Week 4 - topic 2 Flashcards
Drugs that affect synaptic transmissions are categorised as
Antagonists: A drug that opposes or inhibits the effects of a particular neurotransmitter on the postsynaptic cell.
Agonists: A drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell.
Drugs can influence synaptic transmission by
- Serving as a precursor
- Inhibiting the synthesis of a neurotransmitter
Drugs serve as precursor
- Neurotransmitters are synthesized from precursors
- Drugs can act as precursors
- Agonist effect > L-DOPA can be administered as a drug to help synthesize the neurotransmitter dopamine
Drug inhibits NT synthesis
- Neurotransmitter synthesis from precursors is controlled by enzymes
- Antagonist effect > drug inactivating an enzyme
It will prevent the neurotransmitter from being produced.
Effects on storage and release of neurotransmitters
- look up image
3. Drugs can prevent the storage of neurotransmitter in vesicles
4. Drugs can stimulate the release of neurotransmitter into the synapse
5. Drugs can prevent the release of neurotransmitter into the synapse
Antagonist action (step 3)
- Neurotransmitters are stored in synaptic vesicles
- Vesicle transporter molecules are located in the membrane of synaptic vesicles which pump neurotransmitter molecules across the vesicle membrane, filling the vesicles
- Vesicle transporter molecules can be blocked by drugs
Agonist action (step 4)
- Drugs can facilitate the release of neurotransmitters from the terminal button.
- Bind with proteins that cause synaptic vesicles to fuse with the presynaptic membrane and release neurotransmitter into the cleft
Antagonist action (step 5)
- Drugs can prevent the release of neurotransmitters from the terminal button
- Deactivate the proteins that cause synaptic vesicles to fuse with the presynaptic membrane and release neurotransmitter into the cleft
Drug effects on receptors
6) Drugs can stimulate postsynaptic receptors
7) Drugs can block postsynaptic receptors
8) Drugs can stimulate autoreceptors and inhibit neurotransmitter synthesis/release
9) Drugs can block autoreceptors and stimulate neurotransmitter synthesis/release
Competitive binding
Drugs act directly on the neurotransmitter binding site on opening of the ion channel.
1) Direct agonist - Binds with a receptor site that a neurotransmitter would normally bind with- causes postsynaptic potentials (PSPs - Step 6)
2) Receptor blocker (direct antagonist) - Binds with a receptor site that a neurotransmitter would normally bind with - does not cause PSPs (Step 7)
Noncompetitive binding
Drugs act on an alternative binding site and modify the effects of the neurotransmitter on opening of the ion channel.
3) Indirect agonist - Binds with a site on a receptor that a neurotransmitter does not bind with, but facilitates the action of the receptor (Step 6)
4) Indirect antagonist - Binds with a site on a receptor that a neurotransmitter does not bind with, but interferes with the action of the receptor (Step 7)
Autoreceptor stimulation - and drug effects
Stimulation of autoreceptors normally cause less neurotransmitter to be released
5) Antagonist drugs stimulate autoreceptors and inhibit the synthesis/release of neurotransmitter (Step 8)
6) Agonist drugs block autoreceptors and increases synthesis/release of neurotransmitters (Step 9)
Drug effects on Reuptake and destruction of neurotransmitters
10) Drugs can block reuptake of neurotransmitter from the synaptic cleft
11) Drugs can inactive enzymes involved in enzymatic deactivation of a neurotransmitter
Reuptake
Molecules of neurotransmitter are taken back into terminal button
Enzymatic deactivation
Destruction of a neurotransmitter in synaptic cleft by an enzyme