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Neuroanatomy > Signalling > Flashcards

Signalling Flashcards

1
Q

what breaks down ACh?

A

AChE, acetylcholinesterase

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2
Q

What are the two types of cholinergic signalling?

A

Ionotropic/nicotinic (nAChR) and msucarinic (mAChR)

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3
Q

what is the enzyme that forms ACh?

A

ChAT, choline acetyltransferase

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4
Q

Antagonist of nAChRs?

A

curare (plant based toxin)

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5
Q

what are nAChRs permeable to?

A

Na+, K+ and highly variable to Ca2+

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6
Q

whats the role of ACh in somatic nervous system?

A

-voluntary control of body movements
-some reflexes
-NMJ

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7
Q

How is ACh involved at NMJ?

A

-ACh activates nAChRs on motor plate (only pass Na+ and Ca+
- eEPP (excitatory end plate potential)
- when eEPP reaches threshold voltage gated Na+ channles open and causes motor end plate AP

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8
Q

Name 2 toxins that are competitive antagonists for nAChR?

A

Tubocurarine
A-bungarotoxin

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9
Q

Name a AChE inhibitor and how does it work?

A

Physostigimine
- get depolarising block (desensitisation of receptors and deactivated voltage gated Na+ receptors
- used in operative care as a relaxant

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10
Q

Name two toxins that block ACh release?

A

Tetanus toxin
Botulinum toxin (both cause paralysis)

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11
Q

how is nAChRs involved in myasthenia gravis?

A

-autoimmune (antibodies against nAChRs)
- causes muscle weakness and paralysis
-causes membrane attack complex (MAC) which causes internalisation of nAChRs from membrane

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12
Q

Treatment for myasthenia gravis?

A

Neostigmine (AChE inhibitor) and immune system suppressants

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13
Q

what are the pathways of the trisynaptic circuit of the hippocampus?

A

Perforant pathway (Entorhinal cortex to dentate gyrus)
Mossy fibres (dentate gyrus to CA3)
Schaffer collaterals (CA3 to CA1)

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14
Q

What are the 4 basic properties of LTP?

A
  • cooperative (number of fibres simultaneously activated
  • input specific (synapse must be activated during induction)
  • associative (induction at concurrently active synapses)
  • Hebb’s law (spike-timing dependent plasticity)
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15
Q

What are the mechanisms underlying LTP?

A
  • NMDA receptor dependent
  • prolonged depolarisation and alleviation of Mg2+ block (can be associative)
  • large fast increase in Ca2+
  • Kinase activation (calcium calmodulin kinase)
  • insertion of AMPAR
  • retrograde signalling (presynaptic changes)
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16
Q

what can LTP induction be blocked by?

A

Ca2+ chelators

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17
Q

what are some of the mechanisms that contribute to increased AMPAR activity?

A
  • changes in protein phosphorylation
  • AMPAR properties and trafficking
  • cytoskeleton reorganization (remodelling of dendritic spines)
  • local protein synthesis (gene transcription via CREB)
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18
Q

what can LTD be induced by?

A

prolonged low frequency stimulation

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19
Q

what does LTD involved?

A
  • internalization of AMPAR
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20
Q

how is AMPAR internalized in LTD?

A
  • small and slow increases in Ca2+
  • phosphatase activation
  • dephosphorylation of stargazin and endocytosis of AMPAR
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21
Q

what is the induction of LTD (but not LTP) sensitive to?

A

phosphatase inhibitors

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22
Q

LTD in the cerebellum?

A
  • paired stimulation of climbing fibres and parallel fibres causes LTD that decreases purkinje cell EPSP and acts as a corrective mechanism
  • associative (both climbing fibres and parallel fibres must be activated at the same time
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23
Q

Mechanism of LTD in cerebellar?

A
  • Glu release from parallel fibres activated mGluR
  • climbing fibres activation depolarises purkinje cells and voltage gated calcium channels open (increase Ca2+)
  • causes synergistic activation of PKC (and MAPK)
  • internalisation of AMPAR
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24
Q

What is different about electrical synapses compared to chemical?

A
  • electrical synapses can flow backwards
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25
Q

what are the myelinating cells of the CNS?

A

oligodendrocytes

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26
Q

what do oligodendrocytes do?

A

provide metabolic support for aoxns

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27
Q

differences between oligodendrocytes and Schwann cells?

A
  • Schwann cells are PNS, oligos are CNS
  • Schwann cells myelinate a single/single bundle of axons whereas oligos can myelinate multiple axons
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28
Q

components om myelin sheath?

A

70% lipid, 30% protein

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29
Q

what are microglia?

A

resident immune cells of CNS

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30
Q

different states of microglia?

A

‘resting’- highly ramified, motile processes to survey environment
‘activated’- retract processes, become amoeboid and motile

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31
Q

roles of microglia?

A
  • immune surveillance
  • phagocytosis
  • synaptic pruning
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32
Q

which microglia are good and which are bad?

A

M2 and good
M1 are bad

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33
Q

functions of astorcytes?

A
  • developmental (radial glia)
  • structural (brain micro-architecture)
  • envelope synapses (tripartite synapse, buffer K+ etc.)
  • metabolic support (glutamate-glutamine shuffle)
  • neurovascular coupling
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34
Q

what are MND symptoms due to?

A
  • loss of microglia
  • MND spinal cord shows decreases in motor neurons, and increases in microglia and astrocytes
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35
Q

definition of commissures?

A

tracts that cross midline

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36
Q

difference in PNS and CNS terminology for cell bodies?

A
  • nuclei in CNS
  • ganglia in PNS
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37
Q

what drives depolarization?

A
  • influx of Na+
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38
Q

what drives repolarization?

A
  • closure of Na+ and opening of K+
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39
Q

what drives hyperpolarization?

A
  • voltage gates K+ channels remain open after the potential reaches resting level
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40
Q

what is the relative refractory period?

A
  • possible to instigate AP but harder due to hyperpolarization so need even stronger stimulus
  • VGSC need time to rest after conformational changes
  • confers directionality
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41
Q

when does active conduction occur?

A
  • when stimulus is above threshold
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42
Q

why is local passive flow important?

A

-during AP propagation

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43
Q

role of cholinergic signalling?

A
  • septal and basal ganglia
  • consolidation of memory (AD)
  • neocortex (tonically active during ‘awake’ state on EEG
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44
Q

role of serotonin in signalling?

A
  • raphe nuclei of midbrain, pons and medulla
  • largest territorial distribution of any set of CNS neurons
  • role in depression (SSRIs etc.)
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45
Q

role of dopaminergic signalling?

A
  • midbrain DA neurons (substantia nigra (part of BG) and mesolimbic)
  • limbic system
  • role in SZ
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46
Q

role of norepinephrine?

A
  • locus coeruleus in midbrain
  • depression (MAOs work on this system)
47
Q

what can inhibit Na+/K+ ATPase?

A

cardiac glycosides digoxin and ouabain

48
Q

Whats the target of some anti-epileptic drugs such as lamotrigine?

A

Nav channels

49
Q

Sodium channelopathies?

A
  • epilepsy, migraine, autism, episodic ataxia, pain insensitivity and extreme pain disorders
50
Q

Potassium channelopathies?

A
  • epilepsy syndromes
  • episodic ataxia type 1
51
Q

Calcium channelopathies?

A
  • episodic ataxia type 2
  • childhood absence epilepsy
  • X-linked congenital stationary night blindness
52
Q

what does the gap junction GJB1 (Cx32) cause?

A

Charcot Matie-tooth neuropathy X linked 1

53
Q

what does gap junction GJC2 (Cx47) cause?

A

-leukodystrophy, hypomyelinating, spastic paraplegia (non-fatal MND)

54
Q

criteria for NT?

A
  • present in presynatpic neuron
  • released in response to depolarisation of presynaptic neuron and release must be Ca2+ dependent
  • specific receptors must be present on postsynaptic cell
55
Q

small molecule NT?

A

amino acids (Glu, Gly), ACh, ATP (dopamine and 5HT), GABA
- short term effects

56
Q

peptide NT?

A

substance P, vasopressin, CRH, ACTH, opioids and neuropeptide Y
- longer term effects

57
Q

what toxins target SNARE proteins?

A

-BoTX, botulinum (mainly affects peripheral and visceral neuromuscular synapses and causes weakness)
- TeTX, tetanus (mainly affects inhibiotry spinal interneurons)

58
Q

Models for synaptic vesicle recycling?

A
  • clathrin mediated endocytosis (slow and distal to release site)
  • ultrafast endocytosis (very fast and distal to release site, needs dynamin and does not need clathrin)
  • kiss and run (fast and at release site)
59
Q

strategies for upregulation of NT?

A
  • supplement NT or precursor (eg. LDOPA in PD)
  • inhibit cleafrnace by transporters (eg. SSRIs like prozac in depression)
  • inhibit breakdown (eg. AChE inhibitors)
60
Q

strategies for down regulation of NT?

A
  • presynaptically (eg. local application of botox)
  • postsynaptically (eg. block receptors with antagonists of receptors; antipsychotics, D2 dopamine receptors)
61
Q

what does ionotropic mean?

A
  • ligand gated ion channels
62
Q

GABAa ionotropic agonists?

A
  • used as sedative, anxiolytics, antoconvulsants and anaestheitc
  • Barbiturates activate
  • benzodiazepines enhance
63
Q

GABAa ionotropic antagonists?

A
  • Picrotoxin PTZ used experimentally as convulsants (animal models of epilepsy)
  • BZD
64
Q

GABAb metabotropic agonist?

A
  • Baclofen
  • spasticity in MND and MS
65
Q

GABA reuptake inhibitors?

A
  • tiagabine/gabitril
  • used for focal seizures
66
Q

what does glycine work on?

A

ionotropic Cl- channels

67
Q

what are ionotropic Cl- channles inhibited by?

A

strychnine (induces seizures)

68
Q

what is ATP castabolised by?

69
Q

receptors for ATP?

A

-P2X (ionotropic receptors)
- P2Y (metabotropic receptors)
- P1 (adenosine)

70
Q

what is the nigrostriatal pathway used for?

71
Q

what is the mesolimbic projection pathway used for?

A

reward/addication

72
Q

what is the mesocortical projection pathway used for?

A
  • cognition/emotion/motivation
73
Q

MAO-B inhibitors and use?

A

-selegiline and rasagiline
- use din early PD

74
Q

COMT inhibitors and use?

A
  • entacapone and tolcapone
  • used with Levodopa in PD
75
Q

what is noradrenaline used for?

A
  • sleep, wakefulness and attention
76
Q

what type of receptors are adrenergic receptors?

A
  • metabotropic
77
Q

inhibitors of adrenergic receptors and use?

A
  • beta blockers eg. propranolol used to treat cardiac arrhythmias and migraines
78
Q

role of histamine?

A

arousal and attention

79
Q

antihistamines?

A
  • cross BBB
  • promethazine (blocks H1) acts as a sedative
80
Q

role of serotonin?

A

mood, sleep, wakefulness, nausea and appetite

81
Q

therapeutic role of serotonin?

A
  • SSRIs (fluoxetine and prozac)
  • sumatriptan (agonist of 5HT1) helps with migraines
  • atypical antipsychotics are antagonists of 5HT2
  • ondansetron is antagonist on 5HT3 (reduces nausea and vomitting in chemotherapy)
82
Q

what can excess serotonin cause?

A
  • serotonin syndrome
  • shivering and diarrhoae (mild)
  • rigidity, seizures and fever (severe)
83
Q

role of serotonin in PD?

A
  • loss of serotonergic neurons
84
Q

peptide NT involved in pain?

A

substance P and opioid peptides

85
Q

peptide NT involved in stress repsonse?

86
Q

peptide NT involved in food intake?

A

NPY and melanocortins

87
Q

pituitary peptides?

A
  • vasopressin and oxytocin
88
Q

sources of presynaptic glutamate?

A
  • reuptake through glutamate transporters
  • conversion of a-ketoglutarate to glutamate
  • conversion of glutamine to glutamate via glutaminase
89
Q

what is the most abundant excitatory NT in the brain?

90
Q

ionotropic glutatamate receptors?

A
  • ligand gated
  • postsynatpic receptors
  • fast
  • excitatory
91
Q

agonist and antagonist of ionotropic glutamate receptors?

A

agonist: glutamate
antagonist: kynurenic acid

92
Q

types of ionotropic glutamate receptors?

A

NMDA, AMPA, Kainate

93
Q

metabotropic glutamate receptors?

A
  • GPCR
  • post and presynaptic
  • can be excitatory or inhibitory
94
Q

what is AMPA receptors permeable to?

A
  • Na+ and K+
  • can be permeable to Ca2+ but generally not common
95
Q

what does NMDA receptor need?

A
  • coagonist glycine
96
Q

what are NMDA receptors permeable to?

A

K+, Na+ and Ca2+

97
Q

what are NMDA receptors blocked by?

A

Mg2+ channel block

98
Q

difference between NMDA and AMPA receptors?

A
  • NMDA has slower kinetcs and holds onto glutamate longer than AMPA
  • AMPA has quick binding and unbinding of glutamate
99
Q

role of AMPA and NMDA in LTP?

A
  • glutamate binds to both receptors
  • NMDA blocked due to Ca2+
  • AMPA causes partial depolarisation (open NMDA coincidence detector
  • NMDA now permeable to Ca2+
  • Ca2+ influx initiate signalling cascades (calmodulin and activation of CAM kinase II)
  • promotes recruitment of AMPA receptors to postsynaptic membrane
  • more AMPA receptors menas can repsonse with greater strength to sam eamount of glutamate
100
Q

glutamatergic signalling and excitotoxicity?

A
  • excessive glutamate receptor activation can lead to activation of signalling cascades that promote cell death
  • driven by excessive calcium mediated signalling
101
Q

ways in which excessive calcium mediated signalling can drive excitotoxicity?

A
  • mitotoxicity (increased reactive oxygen species)
  • apoptosis via caspase-3 induction
    -nitrous oxide synthase (nNOS) increase mitochondrial permeability transition pore function leading to solute overload and mitochondrial swelling
102
Q

what are NMDA recepotrs involved in?

A
  • synapse to nucleus signalling
  • regulation of transcription
  • function of target genes: dendrite maintenance, protection of mitochondria, acquires neuroprotection, consolidation of plasticity
103
Q

ALS and glutamate?

A
  • glutamate induced motor neuron death is a hypothesis of disease progression of ALS
  • hyperexcitability suggests to be be pre-symptomatic feature or early feature of ALS progression
104
Q

what does tetradoxin block?

A

Na+ channels

105
Q

what does tetradoxin block?

A

Na+ channels

106
Q

what does tetraethylammonium (TEA) block?

A

K+ channels

107
Q

what do cardiac glycosides digoxin and ouabain block?

A

Na+/+ ATPase

108
Q

what does lamotrigine target?

A

Nav channels

109
Q

Potassium channel blockers?

A

-fampridine/ampyra
- amiadarone

110
Q

agonist of TRPA1 channel?

A
  • ## mustard oil
111
Q

agonist of TRPM8 channel?

112
Q

agonist of TRPV1 channel?

A
  • capsaicin (pain)
  • histamine (itch)
113
Q

agonist of TRPV4 channel?

A
  • serotonin
  • histamine

Neuroanatomy (11 decks)

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