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Neuro > neurotransmission > Flashcards

neurotransmission Flashcards

1
Q

chemical synapse

A

50 nm junction
Transmission speed 1-5 ms
Release of neurotransmitters
Excitatory or inhibitory

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2
Q

electrical synapse

A

Close 3-5 nm
Joined by gap junction proteins
Fast response nearly no delay

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3
Q

neuromodulators released from

A

neurosecretory terminals of modulatory neutrons

or conventional presynaptic terminals

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4
Q

neuromodulators effect

A

alter the quality of information passing through a synapse

or the spontaneous activity of a population of post-synaptic neuron

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5
Q

stats of neurons in brain

A

10^12 neurons
each with 1,000 synapses
–> 10^15 synapses in brain

10^15 glial cells ( capable of modulating aspects of neuronal functioning and synaptic transmission )

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6
Q

tripartie synapses

A

refers to the functional integration and physical proximity of the

presynaptic membrane, postsynaptic membrane, and their intimate association with surrounding glia

as well as the combined contributions of these three synaptic components to the production of activity at the chemical synapse.

dynamic two way relationship between glial cells and neurons

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7
Q

gliotransmitters

A

glutamate
adenosine
ATP

–> can modulate synaptic transmission by acting on neurons

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8
Q

the synapse of Held

A

giant synapse surrounding post synaptic cell in auditory system

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9
Q

ribbon synapses

A

spontaneous release

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10
Q

synapses on different parts

A

affect functional role

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11
Q

synapses on different parts

A

affect functional role eg dendrites, cell bodies, axons

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12
Q

gap junctions

A

hemi channels of protein connexin in both pre and postsynaptic membrane –> aligned to form channels along which ions can flow from one cell to another

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13
Q

connexin protein

A

tetra membrane spanning protein with cystine extracellular residues –> important for docking both halves of the hemi-channel

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14
Q

three types of gap junctions

A

homomeric/homotypic: two identical hemichannels

heteromeric: more than one connexin isoform

heterotypic : two different types of hemichannels

each connexion: 6 connexion protein subunits

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15
Q

Electrical synapses common features

A
  • Direct coupling via gap junctions (connexins) (Invertebrates: Innexins and Pannexins)
  • Bidirectional: Transmission in both directions (but examples of rectifying transmission in one direction only)
  • Especially common among between rapidly firing interneurons in the neocortex
  • Synchronize electrical activity between cells

not amplifable

no adaptation

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16
Q

mixed synapses

A

chemical and electrical components of transmission

complex time dependent synaptic signalling, with the appearance of electrical excitation at a synapse when chemical inhibition for instance becomes fatigued. Neuromodulators can alter both chemical and electrical transmission

eg Mauthner neuron

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17
Q

hetero-synaptic interactions

A

same postsynaptic cell

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18
Q

Excitatory transmitters

A

increase time channel spends in open state

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19
Q

chemical synapses , how it works basic

A

presynaptic action potential
calcium influx into presynaptic terminal
fusion of vesicles with synaptic membrane
transmitter release and diffusion across cleft
transmitter binds to receptors
postsynaptic response ( EPSP or IPSP)

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20
Q

EPSP

A

excitatory postsynaptic potentials

–> if big enough opens voltage gated sensitive ion channels in postsynaptic membrane —> these excite postsynaptic cell

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21
Q

IPSP

A

inhibitory postsynaptic potential

–> hyperpolarise postsynaptic membrane , less excitable

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22
Q

Motor neurons

A

Katz at neuromuscular junction of frog

acetylcholine released and binds to receptors
ion channels open –> Na + influx
end plate potential ( like EPSP but at muscle )

TTX blocks opening of sodium channels –> no depolarisation that causes a.p –> graded response

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23
Q

End Plate Potential

A

more than one ion involved

as current-voltage plots show that end plate potentials have a reversal potential of 0 mV
–> as no ion has a rp of 0 more than one have to be involved –> opening of non specific cation channels

–> end plate potential affected by extracellular sodium potassium calcium levels

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24
Q

end plate potential decay

A

consistent with the rate of the time constant of the muscle fibre membrane +

muscle fibre cable properties predicted the amplitude with distance to plate

–> brief surge of inflowing current with passive propagation

–>? end plate potential declines in size as you move away from the junction

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25
Q

GPCRs

A

slower transmission

indirectly modify the action of ion channels via G-proteins or second messenger pathways ( eg Calcium, Cyclic AMP )

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26
Q

mepps : miniature end plate potentials

A

in neuromuscular junction:
discrete spontaneous changes in membrane potential of around 0.5-0.8mV

–> evidence for vesicle hypothesis as when plotting the size of mepps against their frequency then they cluster at multiples of their initial size

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27
Q

what are synapses good for

A

enhances brain power through synaptic connection plasticity –> varying number of physical synapses between cells

varying strength of synaptic connections

functional networks formed through neuromodulation

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28
Q

neuromodulation

A

physiological process by which a given neuron uses one or more chemicals to regulate diverse populations of neurons
neuromodulators diffuse through neural tissue to affect slow-acting receptors of many neurons.

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29
Q

3 largest classes of transmitters

A

amino acids ( glutamate, Gabba, glycine )

biogenic amines ( acetylcholine, noradrenaline, dopamine, serotonine, histamine )

neuropeptides ( 80-100 and increasing )

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30
Q

purines

A

ATP, adenosine

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31
Q

acetylcholine synthesised from

A

( precursor ) AcetylCoA by the enzyme Choline Acetyltransferase ( CAT )

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32
Q

small neurotransmitters

A

are synthesised in terminals by precursors

are transported into vesicles in terminal by specific transporter molecules using energy of the proton gradient set up by the actions of the ATP driven proton pump

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33
Q

Neuropeptides synthesised

A

in cell bodies from larger protein precursor molecules ( DNA )

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34
Q

protein precursor molecules synthesised

A

on ribosomes attached to the endoplasmic reticulum

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35
Q

from the endoplasmic reticulum protein precursor molecules are

A

passed to the vesicular stacks of the Golgi apparatus –> mature there +
modified through sulphating and phosphorylation

packaged to vesicles from membranes of Golgi stacks + transported to release site by axonal transport

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36
Q

How are vesicles released ?

A

calcium sensitive mechanism at specific active zones on the nerve terminal

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37
Q

post synaptic densities

A

array of receptors and effector proteins held in place by scaffolding proteins ( eg gephryn)

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38
Q

in cell calcium channels localised

A

near the release sites in the active zones

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39
Q

vesicle release function RIM proteins

A

linking the calcium channels to the synaptic vesicles via Rabbles proteins

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40
Q

vesicle fusion

A

vesicular Synaptobrevin zips together with terminal SNAREs ( SNAP-25 + Syntaxin ) –> energy of the process brings together the vesicular and presynaptic membranes

calcium binding to synaptotagmin causes the complete zipping of the SNAREs and therefore the fusion of the membranes to form a fusion pore

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41
Q

terminal SNAREs

A

SNAP-25 + Syntaxin

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42
Q

calcium in terminal binds to

A

Synaptotagmin ( –> allows complete zipping of SNAREs)

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43
Q

fusion pore allows

A

neurotransmitter to diffuse into the synaptic cleft

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44
Q

kiss and run

A

partial release of vesicle content

vesicles pinch off after exocytosis without merging with the plasma membrane

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45
Q

vesicle fusion allows

A

complete release of vesicle content

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46
Q

what prevents the terminal from getting too big + recycling specific vesicular proteins

A

Cathrin-dependent mechanisms for membrane recycling

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47
Q

after exocytosis

A

vesicles flatten into the plasma membrane + components recycled via Cathrin -mediated endocytosis + formation of new vesicles

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48
Q

metabotropic: transmitter binding

A

and final effector different proteins

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49
Q

excitatory actions

A

ligand gated ion channels increasing conductance for:
sodium
calcium

decreasing conductance for:
potassium

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50
Q

inhibitory actions

A

ion channels :

increasing conductance for chloride
potassium

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51
Q

Goldman-Hodkin-Katz equation

A

lets calculate the reversal potential of the ion channel

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52
Q

reversal potential of ion channel

A

determines whether an EPSP or IPSP is induced

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53
Q

cys-loop family of receptors

A

five subunits pseudosymetrically arranged forming a rosette with a central ion-conducting pore

some cation selective some anion selective

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54
Q

cation selective ion channels

A

nACh and 5-HT3

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55
Q

anion selective

A

GABA a and Glycine

56
Q

receptor containing

A

extracellular domain containing ligand binding sites

transmembrane domain that allows ions to pass across the membrane

intracellular domain that plays a role in channel conductance and receptor modulation

57
Q

metabotropic receptors

A

7-transmembrane spanning g-protein coupled receptors

kinase-linked receptors

58
Q

kinase linked receptors

A

act directly as enzyme effectors

59
Q

GPCR activations

A

direct: g-protein activates ion channels
indirect: ion channels activated through second messenger pathways

60
Q

cAMP signalling

A

Neurotransmitter docks on receptor

alpha g-protein activated

activity of enzyme adenylyl cyclase ( AC ) regulated

AC makes second messenger cAMP from ATP

cAMP activates protein kinase A ( PKA ) which can phosphorylate –> change activity of numerous proteins eg ion channels

61
Q

modulation of AC by GPCRs

A

can be negative as well as positive

62
Q

ca2+/ IP3 pathway

A

activated alpha g-protein activates phospholipase C which converts PIP2 into IP3 and DAG

IP3 acts on the IP3 gated receptors of the Endoplasmic reticulum . The opened channel allows for Calcium to flow into the cell

DAG activates Protein Kinase C ( PKC ) which phosphorylates targets eg membrane opine channels

63
Q

intracellular Calcium

A

controls huge number of key cellular events

from exocytosis
to gene expression

64
Q

3 main factors influencing transmitter life-time in cleft

A

Diffusion ( all synapses )

uptake ( most synapses eg GABA glutamate

enzymatic breakdown ( esp for cholinergic and peptidergic )

65
Q

transmitter removal determines

A

response duration and frequency of postsynaptic response

66
Q

ACh synapse neuromuscular junction

A

hard but brief postsynaptic hit

due to lots of transmitter vesicle released by each presynaptic AP

rapid breakdown by ACh esterase ( cholinesterase )

–> high fidelity transmission by a wide range of frequencies

67
Q

Transmitter removal of most central synapses:

A

transmitter removed by diffusion and active uptake into presynaptic terminals or surrounding glial cell processes

fewer vesicles released

–> probabilistic transmission with less spill over

68
Q

central synapses drug targets

A

uptake transporters as important drug targets

eg
 function of cocaine blocking dopamine reuptake

SSRIs : specific serotonin reuptake inhibitors

69
Q

synaptic cleft functionality

A

has structural organisation, Is not just an empty gap

nanocolumm organisation –> possibly by diffusible signals crossing synaptic cleft or interactions of pre and post synaptic proteins that project into cleft and interact

70
Q

nanocolumn organisation

A

location of presynaptic active release sites may be coordinated by the RIM proteins to bring them into register with elements of the post-synaptic scaffold proteins ( eg PSD-95) –> organise location of various postsynaptic response elements eg neurotransmitter receptors

71
Q

GPCRs

anatomy

A

7 transmembrane spanning G-protein coupled receptors

variable sequence extracellular N-terminals ( amino )
3 extracellular loops influencing agonist binding

variable intracellular C-terminals ( carboxy )
3 intracellular loops which influence G-protein binding

+ scaffolding protein + other intracellular effectors

72
Q

agonist binding influences

( GPCRs)

A

conformational change in shape of the receptor

–> including a change in relative position of TMs 3 and 6

–> change if the conformation of the intracellular portions of the receptor

–> can now interact and activate with g-protein

73
Q

g-proteins

A

bind guanine nucleotides

trimers of three subunits : alpha beta gamma

74
Q

metabotropic receptors (change)

A

indirect transmission:

not directly inhibiting or exciting

interact with other membrane proteins –>

changes in ion channel activity

changes in metabolic processes within the neuron

amplifiable at a number of different points in the signalling cascade

75
Q

muscarinic receptors

A

binding of ACh activates βγ subunit which binds directly to and opens potassium channels
cell hyperpolarises with an outward potassium current

76
Q

adrenergic receptors

A

GPCRs activated by norepinephrine

77
Q

what mediates appropriate binding of g-protein

A

second and third cytoplasmic loops , amino terminal region of intracellular tail

78
Q

G-proteins grouped into three classes

A

according to structure and target of their α-subunit

Gs

Gq

Gi

79
Q

Gs ( effect)

A

stimulates adenylyl cyclase

–> more cyclic AMP

–> more protein kinase

80
Q

Gi

A

inhibits adenylate cyclase

  • -> less CAMP
  • -> more Potassium channels open
  • -> inhibition

includes
Gt ( transducin )
activates cGMP
Go : interacts with calcium ion channels

81
Q

Gq

A

couples to enzyme phospholipase C ( PLC )

–> more of it –> ITP3

–> protein kinase C

82
Q

activated g-protein

A

GDP displaced by GTP from α-subunit of the G-protein
—> dissociation of α-subunit from βγ-subunit complex

Free α-subunit and βγ-subunit diffuse and bind to target proteins: modulatory effects

–> GTP hydrolysed to GDP on α-subunit by endogenous GTPase activity

–> G-protein re-aggregates , activity terminated

83
Q

resting state g-protein

A

GDP bound to the α-subunit and the three subunits associated as a trimer

84
Q

modulation of ion channels by g-proteins

A

direct interaction: βγ-subunit

indirect interaction: α-subunit through activating one or more enzymes that activate second messengers which interact with ion channels

85
Q

divergence transmitters (GPCRs )

A

when a transmitter interacts with a number of different receptor subtypes this results in divergening signals as each

interacts with a range of different effectors systems

86
Q

convergence

A

each family of receptors contains several members however, C-terminus is indistinguishable

–> different transmitters thus act through the same effector systems although using different receptors

87
Q

non-olfactory GPCRs 5 families

A

based on agonist and subtle structural differences

Rhodopsin family

metabotropic glutamate ( / GABA ) receptors

secretin/calcitonin-like receptors

smoothened/frizzzled-like receptors

adhesion receptors

–>different members of families characterised by different agonist binding sites and different length of N-terminals, C-terminals and third intracellular loops

88
Q

β-2 adrenergic receptor

A

best understood GPCR

inactive crystal structure resolved :
fusion protein bound to its inverse agonist ( carazolol) + to T4 lysozyme to stabilise floppy intracellular loops

89
Q

Ensemble theory

A

receptors are continuously oscillating between a number of different configurations each with different signalling properties

crystalline structures thus represent a snap shot of the receptor in a particular configuration
–> ligands determine the length of time a receptors spends in a configuration

90
Q

GPCR crystalline structures–> why useful

A

diversity of agonist binding sites –> how ligands access those

understand the structural changes involved in receptor signalling : through accumulating info about inactive, agonist bound/ antagonist bound / agonist + g-protein bound structures for indv receptors

identifying dimer forming interfaces : for homo and heterodimeric GPCR forms

identifying action sites of allosteric modulators flexibility : important for internal water pathway

development of new drugs : by finding unknown molecular structures that can act as agonists or antagonists

91
Q

negatives of GPCR crystalline structures

A

need to know influence of various proteins needed for crystallisation

92
Q

Future technologies GPCR

A

• Single-particle negative-stain electron phase-plate cryo-microscopy – 3D structures at almost atomic level and protein-protein interactions – no modifications required
• Hydrogen-deuterium exchange mass spectrometry – dynamic changes
• NMR spectroscopy (Rotationally aligned solid-state NMR) of human chemokine receptor 1
(CXCR1) 2012 – real time dynamic changes

93
Q

protein dimer

A

two monomer proteins ( single proteins ) that are non-covertly bound to form a complex

94
Q

homodimer

A

A protein homodimer is formed by two identical proteins

95
Q

heterodimer

A

a protein heterodimer is formed by two different proteins

96
Q

allosteric

A

changing the activity of a protein by binding an effector ( conformational change )

97
Q

GABA B heterodimers

A

needs to be formed between GABA B1 and GABA B2 subforms before signalling can take place

GABA B2 needed to get GABA B1 receptor to the cell surface –> dimers probably made in ER and transported to plasma membrane

98
Q

GABA B activation

A

GABA B1: binds GABA to Venus fly trap region of N-terminus –>

conformational change –> passed allosterically to GABA B2

GABA B2: binds to g-proteins –> activates signal

99
Q

Biased agonism

A

agonist specific coupling

different agonist induce different receptor conformation each with own distinct repertoire of signalling capabilities to second messenger systems

some compounds can be agonists for one second messenger pathway and antagonists at another through the same receptor

single G-protein coupled receptors –> different pharmacological profiles in different cell types in the same animal –> depending on their local G-protein environment.

100
Q

biased agonism potential benefits

A

reduced side effects of drugs as agonist couple the receptor only to beneficial second messenger pathways and not to those responsible for the production of unwanted side effects

101
Q

homologous desensitization

A

phosphorylation of g-protein coupled receptor specific kinase of agonist activated receptor –> β-arrestin binding

102
Q

heterologous desensitization

A

PKA activated receptor phosphorylation

–> potentially leads to switching between different second messenger pathways

103
Q

causes of receptor desensitisation 1

A

phosphorylation of sites on the third cytoplasm loop and the carboxy terminus by second-messenger related kinases ( eg cAMP dependent protein kinase )

104
Q

Not Dale’s principle of one neuron one transmitter but rather common that

A

one fast acting neurotransmitter is released with

  • slower modulatory transmitter
  • ATP
  • Protons

eg NPY + GABA

105
Q

3 criteria for transmiter system:

A
  1. Substance present in specific neurons together with enzymes that make it, and stored in vesicles in nerve terminals.
  2. Substance released in a Ca2+-dependent way upon depolarization of axon terminal.
  3. Substance has receptors at the synapse and application of substance reproduces (at least partly) the effect of synaptic stimulation. (Note: Co-release means other substances can contribute to synaptic effects.)
106
Q

invertebrate nervous systems transmitter system identification

A

easier

techniques:
large identifiable neurons accessed + dissected + biochemical experiments

107
Q

mammalian brain transmitter system identification

A

harder to identify imdv neurons –> improved through laser techniques

techniques:

immunochemistry

in situ hybridisation –> identify neurotranmitter synthetic enzymes / neuropeptide precursors

induce neurotransmitter release through electrical stimulation / K+ depolarisation
( unsure about exact neuron of release, or is it glial cell? )

iontophoretically apply transmitters to cells in brain slices
- never sure how many different sites they are acting on and whether you are recording from identical neuronal types in different preparations

108
Q

glutamate synthesis

A

from α-ketoglutarate and from glutamine

in presynaptic nerve terminals.

from glutamine made in astrocytic processes from glutamate taken up from synaptic clefts.

109
Q

Glutamate Receptors

A

ionotopic: AMPA, Kainite, NMDA
metabotopic: mGluR ( 8 different )

110
Q

AMPA receptors

A

fast transient excitatory transmissions

agonist binding ( glutamate) opens pore

permeable to Potassium and Sodium –> depolarisation

underlie synaptic plasticity

111
Q

NMDA

A

act slower

coincidence detectors requiring depolarisation

magnesium blocks channel at resting potential due to transmembrane electrical gradient

once post-synaptic cell depolarised to 0, magnesium ion dissociates

–> NMDA receptor permeable to calcium potassium and sodium

glutamate increases Calcium permeability –> induces Long Term Potentiation ( LTP )

112
Q

ionotropic glutamate receptors

A

tetramer of different subunits encoded by separate genes ( usu. dimers of dimers )

non-selective cation channels

differential distribution of subunits in the brain

eceptors with different pharmacology, ionic conductance, desensitization kinetics, calcium permeability and cell surface expression properties

113
Q

Kainate receptors

A

non-NMDA LTP

114
Q

Group II mGluR

A

mGluR 2, 3

Inhibition of adenylyl cylcase
Activation of K+ channels

presynaptically: Inhibition of Ca++ channels –> negative feedback of neurotransmitter release

115
Q

mGluR1

A

predominantly postsynaptically

Phospholipase C stimulation
Stimulation of adenylyl cyclase
(some systems)

increase in Ca2+ concentration in cytoplasm

activate Gq –> produce inhibition of potassium channels ( M& Calcium activated)

116
Q

Group I

A

mGluR1 mGluR5

117
Q

Gaba A receptors

A

members of the Cys-Loop family of ionotropic receptors

pentameric arrangement of 7 different subunit ( 10^ 5 different versions )

gating central chloride channel

GABA binds to the β subunit

all forms contain the γ2 subunit which makes them sensitive to benzodiazepine allosteric modulators.

during neuronal maturation change from excitatory to inhibitory receptors

118
Q

maturation change from excitatory to inhibitory receptors

A

early development:
NKCC transporter –> high intracellular chloride concentration –> m.p negative to equilibrium potential of chloride

receptor opened –> anions flow out of cell –> depolarisation

119
Q

maturation change from excitatory to inhibitory receptors

A

early development:
NKCC transporter –> high intracellular chloride concentration –> m.p negative to equilibrium potential of chloride

receptor opened –> anions flow out of cell –> depolarisation

after maturation:

expression of K+/CL- co-transporter increases –> reduction of intracellular chloride concentration

receptor opened –> Cl- moves into cell ( as Cl- concentration lower than equilibrium potential )
–> outward current : hyper polarisation

120
Q

maturation change from excitatory to inhibitory receptors

A

early development:
NKCC transporter –> high intracellular chloride concentration –> m.p negative to equilibrium potential of chloride

receptor opened –> anions flow out of cell –> depolarisation

after maturation:

expression of K+/CL- co-transporter increases –> reduction of intracellular chloride concentration

receptor opened –> Cl- moves into cell ( as Cl- concentration lower than equilibrium potential )
–> outward current : hyper polarisation

121
Q

GABA inactivation

A

reuptake into presynaptic terminals or glial cells

metabolised to glutamine

transported back to neuron

122
Q

GABA inactivation

A

reuptake into presynaptic terminals or glial cells

metabolised to glutamine

transported back to neuron

123
Q

neuropeptides

A

most numerous transmitters

play specific and critical roles in regulation of brain state and behaviour

124
Q

orexin

A

made by small group of hypothalamic neurons , project everywhere but cerebellum

essential for sustained wakefulness and consciousness –> loss narcolepsy

regulate reward and stress

125
Q

noradrenaline

A

sonata in Locus Coeruleus

innervate: widespread regions of brain and spinal chord

regulates : attention, arousal, sleep/wake

126
Q

Dopamine

A

somata in substantia nigra, ventral tegumental area and arcuate nucleus

regulates:
voluntary movement
reward, addiction

127
Q

serotonin ( 5-HT )

A

somata in raphe nuclei

innervate:
caudal –> spinal chord
rostral: –> nearly all regions of brain

regulates: sleep-wake, mood, perception

128
Q

Histamine

A

somata: tuberomammillary nucleus
regulates: arousal, energy metabolism , general effects

129
Q

active energy currency transferred from glial cells to neurons

A

lactate

not glucose

130
Q

traditional roles of glial cells

A

take up glucose and pass to neuron ( however, pass lactate )

spatial buffering of potassium ions released from active neurons –> prevent building up of potassium ions , interfering with neuronal action potential generation

131
Q

NG2+ glial precursor cells

A

can show Ca2+ dependent action potentials –> potentially to locally coordinate the actions of neurons

not clear if electric property is generalisable

release fibroblast growth factor 2 (FGF2) which supports glutamatrgic signalling

–> without: changes in neuronal activity that contribute to depression

132
Q

examples of dynamic interaction of glial cells and neurons

A

astrocyte control of synaptic NMDA receptors can contribute to the progressive development of temporal lobe epilepsy

astrocyte activation can modulate the response selectivity of visual cortical neurones

133
Q

glial and neuron interaction hippocampus during LTP

A

D-Serine –> co-agonist for NMDA

elease of both glutamate and D-Serine from small vesicles in glial cells
( co-localised in same vesicles )

buffering intracellular changes in Ca2+ in glial cells or blocking D-Serine synthesis
–>
reduce the release of D-Serine from glial cells surrounding hippocampal cell synapses
–> reduction of NMDA receptor induced LTP

glial cells are able to modulate synaptic properties by the release of “gliotransmitters”.

134
Q

release of a wide variety of “gliotransmitters” from Schwann cells at the NMJ

A

Acetylcholine, ATP, Glutamate, Adenosine, Substance P and Calcitonin Gene Related Peptide

135
Q

Denervated NMJs

A

Schwamm cells replace degenerating neuronal nerve terminal

–> memps due to spontaneously released acetylcholine

–> perhaps glial cells to keep neuromuscular architecture intact whilst axon regenerates , re-establishes NMJ

Neuro (13 decks)

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