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Excitable cells > lectures 8-12 > Flashcards

lectures 8-12 Flashcards

1
Q

what is a chemical synapse?

A

electrical –> chemical –> electrical

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2
Q

what are electrical synapses?

A

direct transfer of ions and small molecules between cells.
bidirectional.
fast transmission. used for escape response. drosophila.
less common than chemical.

form a gap junction, through which ions/small molecules can flow.

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3
Q

describe gap junctions.

A

each channel is made of 2 connexon, and each is made of 6 connexon subunits.

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4
Q

describe the synaptic transmission at a chemical synpase

A

action potential arrives in presynpatic nerve.
depolarises the membrane, leading to opening of ca2+ voltage gated ion channels.

ca ions causes release of neurotransmitter.

diffuse across cleft and bind to receptors on postsynaptic membrane. causes opening of ion channels which depolarises the membrane.
if big enough causes an action potential.

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5
Q

What are the types of a postsynaptic membrane?

A

postsynaptic membrane is:
on a dendrite = axodendritic
on the cell body = axosomatic
on another axon = axoaxonic

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6
Q

What are the classification of chemical synapses?

A

Gray type I synapses are usually excitatory and often contact dendrites.
spherical vesicles.
post synpatic is thicker than pre synaptic.

Gray type II synapses are usually inhibitory and may contact the cell body.
flattened vesicles.
symmetrical thickness.

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7
Q

what is the vesicle hypothesis?

A

occasionally a postsynaptic potential can occur in the absense of calcium ions or an action potential.

miniture psp’s (postsynaptic potentials)

accidental release of neurotransmitters.

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8
Q

what is 1 quantum?

A

1 vesicle of neurotransmitter.

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9
Q

how does extracellular calcium ion concentration affect psp amplitude?

A

less ca = lower psp amplitude in a step wise manner.

NT released in packets.

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10
Q

how is the NT released?

A

exocytosis.
fuses with membrane and contents flow out.

docking.

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11
Q

describe docking.

A

t snare proteins embedded in plasma membrane.
v snare proteins are embedded in the vesicle membrane.

calcium dependent.
synaptotagmin changes the snare proteins and causes them to fuse with membrane.
???

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12
Q

botox?

A

destroys snare proteins.

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13
Q

how are vesicles recycled?

A

vesicles are assembled in the ending of the presynaptic cell and loaded with NT.

clathrin forms a coated pit around a patch of membrane and forms it into a vesicle then breaks off.

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14
Q

what is clathrin?

A

a protein used to build intracellular membrane bound vesicles.

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15
Q

what is an agonist?

A

can bind to, and activate, the receptor.

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16
Q

what is an antagonist?

A

binds to, but cannot activate, receptor; occupies the natural ligand site so it cannot bind.

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17
Q

what is a partial agonist?

A

binds and activates the receptor, but with reduced efficacy compared to agonist.

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18
Q

Describe nicotinic acetylcholine receptors.

A

ligand gated ion channel.
membrane spanning protein.

five subunits form a pore.
2 alpha, beta, omega and gamma.

2ACh bind 2alpha subunits to open the channel.

na and k flow into the cell down the electrochemical gradient.
membrane depolarises.

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19
Q

what is co localisation?

A

one neuron may release more than one neurotransmitter.

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20
Q

how do you calculate equilibrium potentials?

A

nernst/goldmann equation.

???

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21
Q

what defines a neurotransmitter?

A

Must be synthesised by the neuron
Must be present in synaptic terminal at sufficient concentrations
Must be released on presynaptic stimulation
Exogenous application to postsynaptic cell evokes a response
Mechanism exists for its removal from synaptic cleft

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22
Q

what are the types of neurotransmitters?

A

amino acids - glutamate, glycine, GABA

amines - ACh, dopamine, noradrenaline, serotonin (5-HT)

peptides - enkephalin, substance p

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23
Q

what is dales principle?

A

???

no longer holds with co localisation???

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24
Q

What is the function of glutamate and GABA?

A

glutamate - excitatory
via Na+ and Ca2+

GABA - inhibitory

amino acids

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25
Q

What is the function of enkephalin and substance P?

A

enkephalin - opiate
substance p - pain

peptides

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26
Q

what is the function of acetylcholine, dopamine and serotonin?

A

acetylcholine – neuromuscular junction, brain
dopamine – movement
serotonin (= 5-HT) – sleep, appetite, arousal

amines

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27
Q

how are amines and amino acids synthesised?

A

?? lecture 9 no podcast

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28
Q

how are peptides synthesised?

A

precursor peptide made in the endoplasmic reticulum.

active peptide split and packaged into vesicles in the golgi apparatus.

secretory vesicles transported down axon to presynpatic terminal where they are stored until release.

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29
Q

give an example of ligand gated and GPCR, difference in speed?

A

ligand gated - nicotinic ACh fast

GPCR - muscarinic ACh slow long lasting.

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30
Q

describe ionotropic and metabotropic receptors.

A

ionotropic - opens cation channels.
excitatory
fast
ie skeletal.

metabotropic - increases K+ permeability
inhibitory
slow

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31
Q

GPCR action?

A

Neurotransmitter activation of a GPCR at the postsynaptic membrane activates a specific G-protein.
G-protein activation leads to: ion channel gating; ion channel modulation; enzyme activation; activation of second messenger pathways - e.g. cAMP, IP3 – which exert downstream effects
Timecourse of response determined by intracellular metabolic processes
GPCRs allow more possibilities in terms of cellular responses and can amplify responses

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32
Q

how is NT removed from the synpatic cleft?

A

Diffusion: e.g. small amines and amino acids
Reuptake: specific neurotransmitter transporter proteins in terminal and glial membranes. e.g. choline transporter
Enzymatic degradation in cleft - followed by uptake of precursors e.g. acetylcholinesterase (AChE)

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33
Q

describe the AMPA receptor.

A

requires glutamate to open then allows na+ influx.

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34
Q

describe NMDA receptors.

A

requires glutamate AND depolarisation to open then allows ca2+ and na+ influx

35
Q

describe glutamate.

A

Glutamate – the most widespread NT in the brain
At high concentrations glutamate overexcites cells and can kill them
The culprit is uncontrolled Ca2+ influx through NMDA channels - high intracellular Ca2+ is toxic
Active (O2-dependent) mechanisms – pumps and transporters – normally keep extracellular glutamate and intracellular Ca2+ low

36
Q

describe GABAa and GABAb

A

GABAa - ionoctropic, increase cl- and fast inhibition

GABAb - metabotropic, increase K+ decrease ca2+, slow inhibition.

37
Q

positive feedback of glutamate?

A

Stroke/heart attack reduced brain O2 X pumps/transporters

↑ glutamate in the synaptic cleft Ca2+ influx though NMDA receptors

↑ intracellular Ca2+ excessive excitation ↑ glutamate release

Positive Feedback

Excess intracellular Ca2+ disrupts mitochondrial function, causes release of more Ca2+, and activates enzymes that can lead to apoptosis (cell death)

?

38
Q

how can you alter the efficacy of a synapse?

A

Pre-synaptic: amount of neurotransmitter released per action potential

Post-synaptic: response of receptor to neurotransmitter

Post-synaptic: excitability of postsynaptic cell

39
Q

Describe cannabinoid CB1 receptors.

A

very common in the brain.
usually found on presynaptic nerve endings.

NT released, post synaptic depolarised, opens ca channels, activate enzyme that releases endocannabinoids in post synaptic.

endo act as retrograde transmitters, go and activate can CB1 receptors which can suppress ca channels on pre synaptic.

40
Q

what is retrograde neurotransmission?

A

feeding back to the pre synaptic nerve.

41
Q

What is allosteric modulation?

A

changing how effectively the post synaptic nerve responds to the NT.

42
Q

give an example of allosteric modulation.

A

GABAa receptor.
multiple sites for other drugs to bind.

barbiturates - increases duration of GABAa channel openings.

benzodiazepines - increased frequency of GABAa channel openings.

43
Q

Describe the mammalian hippocampal neurones - postsynaptic neuromodulation.

A

glutamate main NT.
excitation of post synaptic.

if noradrenaline is present it closes K+ channels.
makes post membrane depolarised.
makes it closer to threshold, more excitable.

Noradrenaline binds to GPCR which releases cAMP to close K+.

useful if brain wants a particular pathway to be prioritised.

44
Q

why is neuromodulation good?

A

increases flexibility and adaptability of pathways.

allows plasticity.

45
Q

give an example of convergence and divergence.

A

alpha motor neurones - convergence.

pain receptors - pain receptor.

46
Q

what do upper motoneurones do?

A

control voluntary movement, located in the brain.

47
Q

what type of signals are post synaptic potentials?

A

graded.

usually very small, summation.

48
Q

what do IPSPs do?

A

inhibitory.

take potential further from threshold.

49
Q

where do psp’s join?

A

axon hillock, above or below threshold.

low threshold, high density of Na+ channels.

50
Q

how does location of synapse matter?

A

graded psp’s travel in a passive decremental fashion, they get smaller.
not like AP.

51
Q

what does attenuation depend on?

A

time constant, length constant, diameter, membrane resistance (Rm) and internal resistance (Ri)

increase resistance of membrane, less loss of current so length constant is longer.

increased diameter, decreased internal resistance so increased length constant.

52
Q

what is the length constant?

A

distance over which PSP travels to 37% of its original size.

53
Q

what is the time constant?

A

time taken for PSP to decay to 37% of its peak value.

membrane resistance x capacitance of membrane ?

54
Q

what is spatial summation and temportal summation?

A

spatial - 3 inputs from 3 sources.

temporal - 3 inputs from 1 source.

higher input from spatial.

55
Q

what is shunting inhibition?

A

inhibitory synapse close to the soma, switches off other inputs to the dendrite.

56
Q

explain hyperekplexia.

A

single amino acid mutation in the glycine receptor-Cl ion channel.
inhibition in the CNS is reduced.

“startle disease”
tiny stimulus startles them.
autosomal dominant

57
Q

how are stimulus encoded at the axon hillock?

A

Amplitude Modulated to Frequency Modulated.

AM - square.
FM - waves.

58
Q

what are the types of electrophysiological recordings?

A

intracellular/extracellular.
ground electrode

intra mV
extra ultraV

59
Q

describe electrophysiological recordings generally.

A

The potential difference between a recording and ground electrode is measured and displayed on an oscilloscope.

Extracellular recording measures the surrounding flow of charge into and out of neurons during action potentials.

Intracellular recording allows measurement of the potential difference between the inside and outside of a neuron.

60
Q

examples of extracellular recording?

A

Established techniques such as electroretinograms (ERG), electroencephalogram (EEG), electrocardiogram (ECG), electromyogram (EMG) all use extracellular recording.

61
Q

describe extracellular recordings.

A

can use multichannel probes, numerous electrodes. each near a different cell.

Advantages:
intact system.

Can help us to understand sensory inputs to the brain as well as brain connectivity.

62
Q

extracellular recordings detect all nearby cells, how do you get around that?

A

neurones have particular waveforms, pick out patterns which correspond to neurones.

63
Q

what are multi/micro electrode arrays? (MEAs)

advantages/disadvantages?

A

flat plates with multiple extracellular electrodes/channels on. Great for cell culture.

Allows continuous recordings of cells (responses can then be spike sorted to approximate spikes from single cells).

Allows recording of long term responses to drugs etc. in vitro (non-implantable) e.g. cell culture.

Disadvantages of extracellular recording: no indication of individual channel activities.

64
Q

what did hodgkin and katz discover?

A

did intracellular recordings, found that less Na+ in extracellular fluid causes a smaller action potential.

65
Q

what is the voltage clamp technique?

Cole version

A

?????

keeps the cell at a constant voltage in relation to the reference electrode.
negative feedback

kenneth cole 1949.

Holds the cell at a predetermined voltage.

Membrane potential set to predetermined level of depolarisation.

Voltage gated channels that would open at the voltage will still open.

Holds the cell at a predetermined voltage.

Membrane potential set to predetermined level of depolarisation.

Voltage gated channels that would open at the voltage will still open.

66
Q

what is the voltage clamp technique?

hodgkin and huxley version

A

look at changes in ion flow (current not voltage) in an AP.

capacitance

??

67
Q

what is capacitance?

A

small outward

68
Q

what is the patch clamp technique?

A

can measure the current through a single channel.

form a tip <1 uM wide.
pipette filled with electrical conducting solution.

69
Q

what are the types of patch clamping?

A

cell attached configuration - used to record currents through 1-2 channels.
Any change between pipette and whole cell is measured.

inside out configuration - rip patch of membrane off the channel, measure in a bathing solution. measures a single active channel away from the cell.

outside out configuration - rip membrane off and hold in pipette, inside of cell is now inside of pipette.

whole cell configuration - once gigaseal has formed a small shock allows pipette to pierce the cell.
looks are entire cell, no leakage or damage.

70
Q

ohms law?

A

current = voltage x conductance

71
Q

describe radioligand binding

A

can tell us about ion channels and GPCRs but no good temporal resolution.

72
Q

describe electrophysiology

A

tells us about ionic changes and conductance but is invasive and tricky.

73
Q

what is temporal resolution?

A

refers to the precision of a measurement with respect to time. Often there is a tradeoff between temporal resolution of a measurement and its spatial resolution.

74
Q

what does fluorescence mean?

A

if right wavelength is applied the molecules will be excited, when they lose energy they give off a longer wavelength of light than was applied.

75
Q

what is a flurophore?

A

fluorescent molecule

76
Q

what is a spectrofluorometer?

A

analyzes before and after flourescence.

77
Q

what is a flow cytometer?

A

sorts/counts out what cells are flourescent or not

78
Q

what is a flourescence microscope?

A

filters weak fluorescent light from other wavelengths.

79
Q

what is a chelator?

A

compound that binds to a metal ion to form a complex, which changes in it’s flourescence.

ie calcium sensitive dye

80
Q

what are Fure molecules?

A

give of green wavelength, excited by UV light.

calcium indicators

81
Q

describe fura 2

A

dye portion absorbs a photon of light, and excites molecules.

ca2+ binds to the dye, this distorts the molecule which changes the absorbance.

82
Q

what is the problem with fura 2?

A

can’t cross cell membrane since it’s polar.

added an ester group to form FURA-2 AM.
can now cross cell membrane but can’t bind Ca2+

send FURA 2 into the cell, esterases inside the cell remove the ester group. can’t leave the cell and will bind.

83
Q

what is GCaMP?

A

a genetically encoded fluorescent calcium indicator.
made of proteins.

ca2+ causes a change in structure and flourescence.

Excitable cells (6 decks)

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