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Current - BFoMH [Private] > Neurotransmitters, receptors and pathways > Flashcards

Neurotransmitters, receptors and pathways Flashcards

1
Q

What does this 2S-3R-2D (SSRRRDD) system stand for?

A
  • Synthesis
  • Storage
  • Release
  • Receptors
  • Reuptake
  • Degradation
  • Drugs and Disease
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2
Q

What are the 3 components of a synapse?

A
  • Presynaptic terminal: synthesis, storage, re-uptake, degradation
  • Synaptic cleft: Release of NT
  • Postsynaptic region: ionotropic/metabotropic receptors
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3
Q

What are the characteristics of Glutamate?

A
  • Amino acid
  • Widely distributed in CNS (Occurs in 70% of all synapses)
  • Very little presence in the PNS
  • Ubiquitous excitatory NT in the CNS
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4
Q

How is Glutamate synthesised?

A

Glutamate (SSRRRDD: Synthesis)

  • In glial cells: α-Oxoglutarate is converted into Glu by GABA Transaminase
  • In neurons: Glutamine is converted into Glu by Glutaminase
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5
Q

How is Glutamate stored in the presynaptic terminal?

A

Glutamate (SSRRRDD: Storage)

Glu is transported by 3 vesicular glutamate transporters (vGluT) into vesicles - vGluT1, vGluT2, vGluT3
vGluT brings Glu into the vesicle
- for Glu to get in: H+ ions are pumped out -> ensuring high concentration of Glu in the vesicle
- H+ is brought in the vesicle by a proton pump which converts ATP-ADP energy into high concentration of H+ which can be exchanged for Glu NT

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6
Q

How are the Glutamate NTs released in the synaptic cleft?

A

Glutamate (SSRRRDD: Release)

> Glu NTs are released by the nerve terminal at the axon terminal bouton
> Ca2+ dependent process: provokes exocytosis of vesicle content

  • Ca2+ required to move and fuse vesicles with the membrane to allow NTs into synaptic cleft
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7
Q

What are the Glutamate receptors?

A

Glutamate (SSRRRDD: Receptors)

> Ionotropic receptors iGluR: ion channels activated by Glu

  • NMDA: allow in Na+ / Ca2+ (significantly)
  • AMPA/kainate: allow in Na+
  • these let out a bit of K+

> Metabotropic receptors mGluR: G-protein coupled receptors, class C

  • Group 1: mGluR1 and mGluR5
  • Group 2: mGluR2 and mGluR3
  • Group 3: mGluR4 and mGluR6-8
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8
Q

What is the process of Glutamate reuptake?

A

Glutamate (SSRRRDD: Reuptake)

Excitatory Amino Acid Transporter (EAAT) regulate this recycling process into the presynaptic neuron or glial cell (e.g. astrocyte)

> EAAT takes Glu back into presynaptic terminal, where its recycled into vesicles and reused
or
> EAAT takes Glu into the astrocyte, where its converted into glutamine by glutamine synthase
- Glu can be transported out of the astrocyte by a glutamine transporter (GlnT) back into the presynaptic terminal
- once into the presynaptic terminal: glutamine is again synthesised into Glu by glutaminase

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9
Q

What is the degradation process of Glutamate?

A

Glutamate (SSRRRDD: Degradation)

Glu is quickly removed from synaptic cleft by EAAT (Excitatory Amino Acid Transporter) into presynaptic neurons for recycling, or into astrocytes
> In astrocytes Glu is converted to glutamine by glutamine synthase
> Glutamine is transferred to the presynaptic neuron where it is converted back to Glu by glutaminase to be reused

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10
Q

What are the drugs related to Glutamate?

A

Glutamate (SSRRRDD: Drugs & Diseases)

> For NMDARs (transferring Na+ and Ca2+)

  • Ketamine: dissociative anaesthetic and channel blocker
  • Memantine: competitive antagonist

> For AMPAR/kainateR (transferring Na2+)
- Perampanel: competitive antagonist

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11
Q

What are the diseases related to Glutamate?

A

Glutamate (SSRRRDD: Drugs & Diseases)

  • Recreational use of drugs (PCP, ketamine etc)
  • Epilepsy is associated with the glutamatergic system (controls brain excitability)
  • Glu is critical to all CNS functions
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12
Q

What are the characteristics of GABA?

A
  • Amino acid
  • Widely distributed in the CNS (30% of all synapses)
  • Very little in the PNS
  • Ubiquitous inhibitory NT in the CNS
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13
Q

How is GABA synthesised?

A

GABA (SSRRRDD: Synthesis)

  • Glutamate -> Glutamic Acid Decarboxylase (GAD) -> GABA
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14
Q

How is GABA stored in the presynatpic terminal?

A

GABA (SSRRRDD: Storage)

  • Vesicular storage by vesicular GABA transporter (vGABAT)
  • vGABAT brings GABA in the vesicle
  • H+ ions are pumped out for GABA to get in
  • H+ is brought in the vesicle by a proton pump which converts ATP-ADP energy into high concentration of H+ which can be exchanged for GABA NT
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15
Q

How is GABA released in the synaptic cleft?

A

GABA (SSRRRDD: Release)

Ca2+ dependent vesicular release (like Glu) and mainly occurs at the axon terminal bouton

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16
Q

What are the GABA receptors?

A

GABA (SSRRRDD: Receptors)

  • Ionotropic receptors
  • GABA-A: allows in Cl-
  • Metabotropic receptors
  • GABA-B coupled to G-proteins Gi and Go
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17
Q

What is the process of GABA reuptake?

A

GABA (SSRRRDD: Reuptake)

  • GAT1 - neuronal GABA transporter - takes GABA NT back into presynaptic neuron
  • GAT3 - glial GABA transporter - takes GABA NT back into glial cells, particularly astrocytes
18
Q

What is the GABA degradation process?

A

GABA (SSRRRDD: Degragation)

By an enzyme: GABA transaminase

  • occurs mostly in glial cells (e.g. astrocytes)
  • ⍺-Oxoglutarate converted to Glutamate; GABA converted into succinct semialdehyde
19
Q

What are the drugs related to GABA-A receptors?

A

GABA (SSRRRDD: Drugs & Diseases)

GABA-A (Ionotropic receptors)

  • Clinically useful:
  • benzodiazepines
  • ethanol
  • anaesthetics
  • barbiturates: sedative
  • Not used clinically:
  • Muscimol: agonist activating the receptor
  • Bicuculine: competitive antagonist
  • Picrotoxin - GABA-A receptor channel blocker
20
Q

What are the drugs related to GABA-B receptors?

A

GABA (SSRRRDD: Drugs & Diseases)

GABA-D (Metabotropic receptors)

  • Baclofen: agonist
  • Saclofen: competitive antagonist
  • Tiagabine: interferes with re-uptake by blocking GAT (GABA transporter)
  • Vigabatrine: blocks GABA transaminase (degradation)
21
Q

What are the diseases related to GABA?

A

GABA (SSRRRDD: Drugs & Diseases)

  • Epilepsy
  • Anxiety
  • Insomnia
    are all associated with GABA

GABA’s major function in the CNS associated with the brain inhibitory actions

22
Q

What are the characteristics of dopamine?

A
  • Monoamine, located in a specific areas of the CNS
  • 4 pathways
  • Mesolimbic (associated with Schizophrenia): VTA (ventral tegmental area) to midbrain
  • Mesocortical: VTA to PFC
  • Nigrostriatal pathway (associated with Parkinson’s): substantia nigra to midbrain
  • Tuberoinfundibular: hypothalamus to brain stem
23
Q

How is dopamine synthesised?

A

Dopamine (SSRRRDD: Synthesis)

  • Tyrosine (diet) is converted into DOPA by Tyrosine hydrixylase
  • DOPA is converted into Dopamine by Dopa decarboxylase
24
Q

How is dopamine stored in the presynaptic terminal?

A

Dopamine (SSRRRDD: Storage)

  • Vesicular storage by vesicular monoamine transporter (VMAT)
  • VMAT1 or VTMAT2 (cell type specific) brings dopamine into vesicle
  • H+ ions are pumped out for DA to get in
  • H+ is brought in the vesicle by a proton pump which converts ATP-ADP energy into high concentration of H+ which can be exchanged for DA NT
25
Q

Why are vesicles acidic?

A

Because they have proton pumps.

26
Q

What is the process of dopamine release?

A

Dopamine (SSRRRDD: Release)

  1. Ca2+ dependent vesicular release mainly occurs at the axon terminal bouton
    OR
  2. ‘en passant’ manner:
    - small release sites located along the axon
    - dopamine can be released at all these points
27
Q

What are the dopamine receptors?

A

Dopamine (SSRRRDD: Receptors)

Only Metabotropic receptors

  • all G-protein coupled, class A
  • D1 and D5 coupled to Gs
  • D2, D3 and D4 coupled to Go/Gi

No ligand-gated ion channels (no ionotropic receptors)

28
Q

What is the dopamine reuptake process?

A

Dopamine (SSRRRDD: Reuptake)

  • DA transported back into presynaptic neuron by dopamine active transporter (DAT)
    AND co-transported by Cl- and 2Na+ (1 chloride ion and 2 sodium ions)
29
Q

What is the dopamine degradation process?

A

Dopamine (SSRRRDD: Degradation)

  • Several biochemical pathways that lead to the breakdown of DA
  • Monamine oxydase (MAO) and COMT (catechol-O-methytransferase) convert dopamine into Homovanillic acid
30
Q

What are the drugs related to dopamine?

A

Dopamine (SSRRRDD: Drugs & Diseases)

  • DA synthesis: Levodopa: precursor of DA -> increase of DA ; for Parkinson’s disease
  • DA storage: Reserpine and Methamphetamine block VMAT
  • DA release: Amantadine
  • DA receptors:
  • full agonist: DA itself, apomorphine, bromocriptine
  • competitive antagonists: haloperidol, chlorpromazine
  • DA reuptake: cocaine, bupropion, methylphenidate (Ritalin)
  • DA degradation:
  • MAO inhibitors: phenelzineu, selegine (MAO-B)
  • COMT inhibitors: entacapone, tolcapone
  • both adjacents with L-Dopa
  • can be used for Parkinson’s
31
Q

What are the diseases related to dopamine? c

A

Dopamine (SSRRRDD: Drugs & Diseases)

  • Parkinson’s, Schizophrenia, Hormonal disturbances, Drug dependance
  • Dopamine is involved in motor control and pituitary control, and may be involved in reward system and thoughts
32
Q

What are the characteristics of 5-HT?

A
  • 5-HT is also called serotonin
  • Monoamine
  • Present in enteric nervous system (gastrointestinal control - part of the PNS) at 80%
  • 5-HT platelet system
33
Q

What are platelets?

A

Smallest blood cells involved in regulation of hemostasis and thrombosis.

34
Q

How is 5-HT synthesised?

A

5-HT (SSRRRDD: Synthesis)

  • Tryptophan (diet) is converted into 5-hydroxytryptophan by Tryptophan hydroxylase
  • 5-hydroxytryptophan is converted into 5-hydroxytryptamine (5-HT) by Dopa decarboxylase
35
Q

How is 5-HT stored in the presynaptic terminal?

A

5-HT (SSRRRDD: Storage)

  • Vesicular storage by vesicular monoamine transporter (VMAT)
  • VMAT1 or VTMAT2 (cell type specific) brings 5-HT into vesicle while ejecting H+ ions
  • H+ is brought in the vesicle by a proton pump which converts ATP-ADP energy into high concentration of H+ which can be exchanged for 5-HT NT
36
Q

What is the 5-HT release process?

A

5-HT (SSRRRDD: Release)

  • Ca2+ dependent release mainly occurs at the axon terminal bouton
  • 5-HT is co-released with neuropeptides, e.g. somatostatin or substance P
37
Q

What are the 5-HT receptors?

A

5-HT (SSRRRDD: Receptors)

  • Ionotropic receptor: 5-HT_3
  • the only 5-HT ligand-gated ion channel
  • mixed cation channel: allows Na+ and Ca2+ into cell and K+ out
  • Metabotropic receptors: G-protein coupled
  • presynaptic: 5-HT1A, 1B, 1D, 1E, 1F
  • postsynaptic: 5-HT2A, 2C
38
Q

What is the 5-HT reuptake process?

A

5-HT (SSRRRDD: Reuptake)

Transported back into presynaptic terminal by serotonin transporter (SERT)
- co-transported by Cl- and 2Na+

39
Q

What is the 5-HT degradation process?

A

5-HT (SSRRRDD: Degradation)

  • 5-HT(hydroxytryptamine) is broken down by MAO into 5-hydroxyindolealdehyde
  • 5-hydroxyindoleadehyde is broken down by Aldehyde hydrogenase into 5-HIAA (hydroxyindoleacetic acid)
  • common metabolite that monitors 5-HT
40
Q

What are the drugs related to 5-HT?

A

5-HT (SSRRRDD: Drug & Diseases)

  • 5-HT synthesis: p-chloropenylalanine (TH inhibitor), L-trytophan (precursor): used in depression
  • 5-HT storage: tetrabenazine
  • 5-HT release: MDMA
  • 5-HT receptors:
  • full agonist: 5-HT itself, sumatriptan (5-HT1D) used for migraines
  • partial agonist: buspirone (5-HT1A)
  • competitive antagonists: ondansetron (5-HT3), ketanserin (5-HT2A)
  • 5-HT reuptake:
  • SSRIs: e.g. citalopram
  • TCAs: e.g. imipramine
  • amphetamine (MDMA)
  • 5-HT degradation:
  • MAOI (phenelzine)
41
Q

What are the disease related to 5-HT?

A

> Depression
> Anxiety
> Hallucinations

> 5-HT helps regulates mood, sleep/wake cycle and appetite

Current - BFoMH [Private] (15 decks)

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