x ln ———————————

F Pk[in]+PNa[in]+PCl[out]

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18
Q

What is the pump ratio for K and Na ions In the K/Na pump

A

3 Na ions are pumped out for every 2 K ions pumped in

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19
Q

What does the Na/K pump require and what can it be describe as

A

Hydrolysis Of ATP

Electrogenic

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20
Q

What is the equivalent of a battery in a neuronal circuit

A

Na/k pump

Stored potential that is maintained

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21
Q

What is the equivalent of a resistor in a neuronal circuit

A

Ion channels

Prevent or allow flow of ions in and out of a cell

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22
Q

What is the equivalent of a capacitor in a neuronal circuit

A

Cell membrane

The charge separation across it

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23
Q

Hyperpolarising current pulses only ______ changes in membrane potential

What does this mean

A

Passive

They decay over time

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24
Q

Small depolarising pulses elicit only _____ responses

A

Passive

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25
Q

When does a depolarising current produce an action potential

A

If it meets or exceeds a threshold, hence why they are all or nothing events

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26
Q

What does increasing the strength of a current do for an action potential

A

No effect on amplitude

Number of spikes increase

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27
Q

What happens if you apply a voltage to a capacitor

What happens when the voltage is removed

A

It begins to store energy until it reaches maximum capacity and stays there

The capacitor discharges it’s voltage across the resistor until it has been fully discharged

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28
Q

What happens if a circuit has a resistor but no capacitor

A

When power is applied the voltage but change to its steady state value and when removed it would then drop to zero immediately

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29
Q

How does the capacitor resist drastic changes

A

It takes time to charge and discharge

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30
Q

What does τ (tau) measure

A

The time constant

How quickly the neuron’s potential decays back to the resting state

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31
Q

How long is τ exactly

A

How long it takes a potential to get to 1/e of its original value

(63% of original value)

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32
Q

What equation describes the rise of voltage

A

V= Vmax(1-e^(-t/τ))

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33
Q

What equation describes the decay of voltage

A

V= Vmax x e^-t/τ

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34
Q

τ=?

A

Rm x Cm

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35
Q

What are the 2 major sources of resistance ions need to overcome in the axoplasm

A

Fibre length

Lack of membrane resistance (too much leaking)

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36
Q

What is the length constant

A

λ

An index of how well a sub threshold potential will spread along an axon as a function of distance

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37
Q

What does it mean to have a length constant of 1mm

A

1mm away from the axon cell body, 37% of the voltage remains

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38
Q

What is the actual equation for the decay of the potential with distance

A

V=Vmax(e^-x/λ)

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39
Q

What actually does λ=

Why can Ro be ignored

A

λ= sqrt (Rm )
(———- )
(Ro + Ri )

Ro«

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40
Q

What ion is the membrane of a resting neuron most permeable to ?

A

K

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41
Q

What did Bernstein suggest about an action potential

What did the peak of the AP represent here then

Who noticed he was wrong

A

Due to a loss of membrane selectivity

The point of maximum conductance so would approach 0 mV

Cole and Curtis (1939)

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42
Q

How does capacitance change in an AP

A

It doesn’t

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43
Q

How did Hudgkin and Huxley experiment with APs originally

What did they observe

A

Modified the concentration of sodium by adjusting the concentration of salt water

The AP and overshoot became slower the more they reduced the Na

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44
Q

What did Huxley’s calculations about Na predict

A

The peak AP amplitude would track the Na equilibrium potential

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45
Q

How does improving insulation improve passive current flow

A

Reduced leakage

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46
Q

How does myelin affect the long motor neuron in the leg, speed wise

A

Without: speed= 1m/s
With: speed= 10-100m/s

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47
Q

What do the Glia do in nodes of Ranvier

A

Secrete specialised proteins that recruit Na channels to the node

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48
Q

What were Rushton’s predictions relating myelin and diameter

A

Myelinated: velocity is proportional to diameter

Unmyelinated: velocity is proportional to the square root of the diameter

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49
Q

What was the general rule of thumb that Erlanger and Gassers discovered in the 1920-30s

A

Larger diameter neurons are heavily myelinated, have low thresholds and are rapidly conducting

Unmyelinated have high thresholds and conduct slowly

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50
Q

Name some symptoms of MS

A

Dizziness, visual problems, headaches, neurological problems that persist for days then remittance

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51
Q

What happens due to demyelination in MS

A

Conduction is slowed and Na channels spread outward from nodes

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52
Q

How does a current clamp work

A

Experimenter injects a current in a ‘step’ fashion and measures how it impacts the membrane potential using a voltmeter and amplifier

Can be used to look at subthreshold stimulation forms of passive membrane currents

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53
Q

What was Hodgkin’s hypothesis concerning conductance of Na

Why Na

A

At a certain membrane potential, conductance (g) of Na increases

At resting potential thete is a high driving force acting on it

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54
Q

What does the voltage clamp amplifier do

A

Clamps the membrane potential at a set level and can detects the difference in current that needs to be injected to stabilise that level

(This required current is proportional to the conductance according to Ohm’s law)

55
Q

What did H and H record from voltage clamp experiment

A

As the membrane was depolarised there was an inward [Na] dependant current

K conductance was found to lead to a time dependent outward current

56
Q

How can the change in current with PD by shown

What drugs will change this graph

A

Am I-V curve

Any treatment that alters ionic conductance will alter its shape and slope

57
Q

What can the slope of the I-V curve be used to calculate

A

Conductance

58
Q

When does the IV curve pass through the voltage axis for a channel specific to ion X

A

At X’s Nernst equilibrium potential

59
Q

What did the toxin TTX demonstrate

Why

A

Slow outward current was mediated by K

It blocks Na voltage gated channels

60
Q

When are leak and gated channels important

A

Leak- to set resting potential

Gated- in active changes

61
Q

In a channel how many helices are in each subunit

Which form the pore

Which segment is charged and how do prevalent models suggest this moves upon depolarisation

A

6 transmembrane domains

S5&6

S4 - translocated from inside to outside the cell

62
Q

Describe the helical screw model

A

Depolarisation causes S4 to rotate and twist up through membrane, changing the exposure of charges from the intra- to extra cellular solution

63
Q

Describe the paddle model

A

S4 makes a large translation such that the most extra cellular charge goes from exposed to the extra cellular medium in the open state to completely buried in the bilateral in the closed state

64
Q

What happens when the channels open upon depolarisation

A

Initially a few Na VGC open, increasing the amount of Na entering the cell, continuing to depolarise the membrane, triggering more Na VGC to open

65
Q

When do Na VGC become inactive

A

It is time dependent- they are inactive after a set time from the VGC opening

The cell is now impermeable to Na, contributing to the refractory period

66
Q

When are the Na VGC closed

A

When the membrane repolarises

67
Q

Why is an action potential self supporting

A

Positive feedback loop of Na VGC opening. This also contributes to the all or nothing quality

68
Q

What is the delayed rectifier

A

The Na VGC take 1ms to open upon depolarisation. This delay and the fact that K conductance serves to rectify the membrane potential.
This delay regulates the relative refractory period

69
Q

What does the refractory period do

A

Limits number of APs in a given nerve per unit time and prevents back propagation of APs

70
Q

What do TTX and TEA stand for and what do they do

A

TTX- tetrodotoxin
- binds to and blocks the Nav channels

TEA- Tetraethylammonium
- targets Kv channels

71
Q

What is a channelopathy

A

Disease caused by disturbed function of ion channel subunits or the proteins that regulate them

72
Q

What is myokymia

A

Reduced activity of K channels which delays AP repolarisation and lowers threshold, producing abnormal spontaneous AP generation

73
Q

What is myotonia

A

Mutations in Na channels cause abnormal tendency for channels to open later or more persistently after depolarisation
Residual Na entry reinitiates the cycle of depolarisation

74
Q

What is a Gap Junction

A

They are formed when 2 cells in close proximity that have channels allowing the propagation of an impulse almost directly

75
Q

How are gal junctions structured

A

Built from 6 connexin subunits that comprise one connexon, then two connexons comprise one gap junction

76
Q

2 advantages of electrical transmissions

A

Speed

They favour synchrony when firing

77
Q

Advantage of chemical transmission

A

Allows for more specificity

78
Q

When and how did Dale shoe transmission could be chemical

A

1913
Injecting acetylcholine into a cat heart, inhibiting the heartbeat
A purified substance produced the same effect as parasympathetic nerve stimulation

79
Q

Describe Ringer’s heart experiments

A

2 beating frog hearts isolated in containers of Ringer’s Solution
The vagus nerve (PNS) was stimulated in heart A, slowing its beat. Fluid from A moves to B, slowing the beat of heart B

80
Q

What did Ringer’s experiments show

A

A soluble substance released by the vagus nerve modulated heart rate, which he called Vagusstoff but is actually ACh

81
Q

Where are NT synthesised and stored

A

In the axon cytosol

Stored in synaptic vesicles

82
Q

What happens when an impulse reaches a presynaptic terminal

A

Depolarisation causes opening of VG Ca channels

Then vesicles can fuse with the presynaptic membrane and release their load

83
Q

How and why are intercellular [Ca] levels kept low in neurons

A

So there is a strong driving force for it to enter once channels open

Transporters and pumps are recruited
Eg Na/Ca exchanger and Ca pumps

84
Q

How is the VG Ca channel deactivated

A

Ca dependant inactivation site providing negative feedback to close the channel when [Ca] increase

85
Q

What do SNARE proteins do

A

They’re on the synaptic vesicles and plasma membrane, and form a complex. This acts like a zip, bringing together the two membranes.
Ca then binds to synaptotagmin causing the cytoplasmic region of this protein to insert into the plasma membrane, bind to SNAREs and catalyse fusion and exocytosis

86
Q

Do neurons need to recover vesicles

A

Yes

They are recovered via endocytosis and the recycled vesicles is refilled with NT

87
Q

What is Dale’s principle

A

A given neuron produces only one type of neurotransmitter (now disproved as co-transmitters, nerve terminal with multiple NTs, have be shown to exist)

88
Q

For ACh in a NMJ, give the following:

a) synthesis
b) vesicles
c) Release
d) action
e) inacitvation

A

a) ChAT
b) Vesicles
c) Ca Dependant
d) nAChR
e) AChE

89
Q

What are ionotrophic receptors

A

Ligand gated channels

90
Q

Give an example of metabotrophic receptors

A

GPCRs

91
Q

Give an important specialisation of the NMJ

A

It’s size- it is one of the largest synapses in the body

92
Q

How does the motor end plate increase surface area

A

It has many folds

93
Q

Give the resting potential and threshold of the motor end plate

A
  • 100mV

- 65mV

94
Q

Give the experiment that shows that the presynaptic signal for full EPPs is Ca dependant

A

If NMJ is bathed in a solution of low [Ca], stimulating the neuron evokes EPPs reduced to the size of MEPPS

95
Q

How could you show post synaptic signals are dependent on the nicotinic subtype of AChR

A

The antagonist, Curare, can reduce the EPP

96
Q

What type of receptor are NAChR in the NMJ

What about in the heart

A

Ionotropic

Muscarinic AChR

97
Q

When is the membrane potential ~0mV

A

When it is equally permeable to Na and K ie when many channels are open

98
Q

What happens if membrane potential is <0mV before ACh was applied

What do you call the critical value when the flow direction changes

A

The direction of flow through ACh-gated ion channels is inward and vice versa

Reversal potential (which is 0 in this case)

99
Q

What is driving force

A

How different the membrane potential is

Vm-Erev

100
Q

Are nAChR permeable to K or Na

What does conductance depend on

A

Both

How many channels are open which depends on [ACh]

101
Q

What is the Quantal Transmission Hypothesis

Give its two main observations

A

EPPs are made of individual units, each equivalent of an MEPP

  1. NT is released in multimolecular packets
  2. Response EPPs fluctuate in steps of unit size corresponding to the size of mEPP
102
Q

What is a simplistic way to determine the possible quantal content of an EPP

A

If you divide an EPP by an mEPP

103
Q

How did Katz analyse the frequency of occurrence of MEPPs with respect to amplitude

A

Poisson Statistics

104
Q

What is myasthenia Gravis

How are MEPPs affected

A

A chronic autoimmune neuromuscular disease that targets the nAChR, disrupting how the cells respond to synaptic transmission

Their amplitude is Greatly reduced

105
Q

How do you treat myasthenia gravis

A

AChE inhibitors to prolong ACh activity

106
Q

Are post synaptic potentials bigger in the brain or in the NMJ

Why

A

Brain PSPs are much smaller

In the CNS, PSPs can be fast acting and short-lived, triggered by iontropic receptors or slow and long lasting driven by metabotropic receptors

107
Q

How can you measure the current produced by an EPP

A

Patch Clamp which measures discrete patches of membrane and the channels there-in

108
Q

How do patch clamps work

A

The transmembrane potential is controlled by the patch clamp amplifier, the extra cellular fluid is considered the “ground/reference”

109
Q

What is the outside-out patch

What does this allow

A

A configuration of the patch clamp where the extra cellular surface is on the external side of the pipette tip

Study of drug action on receptor surface

110
Q

What can single channel recordings with the patch clamp allow

A

Study of unitary conductance and kinetic behaviour of ionic channels

This has shown that individual channel opening and closing are sudden, all or nothing events, triggered by ligand binding causing a conformational change to another

111
Q

What muscle is contracted in the knee jerk reflex and what causes it

What kind of reflex is it

A

Quadriceps femoris
Hitting the patellar tendon

Protective reflex

112
Q

How does hitting the patellar tendon cause a reflex action

A

The pressure stretches the muscles spindles causing contraction

113
Q

What does an intact knee jerk indicate

What is the reflex arc

A

Integrity of the L2-L4 vertebral segments

Sensory efferent neurons project through dorsal root ganglion and synapse directly with the effector extensor motor neuron that projects back to the quadriceps muscle

114
Q

What muscles are indirectly affected by the knee jerk reflex

A

The hamstring is inhibited by inhibitory interneurons which is necessary to avoid both muscles contracting simultaneously against each other

115
Q

Are post synaptic potentials active

A

No they decay exponentially

116
Q

What does the magnitude of a PSP depend on

A

The number of open ion channels which in turn depends on amount of NT released

117
Q

How do the EPSP and ISPS act

A

EPSP -brings a membrane potential closer to threshold

IPSP - hyper-polarises the cell away from threshold

118
Q

What did Brock notice about IPSP’s in the 1950s

A

Reversal only occurred when intracellular microelectromechanical contained KCl, suggesting Cl- is necessary for reversal

119
Q

What is released from the presynaptic terminal of the sensory neurons in the extensor motor neuron of the patella reflex

What does it bind to

A

Glutamate

AMPAR

120
Q

What does AMPAR activation lead to

A

Depolarisation of post synaptic cell via conduction of cations like a ligand gated ionotropic receptor

121
Q

What do glycine receptors conduct?

Are they voltage gated?

A

Conduct Cl- and therefore lead to hyperpolarisation

No they are ligand gated ionotropic receptors

122
Q

Is temporal summation active

A

It is strictly passive

123
Q

What is the spatial summation influenced by

A

The space constant

124
Q

What is equilibrium potential of an ion

A

The voltage that would occur if the membrane were fully permeable to that ion

125
Q

What determines the threshold for an action potential

A

The sodium current exceeding the outward potassium current

126
Q

What is the greatest delay at the NMJ

A

Ca2+ accumulation

127
Q

Which band shorten during contraction

A

A stayed the same length H and I bands shorten

128
Q

What are the effects and noradrenaline on the heart

A

Phosphorylation of phospholamban, troponin I and phosphorylation of calcium channels in the p.m.

129
Q

What is the most important factor influencing brain bloodflow

A

Metabolic autoregulation

130
Q

What determines maximum expiratory flow rate primarily

A

Elastic recoil of the lungs

131
Q

What regulates alveolar ventilation when breathing normal air at sea level

A

PCO2

132
Q

Contraction of the diaphragm and intercostal muscles does what to intrapleural pressure

A

Intrapleural pressure becomes more negative

133
Q

How do glucose, galactose, and fructose cross the luminal border of the small intestine

A

Glucose and galactose: SGLT1

Fructose: GLUT5

All exit via GLUT2

HOM (11 decks)

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