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NSB > Main Chemicals in the Brain > Flashcards

Main Chemicals in the Brain Flashcards

1
Q

Drug targets that may overlap with neurotransmitter’s life cycle:

A
  • AP in pre-synaptic fibre
  • synthesis
  • storage
  • metabolism
  • release
  • reuptake
  • degradation, receptor, receptor induced increase or decrease in ionic conductance, retrograde signalling, second messengers

insert diagram

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2
Q

Neurotransmitter’s:

A
  • endogenous chemical
  • released extracellularrly by a neuron
  • used to signal to neurons, myocytes, endocrine
  • under physiological conditions
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3
Q

How are neurotransmitter’s classified?

A
  • according to chemical class:
  • amino acids: glutamate, aspartate,
    GABA
  • monoamine: dopamine, NA, A,
    serotonin
  • acetylcholine, peptides
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4
Q

Life Cycle of Neurotransmitters:

A
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5
Q

Neurotransmitter Nomenclature:

A

ach = cholinergic neurons, cholinergic receptors
noradrenaline = noradrenergic neurons, adrenoreceptors

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6
Q

CNS: Amino Acids:

A
  • CNS has high concs of certain amino
    acids
  • inhibitory neurotransmitters
    hyperoplarise membranes
  • excitatory neurotransmitters
    depolarise membranes

eg: GABA = inhibitory amino acid
Glutamate = excitatory

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7
Q

Where are neurotransmitters in the CNS located?

A

Ubiquitous distribution in the brain and produce powerful, readily reversible effects

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8
Q

Glutamate:
- class of neurotransmitter
- source?
- synthesis?
- stored?

A
  • amino acid: primary excitatory in
    CNS
  • mainly dietary amino acid so doesn’t
    need synthesis
  • can be synthesised from alpha-
    ketoglutarate or glutamine
  • sequestered in high cons in synaptic
    vesicles by VGLUTs
  • rreleased in glutamatergic synapses
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9
Q

Glutamate: Action:

A
  • 99.9% transmission is excitatory
  • act upon ionotropic (NMDA, AMPA,
    Kainate) and metabotropic receptors
    (ACPD; mGLU recepptors)
  • mainly fast transmission, hence
    mostly through ionotropic receptors
    (fastest)
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10
Q

Ionotropic receptors

A

ion channels (change in ion movement across the membrane)

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11
Q

Metabotropic receptors are

A

G protein coupled receptors

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12
Q

Which is the fastest receptor of glutamate?

A

AMPA receptors
- permeable to Na+, K+ but not Ca2+

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13
Q

NMDA receptors:

A
  • iontropic (four protein subunits)
  • permeable to Ca2+, Na+, K+
    all have Mg2+ blockade, so cell must
    be depolarised by the action of
    glutamate on AMPA receptors before
    glutamate can open NMDA as a
    safety feature
  • glutamate and glycine must bind,
    then strong depolarisation leads to
    removal of Mg2+ and rise in
    intracellular Ca2+

Long term potentiation/synaptic plasticity

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14
Q

What is excitotoxicity?

A

Neuronal damage/death causes by excessive cellular excitation

Pathophysiologic mechanism: neurodegenerative syndromes, stroke and trauma, hyperalgesia, epilepsy

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15
Q

What is wind up?

A

Too much excitation leading to too much Ca2+ influx into cell, which alters mechanisms resulting in altered morphology and cell death

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16
Q

Glutamate: Synaptic Transmission:

A
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17
Q

AMPA and NMDA are receptors unique to glutamate.

True or False?

A

False
alcohol etc (many things)

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18
Q

NMDA and AMPA receptors

A

insert diagram

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19
Q

Glutamate: Signal Termination:

A

Uptake/Re-uptake:
- Glutamate is sequestered from the
synaptic space by specific transport
molecules located on the
membrane of the pre-synaptic
neurone and neighbouring glial
cells
- glutamate taken back up into
glutametergic neurones (Gt(n)
transporters) and can be used again
after packaging into vesicles
- if re-uptake then in glial cells is
metabolised to glutamine (inactive)
before entering glutamatergic
neurons and then synthesised into
glutamate in the pre-synaptic
membrane of neuron

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20
Q

What is the difference between uptake and re-uptake?

A
  • uptake is removal of
    neurotransmitter by a different cell
    than what produced/secreted it
  • re-uptake is removal by the same cell
    that produced/secreted it
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21
Q

If only re-uptake of glutamate what is the disadvantage?

A

Re-uptake is quick and hence if there is depolarisation or continuous stimulation then there will be too much glutamate release and hence excitotoxicity is more likely

Uptake delays and hence acts as a buffer

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22
Q

Glutamate: Signal Termination:

A
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23
Q

Glutamate: Functional Associations:

A
  • excessive activation of NMDA and
    AMPA receptors lead to a significant
    influx of Cas2+
  • leads to excitotoxic cell death in
    stroke and neurodegenerative
    diseases
  • massive release and impaired re-
    uptake of glutamate in the synapse
  • excessive stimulation of glutamate
    receptors and neuronal cell death
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24
Q

Glutamate: Pharmacology:

A
  • most drugs seem to modulate
    glutamate release
  • still serious side effects
  • eg: anticonvulsants,ALS,
    Memantine***
25
Q

GABA is a primary excitatory neurotransmitter.

True or False?

A

False
primary inhibitory neurotransmitter

26
Q

Functional Association of GABA (5):

A
  • attention and arousal
  • memory formation
  • anxiety
  • sleep
  • muscle tone
27
Q

Adverse Effects of drugs that modulate GABA transmission:

A
  • drowsieness
  • lacking co-ordination
28
Q

GABA:
- sources
- synthesis

A
  • synthesised from glutamate within
    GABAergic neurones
  • GABE is sequestered in high concs
    into synaptic vesicles via the
    vesicular GABA transporter GAT
  • and is released when an action
    potential arrives at the synaptic
    bouton
29
Q

GABA: Action: Receptor types:

A
  • GABA A receptors are ionotropic:
    integral Cl- channel and are FAST!!
  • GABA B receptors are metabotropic:
    seven transmembrane domains, G -
    protein linked causing opening of K+
    channels and are SLOW
  • GABA C receptors are ionotropic,
    transmitter gated Cl- channels
  • GABA A = ionotropic, influx of Cl-
  • GABA B = metabotropic, indirectly results in K+ influx
  • GABA C = ionotropic, Cl- influx
  • mostly transmission works through
    GABA A
30
Q

GABA: Action:

A
  • predominantly at GABA A receptors
  • Cl- enters cell
  • increased Cl- conductance in a post-
    synaptic neurone
  • ECl = -70mV
  • hence chloride influx will keep the
    membrane potential at resting of
    -70mV
  • called hyperpolarisation but not
    necessarily for example some cells
    will be at -80mV and will depolarise
    to -70
  • but because so much Cl- enters,
    membrane potential sticks to -70mV
  • hence makes cells less excitable
31
Q

GABA: Signal Termination:

A

Uptake and Re-uptake:
- GABA is sequestered from the
synaptic space by specific transport
molecules located on the
membrane of the pre-synaptic
neurone and neighbouring glial
cells
- GABA is taken back up into
GABAergic neurones (GAT-1) and
can be used again after packaged
into vesicles
- GABA taken up by glial cells
(GAT1/2/3) is converted into
glutamate and then glutamine,
before entering GABAergic
neurones and being converted to
glutamate then GABA then
packaged into vesicles

32
Q

GABA Signal Termination:

A
33
Q

Monoamines: Sources and Synthesis:

A

know the enzymes as well!!
aromatic amino acid decarboxylase

34
Q

Generally, in the CNS NA or Adr?

A

NA
Adr is formed in the adrenal medulla

35
Q

Serotonin is synthesised in a different pathway to adrenaline.

True or False?

A

True

36
Q

Serotonin can produce

A

melatonin which makes you sleepy

37
Q

Dopamine: Receptors:

A
  • D1-D5 are G-protein coupled
    receptors
  • D1 and D5 belong to D1 family:
    increase cAMP through Gs
  • D3 and D4 belong to D2 family and
    decrease cAMP through Gi
  • D1 and D2 receptors are present
    post-synaptically
  • D2 are also autoreceptors which are
    used to control the release
  • D4 present in the cortex but not the striatum
38
Q

Dopamine: Functional Associations:

A
  • control of movement = nigrostriatal
    dopamine
  • emotion = mesocorticolimbic
    dopamine
  • reward pathways, addiction = same
    as above
39
Q

Parkinson’s Disease and dopamine:

A
  • dopamine augmentation (increased
    synthesis)
  • agonists of dopamine
  • inhibition of dopamine metabolism
40
Q

Dopamine and Abuse Drugs:

A
  • reward and addiction pathway
  • amphetamine increases release
  • cocaine blocks re-uptake
41
Q

Adrenoreceptors:

A
  • alpha one and two
  • beta one, two and three
  • Gs on beta receptors
  • Gq on alpha one
42
Q

What is the predominant adrenoreceptor in the forebrain?

A

Beta adrenoreceptors
a lot of presynaptic alpha 2 adrenoreceptors play an important role in modulating NA release and the rate of firing noradrenergic neurones

43
Q

Drugs that act to increase the concentration of noradrenaline in the brain (almost all antidepressants) cause

A

downregulation of beta adrenoreceptors in the forebrain

44
Q

Alpha 2 adrenoreceptor function

A

autoregulation of neurotransmitter release particularly noradrenaline

45
Q

Adrenoreceptors are ionotropic or metabotropic?

A

metabotropic receptors (GPCR)

46
Q

Phentolamine effect on adrenoreceptors

A

antagonist

47
Q

Alpha one adrenoreceptors are found

A

post-synaptically

48
Q

Noradrenaline: Functional Associations:

A
  • increased attention
  • arousal
  • facilitates the responsiveness of
    brain regions to other
    neurotransmitter systems
49
Q

Serotonin: Receptors:

A
  • 5-HT receptors: 14 different subtypes
  • apart from 5-HT3 subtype, all are G-
    protein linked
  • some 5-HT1 receptor subtypes act as
    autoreceptors but most are located
    postsynaptically, where they mediate
    the diverse effects of serotonergic
    neurotransmission
50
Q

5-HT: Functional Associations:

A
  • brain serotonergic nuclei are in the
    brainstem
  • some cells send descending fibres to
    the spinal cord to ***inhibit input
    from nociceptive pathways
    (descending control of pain)
  • other cells send fibres in the medial
    forebrain bundle to forebrain
    structures and cerebral blood vessels
  • diminishes serotonergic
    transmission may lead to depression
51
Q

Monoamines: Signal Termination:

A
  • majority re-uptake via plasma
    membrane transporters
  • Monoamine Oxidase: MAO-A/B
  • Catech-O-methyl transferase (COMT)
  • blockade of monoamine transporters and degradative enzymes such as MAO leads to increased concs of the monamines in the synapse of the neurone itself
52
Q

Monamine: Signal Termination:

A

insert slide
just the first step
most important because then neurotransmitter conc decreases in the cleft/neuron

53
Q

Cholinergic Synthesis

A
  • choline + acetyl CoA = acetylcholine
  • via choline acetyltransferase
54
Q

Cholinergic Synapse:

A
55
Q

How do we limit the action of acetylcholine?

A
  • no uptake or reuptake of ach
  • reuptake of choline
  • acetylcholinesterase (AchE)
  • butyrlylcholinesterase
56
Q

What is the rate limiting step of acetylcholine synthesis?

A

availability of choline (uptake = target)

57
Q

Where is Acetyl CoA mainly derived from?

A

Glycolysis

58
Q

Anti-Cholinergic Side Effects:

A
  • dry mouth
  • urinary retention
  • constipation
59
Q

Application of acetylcholine:

A

NSB (50 decks)

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