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'B33CNS - Biology & Physiology > Neurotransmission and CNS Drug Action > Flashcards

Neurotransmission and CNS Drug Action Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

How do neurons communicate?

A

Synapses:

  • Electrical (gap junctions)
  • Chemical (classical synapse)
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2
Q

Describe the structure of an electrical synapse (gap junction). How many sub-units are there?

A
  • Cells (neurons) connected by Connexons
  • These are ‘bridges/tunnels’ permitting the movement of ions and small molecules between neurons
  • Each connexon is formed of 6 x connexins
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3
Q

What is an indication when the electrical synapse process goes wrong?

A

Indicated in epilepsy (information flow interrupted)

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4
Q

Describe the steps that occur at a chemical synapse.

A
  • Neurotransmitter synthesis in the presynaptic membrane
  • Packing of NTs into vesicles
  • Action potential arrives; permits vesicle movement to membrane
  • Fusion of vesicle w/membrane; excocytosis
  • NT is in synaptic cleft; binding of NT to receptor of postsynaptic membrane
  • NT binding initiates signalling cascade downstream = cellular response
  • Reuptake of NT via reuptake transporter on pre-synaptic membrane
  • OR, termination; NT is broken down by enzyme into metabolites
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5
Q

What handy acronym describes the processes that occur at chemical synapse?

A
  • Synthesis
  • Storage
  • Release
  • Termination
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6
Q

What is the main excitatory NT, and the corresponding ion influx?

A
  • Glu (glutamate)

- Triggers Na+ influx into postsynaptic membrane = depolarisation

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7
Q

What is the main inhibitory NT of the brain, and what drug acts to exploit this?

A
  • GABA
  • Triggers Cl- influx
  • Diazepam binds GABAA receptor, promoting binding of GABA thus inducing a state of hyperpolarisation (increased Cl- influx)
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8
Q

What are the SSRT steps of the classical NT, ACh?

A

Synthesis: Acetyl CoA + choline, via choline-acetyltransferase in the presynaptic membrane
Storage: Vesicles within the presynaptic membrane
Release: Via excocytosis
Termination: Via enzyme acetylcholinesterase in the synaptic cleft, to acetate + choline

  • Acetyl CoA + Choline form Acetylcholine
  • Release via excocytosis
  • Then terminated by acetylcholinesterase, to metabolites acetate + choline
  • Then choline (ONLY) is recycled, acetate goes away
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9
Q

What are the SSRT steps for the excitatory NT, glutamate?

A
  • Synthesis: glutamine precursor is converted to glutamate (Glu) by glutaminase enzyme
  • Storage: Glu is packed into vesicles, vesicle transporter brings vesicle to membrane
  • Release: for release, via excocytosis, interacting with Glu receptors NMDA/AMPA on the postsynaptic membrane (excitatory response downstream; Na+ influx)
  • Termination:
    > Glutamate transporter present in presynaptic membrane takes whole Glu back in to packing process
    > OR, Glu transporter in supporting glial cells takes in Glu, breaks it down to glutamine precursor via glutamine synthetase enzyme, which is then taken up by the presynaptic membrane by a Glutamine transporter
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10
Q

What enzymes are involved in the chemical synapse pathway for the amino acid transmitter, Glutamate?

A
  • Glutaminase; in the presynaptic membrane, responsible for converting Glutamine precursor to Glutamate NT
  • Glutamine synthetase; in glial cells, takes role of acetylcholinesterase in ACh, converting Glu to Glutamine precursor to be recycled.
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11
Q

What are the SSRT steps for the inhibitory NT, GABA?

A
  • Synthesis: initial step same as Glu; precursor molecule glutamine is converted to Glutamate by glutaminase
    > Glu is then converted to GABA via the GAD (glutamic acid decarboxylase) enzyme, with the aid of a pyridoxyl phosphate cofactor
  • Storage: GABA is packed into vesicles, vesicular transporter brings vesicle to membrane
  • Release: Via excocytosis, interacting with GABA receptors (A and B) of the postsynaptic membrane, resulting in Cl- ion influx.
  • Termination:
    > GABA transporter present in presynaptic membrane takes whole GABA back into Storage step (packing vesicles)
    > OR, GABA transporter in supporting glial cell takes up GABA from the cleft, converting it back to Glutamate first via GABA transaminase, then from Glutamate to glutamine via glutamine synthetase (as seen in excitatory Glu processes), where glutamine precursor is recycled back to presynaptic membrane via Glutamine transporter.
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12
Q

What enzymes are involved in the chemical synaptic pathway for the amino acid transmitter, GABA?

A
  • Glutaminase (as per excitatory Glu); in the presynaptic membrane, converting the precursor glutamine to the intermediary (excitatory) molecule, Glutamate.
  • GAD enzyme (glutamic acid decarboxylase); along with a pyridoxyl phosphate cofactor, converts Glu to GABA; extra step over Glu process.
  • GABA transaminase; in glial cells, first break down step of GABA to glutamate.
  • Glutamine synthetase; next step in breakdown of GABA (now Glu), from Glu to glutamine precursor, to be recycled.
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13
Q

What is the endocrine ladder for the catecholamines (DA, NA and A)?

A 
Catecholamines:
- Tyrosine (common precursor)
> tyrosine hydroxylase
- L-DOPA
> DOPA decarboxylase
- Dopamine (DA); acts on receptors
> dopamine β-hydroxylase
- Noradrenaline (NA); acts on receptors
> phenylethanolamine N-methyl-transferase
- Adrenaline; secreted by adrenal medulla, acts on alpha + beta receptors
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14
Q

What is the endocrine ladder for the indolamines (5-HT)?

A 
- Tryptophan (precursor)
> tryptophan hydroxylase 
- 5-hydroxytryptophan (5-HTP)
> 5-HTP decarboxylase
- 5-hydroxytryptamine (5-HT, serotonin; agonists decrease anxiety + depression)
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15
Q

What are the NTs DA, NA, A and 5-HT terminated by?

A
  • MAO (monoamine oxidase)/COMT (catechol-O-methyl transferase)
  • Reuptake
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16
Q

Why is nitrous oxide (NO) described as an ‘atypical’ NT?

A
  • Not stored in vesicles
    > L-arginine (AA) converted to NO by NO synthase
  • Not released via exocytosis
    > Diffuses freely across cell membranes
  • Not confined to presynaptic-postsynaptic direction; retrograde messenger (bi-directional flow)
    > Termination is a passive process
17
Q

What are ionotropic receptors? How fast is their transmission? Give examples.

A
  • Ligand-gated ion channels
  • Very fast; transmission in milliseconds
  • E.g. nACh (nicotinic), NMDA, AMPA (both Glu), GABAA
    > Ligand docks w/ion channel
    > Induces conformational change
    > Ion channel open, ions (Na+, K+, Cl- move through)
18
Q

What are metabotropic receptors? How fast is their transmission? Give examples.

A
  • GPCRs
  • Fairly fast; s/min
  • E.g. α and β receptors
    > NA docks w/α
    > G-protein (GDP) is linked to receptor; dissociates upon NT binding
    > GDP dislodges from α sub-unit, GTP links up in its place (phosphorylation)
    > GTP-α links up w/adenylate cyclase enzyme (2ndary messenger)
    > Leads to increased ATP, cAMP
    > Cellular response
19
Q

How do tyrosine kinase receptors work? How fast is transmission?

A
  • Mins (opposed to metabotropic/GPCRs s/min, ionotropic seconds)
    > Ligand binds to each monomer of TK; associate with each other and form dimer
    > Sum of 6 tyrosine binding sites; these are phosphorylated (ATP > ADP)
    > This results in relay proteins associating w/activated Tyr receptors, bringing about cellular response
    > Hence Tyrosine Kinase is a chemotherapy target (triggers cellular growth)
20
Q

How fast is nuclear receptor transmission? Briefly outline the process.

A
  • Hours/days; making new proteins e.g. insulin
    > Ligand (e.g. hormone) diffuses across cell membrane into cytoplasm
    > Binds to cytoplasmic receptor/or nuclear receptor in the nucleus, forming hormone-receptor complex
    > Initiates transcription, translation etc.
    > mRNA made, new proteins end result
    E.g. PPAR
21
Q

How does Parkinson’s disease affect dopamine synthesis?

A
  • Parkinson’s affects DA synthesis
  • Dopamine (DA) is greatly depleted in Parkinson’s
  • But still have DOPA decarboxylase to convert L-DOPA to DA
  • Thus levodopa (L-DOPA) is given to increase dopamine (DA)
22
Q

What is the pathophysiology behind anxiety and depression WRT 5-HT, and how is it treated?

A
  • Effect on storage/release (thus inhibit reuptake w/SSRIs), termination (thus inhibit termination)
  • Combat low 5-HT by inhibiting MAO/COMT (which terminate 5-HT)
  • 5-HT thus not broken down in the synaptic cleft/presynaptic neurone
    »> SSRIs
23
Q

Where do drugs of abuse e.g. amphetamine and MDMA act? What are the dangers of amphetamine?

A
  • Effect on release
  • Amphetamine causes non-exocytotic release of NA and DA = stimulant
    »> Too much NA in cleft = could bind to α-receptors = vasoconstriction, increased BP
  • MDMA (ecstasy); increases release (excocytosis) of 5-HT, DA and NA
24
Q

How is Alzheimer’s disease combatted? What is an example treatment?

A
  • Effects on termination
  • Low ACh affects cognitive function
  • Therefore target acetylcholinesterase enzyme
    »> Aricept inhibits ACherase (cognitive enhancer)
    > Modest effects in increasing cognitive fucntion
25
Q

What receptor is a drug target for migraines, and what drug class combats them?

A
  • 5-HT (agonist)

- Triptans

26
Q

What receptor is a target for schizophrenia therapy, and by what drug class?

A
  • D2 (antagonists)

- Antipsychotics

27
Q

What receptor is a target for pain, and by what drug class?

A
  • μ-opioid (agonist)

- Opioids

28
Q

What receptor is a target for anxiety, and by what class?

A
  • GABAA (modulator)

- Benzodiazepines

29
Q

What receptor is a target for anesthesia, and by what class?

A
  • NMDA (antagonist)

- Ketamine, PCP

'B33CNS - Biology & Physiology (3 decks)

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