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Pharmacology > Introduction to pharmacology of the CNS > Flashcards

Introduction to pharmacology of the CNS Flashcards

1
Q

what type of receptors do acetylcholine, dopamine and noradrenaline used?

any exceptions?

what type of affect do they have?

A

they all use metabotropic receptors

only exception is the 5HT3 receptor which is ionotropic

they have mixed effects

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2
Q

what type of effects do the peptide neurotransmitters have?

A

opioid NT - inhibitory

NPY - excitatory

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3
Q

list some of the problems associated with drugs of the CNS

A

measurement and assessment of disorder
- not really applicable for epilepsy

multiple receptors
cellular tolerance
- most CNS conditions are chronic, so require prolonged drug use, but receptors can be dynamic

side effects:
- numerous and hinder compliance

drug delivery:
- problem with crossing the blood - brain barrier
particularly with peptide based drugs

neuronal circuitry
- e.g. inhibition leading to disinhibition
co-existence of peptides

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4
Q

how are peptides different from the normal neurotransmitters

A

they’re produced in precursor form, and processed en - route (they’ve slow axonal transport)
they’re not re-uptaken, but broken down by peptidases

in active neurones, if synthesis lags behind release - depletion occurs

peptide can be broken down by peptidases, and thereby diffuse into other cells further from cell that released them:

  • thus they have important effects at distant sites
  • volume transmission is very important

the type of peptides produced from the same gene, is very important on external factors

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5
Q

what are opioid receptors involved in? what can they cause?

A

receptors:

  • anxiety
  • pain
  • dependance

indication in:

  • chronic pain
  • addiciton
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6
Q

what are tachykinin functions? what is their possible indication?

A

function:

  • inflammation
  • anxiolysis

indication:

  • headache
  • anxiety
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7
Q

what are CCK functions? what is their possible indication

A

function

  • axiogenesis
  • satiation
  • dopamine function
  • pain

indication:

  • PD
  • eating disorders
  • physcosis
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8
Q

what are NPY function? what is their possible indication?

A

function:
obesity
mood

indication:

  • eating disorder
  • depression
  • epilepsy
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9
Q

what is the function of vasopressin? what are the possible indication?

A

function:
- learning and memory

indication:
- amnesia

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10
Q

what is the function of somatostatin? what are the possible indications?

A

function:
- analgesia

indication:
pain

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11
Q

what are the functions of Galanin? what are the possible indications?

A

function

  • sensory transmission
  • feeding

indication:

  • pain
  • eating disorder
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12
Q

most neurotransmitters are amino acid derivatives, what are the exceptions?

A

acetylcholine
cannabinoids
adenosine
NO

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13
Q

what type of vesicles are involved in

  • fast neuronal transmission
  • slow peptide transmission
  • slow synaptic transmission
A

small, synaptic vesicles

  • large dense core synaptic vesicles
  • small dense core synaptic vesicles
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14
Q

what are the GCPRs of the Gi type coupled to?

what toxin acts on this receptor

A

negatively coupled to AC

pertusis

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15
Q

what are the GCPRs of the Gs type coupled to

what toxin acts on this receptor

A

positively coupled to AC

cholera toxins

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16
Q

what are the GCPRs of the Gq type coupled to

A

positively coupled to PLCb

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17
Q

what are the roles of glutamate?

what receptors is it coupled to?

A

glutamate is coupled to post-synpatic receptors: NMDA AND AMPA

it is coupled to pre-synpatic receptors which are slow metabotropic
and kainaite receptors

involved in:

  • LTP (memory)
  • delayed hyperexciation
  • neuronal development
  • epilepsy
  • neuronal death
  • point - point transmission
  • pain wind up in the spinal cord
  • neuromodulation (through the GCPRs)
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18
Q

what are the metabotropic receptors of glutamate linked to?

A

so the metabotropic receptors can either be positively or negatively linked
Gi receptors: which are negatively coupled to AC
or Gq receptors: which are positively coupled to PLC
- the only one linked to this is mGLU R1/5 - this one is the positively linked one

19
Q

what pathologies are the NDMA receptors involved in? and how?
recall they’re also involved in development of the visual system and LTP in hippocampus

A 
pain transmission (wind up) 
- due to amplification and prolongation of impulses 
cell death 
- due to excessive calcium influx
- alzheimer's 
- PD?
- cerebral ischameia

epilepsy

20
Q

explain how the NMDA receptor work?

A

both voltage and ligand gated

ligand required:
- glutamate and glycine

voltage gated:

  • at physiological range, the gates are blocked from the inside by magnesium
  • depolarisation, removes the magnesium

means:

  • receptor not active at physiological range
  • delayed in action, because required prior depolarisation
21
Q

what two calcium channel types are involved in pre-synpatic transmission

A

N and P calcium channel types

22
Q

explain wind up pain and LTP?

what nerve fibres are involved

A

LTP: long lasting enhancement of signal transmission between two neurones, even after neuronal firing is inactivated

it occurs when:

  • high stimulation of C-nerve fibres occurs, causing a high rate of C fibre depolarisation
  • this prior depolarisation activates NMDA receptors
  • activation of NMDA receptor causes increase in the response to the same stimuli over a long period of time

this only occurs in C fibres

23
Q

what are the two types of GABA receptors? how are they different?
how can the function of GABA receptors be modulated using two different classes of drugs?

A

GABA a - fast ionotropic - uses Cl- channels
GABA b - slow ionotropic - uses potassium and calcium channels

GABA receptors:

  • allosteric modulation of GABAa receptors via benzodiazpenes, increasing the receptor affinity to GABA
  • barbiturates: those hold open the Cl- channels of the receptors
24
Q

what is glycine?

what antagonist is its sensitive to?

A

peripherial equivalent of GABA

sensitive to strychnine as an antagonist

25
Q

what type of GCPRs are A1 receptors coupled to?

A

Gq/11 which are positively linked to PLC B

26
Q

what type of GCRPs are A2 receptors coupled to?

A

Gi/o which are negatively coupled to AC

27
Q

What type of GCRPs are B1 receptors coupled to?

A

Gs receptors which are positively coupled to AC

28
Q

what type of GCRPs are dopamine receptors coupled to?

classes 1 - 5

A

1/5: G/s which is positively coupled to AC

2-4: G/i which are negatively coupled to AC

29
Q

what are the precursors for:

  • acetylcholine
  • glutamine
  • glycine
  • GABA
  • noradrenaline
  • adrenaline
  • 5HT
  • dopamine
  • histamine
A

precursors

  • choline
  • KG/ glutamate
  • L serine
  • L glutamine
  • dopamine
  • noradrenaline
  • L tryptophan
  • L tyrosine
  • L histidine
30
Q

give two examples of drugs that affect the availability of a neurotransmitter

A

LEVODOPA:

  • increases the precursor for dopamine
  • used in PD

metirosine:

  • competitive antagonist for tyrosine hydroxylase
  • prevents noradrenaline formation
  • used in phaechromocytoma
31
Q

how is the role of calcium in vesicle release different in peptide synapses and fast synapses?

A

in fast synapses:

  • the calcium channels are released close to the active site
  • form low affinity complex with vesicle and membrane

in peptide synapses:

  • calcium not involved in fusion of vesicle to membrane
  • but involved in moving vesicle to membrane
  • requires fast depolarisation
  • form high affinity complex with vesicle
32
Q

what evidence is there to support the need for calcium for vesicle release?

A

removal of calcium blocks transmission
ions permeating calcium channels, aid transmission (Ba and SR)
ions that do not permeate the channels, block transmission (Co, Mn)

specific antagonists of the N and P type calcium channels block transmission
- conotoxin and agatoxin

33
Q

how do Gi/o type GCPRs inhibit transmitter release?

A
  • inhibit vescile fusion
  • block calcium voltage gates
  • increase potassium channel permeability
34
Q

give two ways in receptor function can be modulated?

A

allosteric modulators:

  • substances binding to a distinct binding site of receptor
  • changing its shape, thereby its affinity for the NT

intracellular:

  • phosphorylation of the receptor
  • activates or inactivates the receptor
35
Q 
these are some potassium sites:
- inwards rectifying potassium channels 
- two pore potassium channels, TASK 
- GIRK, G coupled inwards rectifying potassium channels 
how can they be modulated?

can you think of the slow potassium channels?

A

Kir - if inhibited causes depolarisation
TASK - if inhibited causes depolarsation
GIRK - e.g. GABAb
they cause hyper polarisation by opening

calcium activated calcium channel 
voltage gated M channels 
they remain open a long time after depolarisation 
closed by Ach on muscuraninc receptors 
glutamate on metabotropic receptors
36
Q

list some drug types, and the uptake mechanisms they inhibit to increase NT concentration

A

tiagabine - GABA uptake blocker (epilepsy)

amitriptyline - noradrenaline and 5HT blocker (tricyclic anti-depressants)

fluoxetine: selective 5HT blocker (depression

37
Q

give drug names, that inhibit enzyme that break down NT

A

Selegiline - MAO-B inhibitor - prevents dopamine metabolism - used in PD

valoproate GABA transaminase inhibitor -epilepsy

Vigabatin GABA transaminsae inhibitor - prevents GABA metabolism - Epilepsy

moclobemide MAO-A inhibitior - prevents noradrenaline metabolism - major depression

38
Q

what type of receptors are cannabinoid receptors?

A

G coupled receptors (coupled with Gi/o)
CB1 in brain
CB2 in immune system

39
Q

what are the effects of cannabinoids in the hippocampus?

A

CB1 receptors are coupled to glutamate and GABA releasing neurones, therefore because they inhibit calcium voltage gates - they will cause inhibition to BOTH excitatory and inhibitory signals

40
Q

what are the effects of cannabis

A 
depressant 
euphoria 
impaired learning and motor preformance 
analgesic and anti-emetic 
pyscomimetic
41
Q

what are the clinical uses of cannaboid agonists?

A

glaucoma
anti-emetic in chemotherapy patients
prevent weight loss in cancer patients
neuropathtic pain

42
Q

what are the clinical uses of cannabionoid antagonists?

A

obesity and drug addiction

43
Q

how does cannabinoid neuromodulation work?

A

depolarisation induced cannabionoid production in post-synpatic cell

depolarisation activates DAG lipase, which breaks down DAG into 2DA
2DA is lipophillic and diffuses across the membrane to act on CB1 receptors
the CB1 receptors inhibit AP induced neurotransmitter release (by inhibiting calcium influx)
this causes short term suppression of excitatory and inhibitory signals

endocannibinoids and CB1 receptors are thought to play a role in long term suppression, involving long lasting decrease in neurotransmitter release

44
Q

what type of activity do NO and adenosine have?

A

NO- excitatory

Adenosine - inhibitory

Pharmacology (17 decks)

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