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Physiology and Pharmacology 2 > Synapses > Flashcards

Synapses Flashcards

2
Q

Lecture 1

A

Synaptic Transmission

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3
Q

What is the fast chemical transmission? Give an example.

A

NT binds to ion channels causing influx. nAChr/GABAA/NMDA

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4
Q

What is the slow chemical transmission? Give an example.

A

NT binds to receptors which cause release of postsynaptic cell NT which binds to ion channels. GPCR modulated. mAChr/Adrenoceptors/GABAB/Metabotropic Glu R/Opioid Receptors.

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5
Q

What are combined synapses? Give an example.

A

Both chemical and electrical synapse in one. Spinal motor neuron in the frog.

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6
Q

What are connexons?

A

Hydrophilic bidirectional channels made up of 6 connexin monomers.

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7
Q

How are small NTs synthesised? Give examples.

A

In situ of the nerve terminal. By synthesising enzymes. Ach/Glu

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8
Q

How are peptide NTs synthesised?

A

Transcription of gene in nucleus. Translation of mRNA and transfer of protein to ER. Packaging of protein into vesicles and transport to Golgi. Proteolytic cleavage of protein (post-translational modification). Transport of vesicles down the axon to terminal.

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9
Q

Give 2 examples of peptide NTs.

A

Met-enkephalin. Neuropeptide-Y.

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10
Q

Give 2 examples of NT that fit neither category.

A

Nitric oxide. Zinc ions.

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11
Q

What is the difference between vesicles of small and peptide NTs?

A

Small NTs are in small clear vesicles. Peptide NTs are in dense core vesicles.

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12
Q

Describe synthesis of catecholamines.

A

Tyrosine via tyrosine hydroxylase to DOPA, via DOPA decarboxylase to Dopamine, via Dopamine Beta-hydroxylase to Noradrenaline, via Phenylethanolamine N-methyltransferase to Adrenaline.

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13
Q

How is the NT signal terminated?

A

Re-uptake of NT into presynaptic cell via presynaptic transporters. Uptake into glial cells. Breakdown of Ach in the cleft by acetylcholinesterase. Recycling of NT for resynthesis.

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14
Q

Describe the process of vesicular fusion and release.

A

Synaptotagmin senses calcium concentration and induces a conformational change in the calcium VGCs. Synaptotagmin fuses to membrane briefly causing a small NT release (Kiss&Run).

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15
Q

What is the SNARE complex?

A

Soluble NSF Attachment Protein Receptor.

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16
Q

What are the common features of EPSPs?

A

Depolarisatory - Cause influx of +ve charge (Na+/Ca2+); Increase firing frequency; Mediated by Glutamate (Na+/Ca2+).

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17
Q

What are the common features of IPSPs?

A

Hyperpolarisatory - Cause efflux of +ve (K+) or influx of -ve (Cl-) charge; Decrease firing frequency; GABA-mediated (Cl-).

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18
Q

Lecture 2

A

Chemical Synapses

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19
Q

How are synaptic vesicles recycled directly?

A

Vesicles delivered to presynaptic membrane. Endocytosis of vesicle components to form new vesicles.

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20
Q

How are synaptic vesicles recycled indirectly?

A

Endocytosis of vesicle components and delivery to endosome. Budding of endosome to form vesicles.

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21
Q

What are the advantages of a vesicular storage system?

A

Concentrations within can be manipulated by binding proteins and proton pumps. Protection from proteases/esterases. Provide a storage system. Allow to be regulated.

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22
Q

How does NT release vary within a neuron?

A

Cortical pyramidal neurones show increasing stimulation (facilitation) at bipolar synapses but decreasing stimulation (depression) at multipolar synapses

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23
Q

What is the evidence for the need of calcium for NT release?

A

No release if intracellular calcium removed. Facilitated release if intracellular calcium increased. Injection of calcium into terminal - facilitated release. Calcium indicator dyes show influx before NT release.

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24
Q

Which type of calcium channels mediate release of NT?

A

P/Q-type.

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25
Q

Describe N-type calcium channels.

A

Neutral type. Presynaptic. Blocked by w-conotoxins and GABA pentin (analogue).

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26
Q

Describe L-type calcium channels.

A

Long lasting. Ventricular and purkinje fibres. Blocked by nidedipine, diltiazem and verapamil.

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27
Q

When would one calcium channel be able to elicit NT release?

A

If the vesicles are closely associated with calcium channels.

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28
Q

Which channels are responsible for NT release in absence of P/Q channels?

A

N & R channels.

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29
Q

Describe the evidence for cooperative action of calcium channels.

A

If two channel types are present, blocking one will decrease the NT release by less than if both are blocked.

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30
Q

Describe the basis of quantal release of NT.

A

Postsynaptic signal magnitude is proportional to the amount of NT released. Single vesicles may be released without stimulation - give 1 quantum of signal (MEPPs). Stimulation of the synapse will give a signal amplitude which is a multiple of a MEPP amplitude.

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31
Q

What is the vesicular concentration of ACh? How many molecules does that equate to?

A

100mM; 10,000 molecules.

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32
Q

What is 4-AP?

A

4-Aminopyridine.

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33
Q

What is the effect of 4-AP on quantal release?

A

Blocks repolarisation by blocking potassium VGCs. Extends the period of presynaptic AP allowing for release of most vesicles - increases efficienct of quantal release.

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34
Q

Describe the evidence for quantal release.

A

Stimulation causes small depolarisation with an amplitude of a multiple of MEPPs. Same trend observed if 4-AP is used.

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35
Q

How is the number of vesicles released estimated?

A

Average amplitude of EPSP / Average amplitude of MEPP.

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36
Q

Describe Katz’s model for quantal release.

A

n quanta released with probability p of release.

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37
Q

Describe Bernoulli’s trial model for quantal release.

A

n repeated trials, representing number of vesicles. Two possible outcomes - Release or not. Probability of success 0<1. Probability for each vesicle/trial is equal. Trials independent.

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38
Q

How is the mean number of vesicles released calculated using binomial models?

A

mu = np

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39
Q

How is the variance of release calculated?

A

sigma^2 = np(1-p)

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40
Q

How is the standard deviation calculated?

A

sigma = _/np(1-p)

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41
Q

What changes in quantal release have been observed in mice with chronic pain?

A

Increased number of vesicles and probability of release in mice with Inflammatory pain. Increased probability of opening in mice with neuropathic pain.

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42
Q

What factors affect vesicular release?

A

Size/shape of depolarisation. Number and functional state of calcium channels. Distance between vesicles and calcium channels. Baseline formed by calcium influx. Number of docked, primed vesicles. Phosphorylation state of presynaptic proteins.

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43
Q

What is the clostridial toxin?

A

Toxin of Clostridium botulinum.

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44
Q

What is the action of clostridial toxin?

A

Toxin is a zinc protease which cleaves either Synaptobrevin, SNAP-25 or Syntaxin 1a needed for vesicle fusion/release. Types B, D, F and G have different cleavage sites.

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45
Q

What are the symptoms of clostridial toxin action?

A

Respiratory failure and paralysis (may lead to death).

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46
Q

What is botox?

A

Botulinum toxin type A.

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47
Q

What is the effect of botox?

A

Blocks nerve transmission reducing facial muscle contraction hence frown lines/wrinkles.

48
Q

Lecture 3

A

Synaptic Integration

49
Q

Describe the distribution of Glutamate receptors in neurones.

A

EAAT1 (GLAST)/EAAT2 (GLT-1) on glial cells. EAAT3-5 on pre and postsynaptic membranes. EAAT5 only in retina.

50
Q

How is glutamate recycled?

A

Glutamate transported into glial cells via GLAST or GLT-1. Converted to glutamine. Glutamine transported into presynaptic neuron. Converted into glutamate and packaged into vesicles by vesicular glutamate transporters.

51
Q

How are glutamate transporters electrogenic?

A

Induce a net uptake of 3+ since they cause influx of 1 glutamate, 3Na+ and 1H+ for every K+ out.

52
Q

How are GABA transporters electrogenic?

A

Induce a net uptake of 1+ since they cause influx of 1 GABA, 2Na+ and 1Cl-

53
Q

What are the types of GABA receptors?

A

GAT1/2/3/4

54
Q

Where are GAT-1 found?

A

Neurones.

55
Q

Where are GAT-3 found?

A

Glial cells.

56
Q

Give an example of a Glutamate transporter blocker.

A

L-Threo-Beta-Benzyloxyaspartate

57
Q

What is the importance of EAAT2 in hippocampus?

A

Produces LTP potentiation. Controls extracelular glutamate allowing appropriate NMDA activation.

58
Q

What is the effect of L-TBOA application? How else can the effect be achieved?

A

Glutamate spillover. Extracellular glutamate so high it may activate neighbouring synapses. EAAT1 knock out in transgenic animals has the same effect.

59
Q

How may mice with no GLT-1 have epilepsy?

A

GLT-1 maps near the QTL of EL-2 (gene associated with epilepsy) on chromosome 2.

60
Q

Describe the experiments proving GLT-1-less mice showed epilepsy.

A

Wt and mutant homozygotes treated with pentylenetetrazole (PTZ) - GABA receptors antagonist. Wt showed no epileptic symptoms because they had GLT-1 to bypass the signalling block. Mutant mice showed sharp high voltage wave bursts and behavioural changes.

61
Q

Describe the neuronal degeneration patterns of mutant GLT-1 mice.

A

Degeneration of CA1 in hippocampus shown by Nissl staining. Neuronal loss in hippocampal dentate gyrus. Increased tonic GABAA mediated conduction and prolonged postsynaptic currents in cerebellar cells.

62
Q

What is the difference in behaviour observes in mutant GLT-1 mice?

A

Fall off a rotating rod sooner. Paw print pattern wider than normal.

63
Q

What are the effects of ischaemia?

A

Decreased cerebral bloodflow. Decreased ATP. Increased intracellular Na+/Ca2+/Cl-/H2O. Increased extracellular K+. Increased NT release. Swelling. Cell damage/death.

64
Q

What is hemodynamic compromise?

A

Blood-flow blockage.

65
Q

What does glutamate transport depend on mostly?

A

Electrochemical gradient set by Na+/K+ ATPases.

66
Q

Where is most of neurones’ ATP used?

A

Na/K ATPases.

67
Q

What is the effect of 5 minute bloodflow interruption in the brain?

A

Death of neurones in several brain regions.

68
Q

What causes increase in postsynaptic calcium in ischaemia?

A

High extracellular glutamate drives calcium influx via symporters. Activation of PLC by glutamate leads to IP3 formation, increasing postsynaptic calcium further by release from ER.

69
Q

What is the effect of NMDA inhibition in ischaemia?

A

Protects myelin from ischaemic damage.

70
Q

How is glutamate release calcium independent in ischaemic tissue?

A

Imbalance in ionic concentrations causes reversal of uptake which means GLT-1 and GLAST transporters of glia pump out glutamate. So do EAAT3/4/5.

71
Q

Lecture 4

A

Synaptic Plasticity

72
Q

What factors affect synaptic integration?

A

Distance from synapse to soma. Relative position of all synapses. Amplitude of current at synapse. Time constant. Length constant.

73
Q

What is spatial integration?

A

Integration of signals which reach the synapse at the same time. Simultaneous signalling between 2 neurones or coincidence of multiple neurons.

74
Q

Describe the signalling between climbing fibres and Purkinje cells.

A

One climbing fibre per Purkinje cell. 100s of synapses. Large synaptic current/potential. Complex spike.

75
Q

Describe the signalling between parallel fibres and Purkinje cells.

A

1000s per Purkinje cell. Single contact site each. Small synaptic current/potential.

76
Q

What is the effect of the length constant on spatial integration?

A

Long length constant allows more distant synapses produce an AP with less coinciding inputs.

77
Q

Why is the total depolarisation caused by multiple inputs not equal to the sum of individual inputs?

A

More proximal input will open channels reducing the Rm (hence length constant) for the distal input.

78
Q

What is temporal integration?

A

Integration of inputs from either a single neuron firing a train of APs or multiple neurons firing in quick succession.

79
Q

What is the effect of the time constant on temporal integration?

A

Interval between summating inputs may be longer.

80
Q

Lecture 5

A

Synaptic Information Processing

81
Q

How is coincidence detection achieved?

A

By setting the threshold for an action potential so high that only 2 summating EPSPs will evoke a response. Short time constant to let only near-simultaneous EPSPs evoke an action potential.

82
Q

How is rate coding different to coincidence detection?

A

Long time constant is used to determine the average rate of EPSPs

83
Q

Describe how EPSPs and IPSPs summate.

A

Summate linearly if from different dendrites. If IPSP on the same dendrite and more proximal - affects spread of EPSP by lowering Rm of membrane - Non-linear summation.

84
Q

What are silent IPSPs?

A

IPSP which equals the resting potential.

85
Q

What effect do silent IPSPs have on EPSPs?

A

Cause a shunt - stunted excitatory effect due to Rm decrease triggered by the Rm.

86
Q

Give an example of silent IPSPs in the CNS.

A

GABA receptors cause influx of Cl-. Reversal potential of Cl- is close to -70mV (resting potential)

87
Q

What is presynaptic inhibition?

A

Inhibition of an EPSP by an IPSP which inhibits the presynaptic terminal by reducing calcium influx.

88
Q

What are the limitations of computational approaches of studying synaptic integration?

A

Only as good as the assumptions used.

89
Q

What is the common approach to studying synaptic integration?

A

Using caged NT. Brain slices in solution of NT activated by UV. Brief flashed of UV mimic calcium influx.

90
Q

What is the effect of UV on

A

Cleaves the C-O bond between glutamate and alpha-carboxy-2-nitrobenzyl.

91
Q

How do neuronal responses vary?

A

Different synaptic input patterns form distinct responses which are distinguished by neurons.

92
Q

Why does the order of synaptic inputs matter?

A

Distal=>Proximal activation yields a greater summation response than Proximal=>Distal. Difference depends on time constant and intervals.

93
Q

Lecture 6

A

Synaptic Plasticity

94
Q

What is synaptic facilitation? Give an example.

A

Next of a train of EPSPs has a greater amplitude. Parallel fibres of Purkinje cell.

95
Q

What are the mechanisms of synaptic facilitation?

A

1st AP induces calcium influx. Some NT released. Rest mostly primed. 2nd AP releases more NT. Postsynaptic receptors sensitise. More receptors expressed - greater chance of binding.

96
Q

Why does the spike broaden during synaptic facilitation?

A

Longer presynaptic depolarisation causes more calcium influx hence more NT release and an increased synaptic response.

97
Q

What is synaptic depression? Give an example.

A

Next of a train of EPSPs has a smaller amplitude. Climbing fibres of Purkinje cell.

98
Q

What are the mechanisms of synaptic depression?

A

1st AP causes release of most of the vesicles. Less NT left for subsequent APs.

99
Q

How does release probability differ at different synapses?

A

Low probability synapses show higher chance of release by next APs (facilitation). High probability synapses show lower chance of release by next APs (depression).

100
Q

What other mechanisms may give rise to synaptic depression?

A

Altered coupling between calcium and vesicles. Modulation of vesicle recycling. Reduction of amount of NT in vesicles. Reduction in calcium influx. Reduction in postsynaptic receptor sensitivity.

101
Q

What is a homosynapse?

A

One presynaptic and one postsynaptic membrane.

102
Q

Describe postsynaptic modulation.

A

Second presynaptic terminal synapses with the postsynaptic membrane. May modulate sensitivity.

103
Q

Describe presynaptic modulation.

A

Second nerve synapses with the presynaptic nerve and facilitates or inhibits it.

104
Q

Describe GABAA modulation via phosphorylation.

A

Activation of a serotonin GPCR receptor activates PKA. PKA phosphorylates GABAA enhancing or suppressing its function depending on phosphorylation site/subunit composition.

105
Q

How can the number of postsynaptic receptors be altered? Use an example.

A

GABAA receptor expression is promoted by insulin. Brain Derived Neurotrophic Factor (BDNF) promotes removal of GABAA.

106
Q

Give an example of heterosynaptic facilitation. Describe.

A

Sensitisation of gill withdrawal reflex in Alpysia californica. Touch of siphon alone elicits weak withdrawal. Touch of siphon after shock of tail givea an enhanced response.

107
Q

Describe the mechanism of heterosynaptic facilitation.

A

Serotonin activates metabotropic 5HT GPCRs. Causes activation of Adenylyl Cyclase. Increase in cAMP. Activation of PKA. PKA phosphorylates potassium VGCs. Decrease in potassium current during AP. Broader AP spike. Calcium VGCs open for longer. Increased intracellular calcium. Increased NT release.

108
Q

Give an example of long-term plasticity.

A

Tetanus causes future EPSPs to have a greater amplitude. Effect lasts for a long time suggesting learning.

109
Q

What are the 2 categories of postsynaptic ionotropic glutamate receptors?

A

NMDA and non-NMDA.

110
Q

Describe the action of non-NMDA receptors. Give examples.

A

Glutamate binds causes opening of channel and influx of sodium. AMPA. Kainate.

111
Q

Describe the action of NMDA receptors.

A

Glutamate binds and activated but pore blocked physically by magnesium. Blocked unless membrane is depolarised. If depolarised - causes influx of calcium.

112
Q

Why is tetanus more likely to induce LTP than a single presynaptic potential?

A

Tetanus causes large release of NT therefore large postsynaptic depolarisation which is more likely to activate NMDA receptors upon which LTP depends.

113
Q

What is the importance of LTP? Support with evidence.

A

Important for memory formation and learning in hippocampus. HM patient suffering from epilepsy. After operation involving bilateral medial temporal lobe resection (removal of most of the hippocampus) he couldn’t form any new memories.

114
Q

What are other forms of LTP?

A

Long-term potentiation - NMDA dependent and independent. Long-term depression - NMDA dependent and independent.

115
Q

Give an example of long-term potentiation.

A

NMDA independent LTP of claw opener muscle in crayfish.

Physiology and Pharmacology 2 (8 decks)

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