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intro to neuro 1006 > neurotransmitter receptor signalling > Flashcards

neurotransmitter receptor signalling Flashcards

1
Q

what is the key excitatory fast transmitter in the CNS

A

glutamate

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2
Q

what are ionotropic GluRs (iGluRs) and examples

A

are ligand-gated ion channels that produce excitatory glutamate-evoked currents. e.g. AMPA, Kainate, NMDA receptors

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3
Q

what are mGluRs and examples

A

are GPCRs that control cellular processes via G protein signaling cascades. e.g. grp I, grp II, grp III

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4
Q

what are the key inhibitory fast transmitters in the CNS

A

γ-Aminobutyric acid (GABA) and glycine

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5
Q

what are examples of slow transmitters that work by ‘volume transmission’

A

DA, NA 5HT, ACh, neuropeptides, histamines etc

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6
Q

what are the names for the ionotropic gaba receptor and the metabotropic gaba receptor

A

ionotropic - iGABARS (GABAA & GABAC)
metabotropic - GABAB

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7
Q

what neurotransmitter accounts for 90% synaptic connections in human brain

A

glutamate

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8
Q

what is the Q/R site on the AMPA receptor do

A

determines calcium ion permeability of GluA2

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9
Q

why is AMPA a tetramer

A

because it has four GluA1-4 subunits in any combination

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10
Q

what does AMPA receptor bind to?

A

glutamate

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11
Q

what is an example of an selective AMPA receptor antagonist that would completely block an EPSP

A

telampanel

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12
Q

what property do AMPA receptors containing GluA2 subunit have

A

have very low Ca2+ permeability due to mRNA editing

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13
Q

what does the activation of all AMPA receptors lead to

A

an influx of Na+ and are only permeable to Ca2+ too if there is absence of any GluA2(R) subunits

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14
Q

what are the four different AMPA receptor subunits in mammals

A

GluA1, GluA2,GluA3. GluA4

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15
Q

what does Q/R site determine in Kainate Receptor subunit topology

A

determines Ca2+ permeability of GluK1 & K2

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16
Q

what neurotransmitter binds to kainate receptor

A

glutamate

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17
Q

what is the structure of NMDA receptor

A
  • cation channel for Na+ and Ca2+. channel opening -> depolarisation
  • activation requries glutamate + co agonist
  • has voltage sensitive Mg2+ block which is present at physiologic conc. of Mg2+ but disapears when cell is depolarised
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18
Q

what must occur for Mg2+ block of NMDAR to occur

A

channel must be open i.e. glycine and glutamate must be bound t their binding sites on the NMDA receptor

19
Q

how does the NMDA receptor act as a coincidence detector

A

AMPARs are often present at same synapse as NMDARs. activarion of AMPARs depolarises membrane sufficiently to remove Mg2+ block of NMDARs. thus Ca2+ entry through NMDARs dependent on pre&post synaptic elements being active at same time

20
Q

what is long term potentiation (LTP)

A

long lasting potentiation of synaptic transmission

21
Q

what is long term depression (LTD)

A

long lasting of synaptic transmission depression

22
Q

what does Ca2+ do inside postsynaptic cells

A

can activate enzymes, regulate ion channel and affect gene expression

23
Q

how is NDMARs involved w/ synaptic plasticity

A

long term potentiation and long term depression

24
Q

what is structure of mGlu receptor

A
  • bi lobed N terminal extracellular domain contains glutamate binding site
  • cysteine rich domain involved in maintaining tertiary structure
  • 7 transmembrane domains (7-TMD) in common w/ other GPCR families
  • 2nd intracellular loop involved in G protein coupling & in determining transduction mechanism
25
Q

properties of metabotropic glutamate receptors

A
  • depending on subtype can be pre&posynaptically localised
  • generally play modulatory role in synaptic transmission
  • involved in modulation of signalling through K+ and Ca2+ - control excitability of neurones
26
Q

what does postsynaptic group 1 mGlu receptors do

A

mediate slow depolarisation (EPSP)

27
Q

what does presynaptic group 2 and 3 mGlu receptors do

A

decrease neurotransmitter release

28
Q

what is the structure of GABAA receptor structure

A
  • anion channel (Cl- entry). channel opening -> hyperpolarisation
  • made up of 5 subunits
  • different isomers have diff. sensitivity to alcohol
  • found synaptically and extrasynaptically
  • sedative/ hypnotic drugs enhance GABAA receptor activity via the modulatory site
29
Q

what type of modulators are GABA

A

positive allosteric modulators

30
Q

how does GABA produce inhibition

A

acts both as a fast ‘point to point’ transmitter & as an ‘action at a distance’ neuromodulator

31
Q

what is the structure of GABAB receptors

A

dimer made up of two 7td subunits held together by coil/s interaction between their C-terminal tails
- activation occurs when GABA binds to extracellular domain of B1 subunit
- located pre & postsynaptically
- GPCR that coyple through Gi/Go

32
Q

what does acute alcohol (ethanol) modulate

A

glutamergic neurotransmission

33
Q

what does alcohol reducing glutmate release from presynaptic terminal do

A

increases activity of mGluR2/3 (group 2 metabotropic glutamate receptor

34
Q

what does acute ethanol inhibit

A

reversibly inhibits NMDA induced inward currents in cultured neurons (voltage clamp)

35
Q

how does chronic alcohol intake leads to compensatory adaptations in glutamergic neurotransmission

A
  • increased NMDA & AMPA receptors on post synaptic membrane
  • increased ion channels conductance
  • reduced glial reuptake of glutamate from synaptic cleft
  • desensitisation/downregulation of presynaptic mGlu receptors leading increased glutamate release
36
Q

what are the behavioural effects of acute alcohol mediated by changes in glutamergic signalling

A

amnesia/memory loss (intact NMDA signalling is required for memory formation, long term potentiation)

37
Q

behavioural effects of chronic/withdrawal alcohol mediated by changes in glutamatergic signalling

A
  • seizures/brain damage/ excitotoxcity (withdrawal)
  • anxiety, disorientation (hyper-excitability associated w/ withdrawal)
38
Q

what are neurosteroids and how does acute alcohol affect it

A

they are positive allosteric modulators of GABAA receptors and acute alcohol may also increase neurosteroid release in brain

39
Q

how does chronic exposure to alcohol affect GABAergic transmission

A

change in GABAA receptor subunit composition - reduced sensitivity of GABAA receptor to alcohol and/or neurosteroids & chang3w in localisation (synaptic vs extra synaptic)

40
Q

what are opiods

A

chemicals that act on opiod receptors can be endogenous (made by body) or exogenous

41
Q

what are opiates

A

naturally occuring biochemicals that modulate opiod receptors e.g. morphine, heroin

42
Q

how does acute alcohol (ethanol) affect opiod synthesis and release

A

increases endogenous opiod synthesis and release

43
Q

how do glial cells modulate synaptic transmission

A

they release gliotransmitters and impact excitatory transmission - release glutamate & D-serine - also release neuromodulators like ATP and adenosine

44
Q

how do ethanol impact glial cell function

A
  • ethanol increases excitatory amino acid transporter (GLAST & GLT-1) expression on astrocytes
  • inhibiting GLAST or GLT-1 activity reduces rewarding/reinforcing properties of alcohol

intro to neuro 1006 (10 decks)

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