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neuropharmacology Flashcards

1
Q

what is a drug

A

a chemical substance of known structure, other than a nutrient or essential dietary ingredient which, when administered to a living organism, produces a biological effect.

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2
Q

what targets do drugs act on

A

receptors
enzymes
carriers
ion channel

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3
Q

what is a receptor

A

protein molecules whose function is to recognise and respond to endogenous chemical signs.

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4
Q

when is a receptor activation

A

when a ligand binds
higher affinity for activated state
conformational change

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5
Q

agonist

A

drugs which activate receptors
towards activated state

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6
Q

antagonist

A

a drug that binds to the receptor without causing activation
blocks activation reduces ability of ligand binding

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7
Q

e max

A

maximal drug response

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8
Q

EC50

A

concentration of drug that gives half maximal response

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9
Q

concentration respose graph shape

A

non linear relationship
sigmoidal curve

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10
Q

neural antagonist

A

an antagonist that doesn’t have positive or negative efficacy
blocking binds to receptor without producing an effect
efficacy = 0

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11
Q

inverse agonist

A

binds to receptor produce opposite response
as the conc increases, it decreases the amount of receptors in the activated state
directly causes a change from the active to resting state.

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12
Q

reversible antagonist

A

compete with agonist binding typically at the same site
binds reversibly

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13
Q

irreversible / covalent antagonist

A

binds irreversible to receptor
may change the conformation of the receptor to reduce ability of agonist to bind
lower curve

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14
Q

full agonist

A

sigmoidal curve
all receptors in activated state
increases as ligand binds

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15
Q

partial agonist

A

60% of receptors in activated state
lower efficacy
smaller response curve

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16
Q

affinity

A

how well a drug binds its receptor

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17
Q

efficacy

A

how well a drug once bound to a receptor elicits a response

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18
Q

potency

A

a measure of the amount of drug required to elicit a response of a given intensity

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19
Q

how does a irreversible antagonist work

A

the covalent bond produces a conformational change that the receptor is unable to become acivated again.

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20
Q

potency on the graph

A

location of curve along dose axis
more to the left = more potent

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21
Q

efficacy on graph

A

location of the curve on the resoponse axis
higher the curve = higher efficacy

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22
Q

orthosteric site

A

the primary ligand binding site of a receptor

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23
Q

allosteric site

A

a site distinct from the endogenous ligand

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24
Q

positive allosteric modulator effect on signalling

A

increase signalling
site separate to orthosteric site
increase affinity and efficacy
causes curve to shift to the left and up

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25
negative allosteric effect on signalling
decrease signalling decrease affinity and efficacy causes curve to shift to right and down
26
neurotransmitter
biochemical that mediated fat action direct communication between 2 neurons (pre and post synaptic)
27
neuromodualtor
biochemical that modulates activity of neurons and neural networks by changing the ability of neurons to repose to neurotransmitters can act at sites remote from where they are synthesised
28
glutamate
excitatory
29
aspartate
excitatory
30
GABA
inhibitory
31
glycine
excitatory or inhibitory
32
Biogenic amines
ACh Mono-amines Histamine Catecholamines Serotonin (5HT) Noradrenaline Adrenaline Dopamine
33
give examples and targets of small molecule transmitters
glutmate, serotonin, GABA, dopamine, ACh Ligand gated ion channels, GPCRs
34
give examples and targets of neuropeptides
substance P, neuropeptide Y , endorphins GPCRs
35
give examples and targets of lipid mediators
prostoglandins endocannabioids GPCRs
36
give examples and targets of nitric oxide
Guanylyl cyclase
37
give examples and targets of neutorophins, cytokines
brain derived neurotropic factor, IL-1 kinase linked receptors neuronal growth plasticity
38
give examples and targets of steroids
androgens, oestrogens nuclear and membrane receptors plasticity
39
how does nitric oxide signalling modulate neurotransmission
-Ca2+ influx into cells downstream of ion channels opening leads to activation of nNOS - increases intracellular NO levels -NO activates cGMP and MAPK signalling --> modulated function of the postsynaptic neurone - NO can diffuse retrogradely and impact NT release from the presynaptic neurones.
40
what do glial cells do with neurotransmitter
release transmitters which can modulate neuronal activity
41
what do glial cells do with neurotransmitter
release transmitters which can modulate neuronal activity
42
examples of gliotransmitters
glutamte ATP adenosine D serine Eicosanoids (prostaglandins) cytokine(TNFalpha) neuopeptides
43
inotropic receptors
ligand gated ion channels NMDA, AMPA, Kinate fast
44
metabotropic receptors
receptors that coupe through secondary messenger GPCRs and tyrosine kinase linked receptors may indirectly regulate ion channel openings
45
features of ligand gated ion channels
Heteromeric assemblies of 4/5 subunits each subunit has transmembrane spanning helices which when assembled form a central aqueous channel ligand binding - channel opening = millisecond - fast
46
mechanism of GPCR
ligand binding induced GDP to GTP exchange on G alpha subunit G alpha subunit dissociates from beta-gamma complex G alpha and beta-gamma complex activate downstream targets when bound to target GTPase activity of G alpha subunit is increased leading to hydrolysis of GTP to GDP
47
name some downstream effectors of stimulation of GPCRs
Adenyl cyclase - cAMP formation Phospholipases PLC = inositol phosphate and diacylglycerol formation PLA2 = arachidonic acid and ecodanoid formation kinase = MAPK, PI3K ion channels gene transcription = via MAPK, PKA/CREB
48
G alpha s
- stimulates adenylyl cyclase = causing increased cAMP formation
49
G alpha i/o
inhibits adenylyl cyclase = causing decreased cAMP formation
50
G alpha q
activated phospholipase C = increasing production of second messengers = Inositol triphosphate and diacylglycerol
51
what metabotropic glutamate receptors single through Gq
group 1 = mGlu1, mGLu5 slow excitatory
52
what metabotropic glutamate receptors single through Gi/o
group 2 mGul2,mGlu3 and group3 3 mGlu4, mGlu6-8 slow inhibitory
53
how do kinase linked receptors work
ligand binding leads to dimerisation of receptors receptor dimers undergo autophosphorylation at tyrosin residues pTyr sites recruit proteins with Sh2 domains leading to activation of downstream signalling
54
what downstream signalling can be activated by kinase linked receptors
STAT, RAS/Raf/MAPK
55
what type of receptor are cytokine receptors
tyrosine linked receptors cytokines = neuromodulators in CNS activate multiple down stream signalling cascades = transcription factors
56
how is cytokine signalling regulated
regulated by endogenous negative feedback mechanisms
57
examples of nuclear (hormone) receptors
glucocorticoid receptor oestrogen receptor androgen receptors
58
how do nuclear (hormone) receptors work
steroid hormone passes through plasma membrane inside target cell - steroid hormones binds to a specific receptor protein in cytoplasm or nucleus receptor/ steroid hormone complex enters the nucleus and binds to DNA gene transcription protein synthesis induced protein is produced
59
when does receptor desensitisation occur
high levels and chronic agonist exposure
60
what is receptor desensitisation
reduced signalling response to agonist binding - uncoupling of agonist binding from signalling - receptor internalisation - reduced receptor expression (increased degradation and reduced synthesis)
61
tachyphylaxis
medical term for actor sudden decrease in response to drug after administration
62
tolerance
reduced response to drug after chronic use
63
addiction
behavioural manifestation of tolerance
64
what is homologous desensitisation of GPCRs mediated by
Arrestins
65
how are GPCRs desensitised
agonist binds to receptors activated receptor receptor phosphorylated by GPCr specific kinase Beta arrestin is recruited loss of G protein coupling endocytosis and internalisation
66
how does densensitiation lead to drug tolerance
rapid desensitisation - phosphorylation - arrestin bindng - endocytosis short term tolerance long term tolerance

Neuroscience (14 decks)

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