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202 theme 1 > Chemistry and Physiology of the Synapse > Flashcards

Chemistry and Physiology of the Synapse Flashcards

1
Q

what are the 2 types of postsynaptic recepetors?

A

ionotropic and metabotropic

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2
Q

what are ionotropic receptors?

A

ligand gated ion channels = responsible for fast transmission of information to postsynaptic neuron
channels are made up of 2/4 subunits which fold together to form a central pore
similar to voltage gated Na+ and K+ channels, but open to ligand binding, rather than voltage changes

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3
Q

what do ligands do?

A

neurotransmitter
binds to channel, changing its conformation
opens channel, allowing ions to flux through the central pore

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4
Q

receptor variation: pharmacology

A

what transmitter binds to the receptor and how drugs interact with them

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5
Q

receptor variation: agonist

A

a drug that can combine with a receptor on a cell to produce a physiological reaction

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6
Q

receptor variation: antagonist

A

a drug which blocks the activity of the agonist/endogenous ligand (neurotransmitter)

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7
Q

receptor variation: kinetics

A

rate of transmitted binding and channel gating determining duration of their effects

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8
Q

receptor variation: selectivity

A

which ions are fluxed

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9
Q

receptor variation: conductance

A

the rate of flux helps determine effect magnitude

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10
Q

what do glutamate ionotropic receptors do?

A

in general, flux Na+
cause EPSP (excitatory post synaptic potential)
depolarises postsynaptic neuron
if enough occurs, post synaptic neuron will fire an AP

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11
Q

what do GABA ionotropic receptors do?

A

flux Cl-
cause IPSP (inhibitory post synaptic potential)
hyperpolarises postsynaptic neuron
inhibits neuron from firing UNLESS there is sufficient glutamate stimulation to counteract hyperpolarisation

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12
Q

which are the most well studied ionotropic receptors?

A

nicotinic receptors at NMJ
activated by acetylcholine
causes excitation and contraction of muscle cells

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13
Q

what can activate ionotropic recpetors?

A 
glutamate
GABA
acetylcholine
serotonin
ATP
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14
Q

what is the relevance of synaptic integration?

A

determines whether or not a postsynaptic neuron will fire an AP or not
summation of all excitatory and inhibitory signals - depolarisation must surpass threshold

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15
Q

types of glutamate ionotropic receptors

A

NDMA
AMPA
Kainate
names based on agonists selective for them (NMDA, AMPA, Kainic acid)

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16
Q

non-NMDA receptors (AMPA and Kainate) selectivity and conductance

A

fast opening channels
permeable to Na+ and K+
responsible for early phase EPSP

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17
Q

NMDA receptor selectivity and conductance

A

slow opening channel
permeable to Na+, K+ and Ca2+
requires extracellular glycine as a cofactor to open the channel
gated by membrane voltage - Mg2+ plugs pore - ejected on depolarisation
responsible for late phase EPSP

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18
Q

how is Mg2+ related to NMDA receptors?

A

plugs pore at resting state
on membrane depolarisation, Mg2+ is ejected by electrostatic repulsion
allows for conductance of other cations
= activity dependent synaptic modification

19
Q

how is NMDA channel opening regulated?

A

EPSPs are measure from resting potential higher than Mg2+ blockade, regardless of antagonist being present (or not)influx Ca2+ and Na+, leading to activation of enzymes and other cellular events, causing widespread changes

20
Q

which channel may be responsible for memory?

A

NMDA receptors + resultant neuroplasticity may be the molecular mechanism which leads to long term memory formation

21
Q

which conditions can result from NMDA receptor dysregulation?

A

schizophrenia, glutamate excitotoxicity

22
Q

how are schizophrenia and NMDA recpetors related?

A

NMDA receptors are inhibited by PCP and MK801
blockage of NMDA receptors produced symptoms resembling hallucinations associated with schizophrenia
certain antipsychotic drugs enhance current flow through NMDA channels

23
Q

how are NMDA receptors and glutamate excitotoxicity related?

A

excessive Ca2+ influx into cell activates calcium-dependent enzymes
degrade proteins, lipids and nucleic acids
occurs after cardiac arrest, stroke, oxygen deficiency, repeated intense seizures

24
Q

ionotropic receptors: examples

A

glutamate - excitatory GABA - inhibitory (brain)
glycine - inhibitory (spinal cord and brain stem)
nicotine - excitatory at NMJ, excitatory or modulalatory in CNS
serotonin - excitatory or modulatory
ATP - excitatory

25
Q

what are metabotropic receptors?

A

transduce signals into cell, not directly through an ion channel
activate G-protein, triggers series of intracellular events, leading to ion channel opening

26
Q

what are G-protein coupled receptors?

A

seven transmembrane domain protein

multiple receptors described for every neurotransmiter

27
Q

how do G-protein coupled receptors work?

A

transmitter binds to extracellular domain of receptor
binding triggers uncoupling of heteromeric G-protein on intracellular cell surface
signal is transduced across cell membrane

28
Q

noradrenaline second messenger system

A

NE binds to beta-adrenergic receptor, coupled with Gs
Gs activates adenylyl cyclase, which activates cAMP
cAMP activates protein kinase A
protein phosphorylation increases

29
Q

glutamate second messenger system

A

glutamate binds to metabotropic glutamate receptor, coupled with Gq
Gq activates phospholipase C
Phospholipase C converts PIP2 to diacylglycerol (activates protein kinase C) and IP3 (causes Ca2+ release)
protein phosphorylation increases and calcium-binding proteins are activated

30
Q

dopamine second messenger system

A

dopamine binds to D2 dopamine receptor coupled with Gi
Gi inhibits andenylyl cyclase
cAMP is not activated,, so cannot activate protein kinase A
protein phosphorylation decreases

31
Q

what are G proteins?

A

GTP binding proteins of 3 subunits: alpha, beta, gamma

32
Q

activity of G proteins

A

in resting state, is bound to GDP
when ligand binds to receptor, GDP is swapped for GTP, causing heteromer to split in 2
G-alpha subunit and G-beta-gamma complex divide, diffusing separately through membrane
individual entities stimulate activity of other effector proteins
alpha subunits have intrinsic GTP-GSP activity - allows signal to be transient (breakdown from GTP to GDP switched off activity)
hereromer recomplexes and awaits activation by ligand binding to another receptor

33
Q

alpha subunits of G-proteins

A

~20
Gs: stimulates adenylyl cyclase
Gi: inhibits adenylyl cyclase
Gq: stimulates phospholipase C

34
Q

beta-gamma complexes of G-proteins

A

5 beta, 12 gamma
activate K+ channels directly (G-protein gated ion channel)
= mode of action for muscarinic ACh receptors in heart and GABA receptor
relatively fast acting and local effect - ‘shortcut pathway’

35
Q

what is the shortcut pathway?

A

receptor - G-protein - ion channel
signal binds to receptor, causing ADP to be swapped for ATP on G-protein
G protein splits
beta-gamma complex directly activates ion channel - no other chemical intermediates

36
Q

what is the cAMP second messenger cascade?

A

Gs and Gi have opposite effects on adenylyl cyclase
stimulate or inhibit cAMP synthesis
affects subsequent activation of protein kinase A

37
Q

what is the PIP2 second messenger cascade?

A

Gq activates phospholipase C (PLC)
PLC converts PIP2 to IP3 and diacyglycerol (DAG)
DAG ativates protein kinase C
IP3 releases Va2+ from internal stores, activating Ca2+ dependent enzymes

38
Q

why are kinases and phosphatases important?

A

activity of many proteins depends on phosphorylation state
kinases and phosphatases regulate by variety of intracellular second messengers
e.g. phosphorylation gate channels - influences membrane potentials and excitation state

39
Q

how can G protein signals be amplified?

A

G protein signalling can amplify signals between neurons
one transmitter bound receptor can uncouple multiple G-protein heteromers
signal can be amplified at each stage
weak signals can hence cause an amplified response in the postsynaptic cell

40
Q

how can presynaptic receptor activation modulate activity?

A

change the amount of transmitter released

autoreceptors: regulate release of transmitter by modulating its: synthesis, storage, release or reuptake
e. g. phosphorylation of tyrosine hydroxylase
heteroreceptors: regulate synthesis and/or release of transmitters other than their own ligand
e. g. NE can influence release of ACh by modulating alpha-adrenergic receptors

41
Q

how can postsynaptic receptor activation modulate activity

A

change firing pattern or activity
increase/decrease rate of cell firing (directly by action at ligand gate ion channels, or indirectly at G-protein/phosphorylation coupled channels
or long term changes

42
Q

metabotropic receptors: examples

A 
metabotropic glutamate receptors - Group I (Gq), II (Gi) and III (Gi)
GABA(b) receptor 
muscarinic ACh recpetors 
dopamine receptors 
noradrenergic and adrenergic receptors 
serotonin receptors
neuropeptide receptors
43
Q

other receptors found on or in neurons

A

enzyme linked receptors eg receptor tyrosine kinases
= transmembrane proteins with intrinsic tyrosine kinase activity
activated by neurotrophin binding
autophosphorylate on activation: phosphorylate regulatory subunits signal transduction cascades

membrane permanent signalling molecules - activate intracellular receptors

202 theme 1 (13 decks)

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