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Neuroscience > neuropharmacology > Flashcards

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
Q

negative allosteric effect on signalling

A

decrease signalling
decrease affinity and efficacy
causes curve to shift to right and down

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26
Q

neurotransmitter

A

biochemical that mediated fat action direct communication between 2 neurons (pre and post synaptic)

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27
Q

neuromodualtor

A

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
Q

glutamate

A

excitatory

29
Q

aspartate

A

excitatory

30
Q

GABA

A

inhibitory

31
Q

glycine

A

excitatory or inhibitory

32
Q

Biogenic amines

A

ACh
Mono-amines
Histamine

Catecholamines
Serotonin (5HT)

Noradrenaline
Adrenaline
Dopamine

33
Q

give examples and targets of small molecule transmitters

A

glutmate, serotonin, GABA, dopamine, ACh

Ligand gated ion channels, GPCRs

34
Q

give examples and targets of neuropeptides

A

substance P, neuropeptide Y , endorphins
GPCRs

35
Q

give examples and targets of lipid mediators

A

prostoglandins
endocannabioids

GPCRs

36
Q

give examples and targets of nitric oxide

A

Guanylyl cyclase

37
Q

give examples and targets of neutorophins, cytokines

A

brain derived neurotropic factor, IL-1
kinase linked receptors
neuronal growth plasticity

38
Q

give examples and targets of steroids

A

androgens, oestrogens
nuclear and membrane receptors
plasticity

39
Q

how does nitric oxide signalling modulate neurotransmission

A

-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
Q

what do glial cells do with neurotransmitter

A

release transmitters which can modulate neuronal activity

41
Q

what do glial cells do with neurotransmitter

A

release transmitters which can modulate neuronal activity

42
Q

examples of gliotransmitters

A

glutamte
ATP
adenosine
D serine
Eicosanoids (prostaglandins)
cytokine(TNFalpha)
neuopeptides

43
Q

inotropic receptors

A

ligand gated ion channels
NMDA, AMPA, Kinate
fast

44
Q

metabotropic receptors

A

receptors that coupe through secondary messenger
GPCRs and tyrosine kinase linked receptors
may indirectly regulate ion channel openings

45
Q

features of ligand gated ion channels

A

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
Q

mechanism of GPCR

A

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
Q

name some downstream effectors of stimulation of GPCRs

A

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
Q

G alpha s

A
  • stimulates adenylyl cyclase = causing increased cAMP formation
49
Q

G alpha i/o

A

inhibits adenylyl cyclase = causing decreased cAMP formation

50
Q

G alpha q

A

activated phospholipase C = increasing production of second messengers = Inositol triphosphate and diacylglycerol

51
Q

what metabotropic glutamate receptors single through Gq

A

group 1 = mGlu1, mGLu5
slow excitatory

52
Q

what metabotropic glutamate receptors single through Gi/o

A

group 2 mGul2,mGlu3
and
group3 3 mGlu4, mGlu6-8
slow inhibitory

53
Q

how do kinase linked receptors work

A

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
Q

what downstream signalling can be activated by kinase linked receptors

A

STAT, RAS/Raf/MAPK

55
Q

what type of receptor are cytokine receptors

A

tyrosine linked receptors
cytokines = neuromodulators in CNS
activate multiple down stream signalling cascades = transcription factors

56
Q

how is cytokine signalling regulated

A

regulated by endogenous negative feedback mechanisms

57
Q

examples of nuclear (hormone) receptors

A

glucocorticoid receptor
oestrogen receptor
androgen receptors

58
Q

how do nuclear (hormone) receptors work

A

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
Q

when does receptor desensitisation occur

A

high levels and chronic agonist exposure

60
Q

what is receptor desensitisation

A

reduced signalling response to agonist binding
- uncoupling of agonist binding from signalling
- receptor internalisation
- reduced receptor expression (increased degradation and reduced synthesis)

61
Q

tachyphylaxis

A

medical term for actor sudden decrease in response to drug after administration

62
Q

tolerance

A

reduced response to drug after chronic use

63
Q

addiction

A

behavioural manifestation of tolerance

64
Q

what is homologous desensitisation of GPCRs mediated by

A

Arrestins

65
Q

how are GPCRs desensitised

A

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
Q

how does densensitiation lead to drug tolerance

A

rapid desensitisation
- phosphorylation
- arrestin bindng
- endocytosis
short term tolerance
long term tolerance

Neuroscience (14 decks)

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