Week 2- Part 5- Mechanisms of drug action (after NT release). Flashcards
What do they target?
Processes that normally happen after NTs are released into the synapse.
Effects on receptors:
What is the most important and most complex site of action for psychoactive drugs?
What can some drugs do?
What are the two additional categories?
On both the presynaptic and postsynaptic receptors.
Bind to receptors and act as either agonists or antagonists.
Inverse agonists and neuromodulators.
What is a direct agonist?
What does it increase?
Drug which slots into the same receptor as the NT would- has the same effect- mimicking the NT.
Activity within that NT system.
What is a direct antagonist?
What is this useful in?
Drug goes into the receptor used by the NT- blocks or reverses the effects of the NT- e.g. pushing it out.
Treating overdoses- reverses the effects of drugs.
What is an inverse agonist?
What is a neuromodulator?
Drug combines to receptor site as the NT would- has the opposite effect to NT.
Have a drug which does not bind directly to where the NT would bind but somewhere else on the receptor complex- modifies the effect of NT- makes the NT effects stronger or weaker- can increase or inhibit effects of a neurotransmitter.
What is the sixth one?
What can a drug do?
Give an example of what some drugs do.
What happens at neuromuscular junctions?
Drugs stimulating postsynaptic receptors.
Bind to postsynaptic receptors + mimic the effects of the NT- i.e., act as an agonist.
Mimic effects of acetylcholine (major NT in the ANS + neuromuscular junctions + CNS).
Nerves connect to your skeletal muscles and activate them.
Continuation from the sixth one:
What is there?
What is the first?
What would they be considered?
What happens with it?
Two major types of acetylcholine receptor.
Nicotinic ACh receptors.
Ionotropic.
Ion channel gets opened when acetylcholine binds- normally a sodium channel- sodium ions rush in- are excitatory- due to influx of positively charged sodium ion- cause an excitatory postsynaptic potential.
Continuation from the sixth one- Nicotinic ACh receptors:
What binds together?
How do they respond?
Nicotine in cigarettes- binds to- nicotinic acetylcholine receptors- mimics acetylcholine- opens the channels.
Fast.
Continuation from the sixth one:
What is the second type?
What would they be considered?
What are they varied in?
What is a crucial thing to remember?
Where does muscarinic come from?
Muscarinic ACh receptor.
Metabotropic.
What they do.
It is not directly associated with an ion channel- are associated with metabotropic second messenger system- open other ion channels and trigger all sorts of cellular effects.
Mushrooms- binds to muscarinic acetylcholine receptors- mimic the effects of acetylcholine there.
What kind of muscle is the nicotinic in?
What kind of muscle is the muscarinic in?
What is there for the previous?
Are they fast or slow?
Skeletal muscle (neuromuscular joints), ganglia and CNS.
CNS + smooth muscle of the ANS (controls things like blood vessel dilation, cardiac muscle etc).
Different types- some can be excitatory + some inhibitory.
Slower.
Neuromodulator:
What is GABA?
What would it be considered?
Give examples.
What does the previous do?
Major inhibitory NT in the CNS.
Ionotropic receptor- normally opens chloride ion channels- leads to hyperpolarization- makes neurons less likely to fire.
Sedatives + anxiolytics such as benzodiazepines.
Bind to a different part of the complex- facilitate action of GABA- do not mimic it- make it more potent.
What is seventh?
What might a drug bind to?
Give two examples.
Drugs can act as antagonists and block postsynaptic receptors.
Postsynaptic receptors and block effects of NTs- i.e., act as an antagonist.
Atropine + Curare.
Continuation from the seventh:
What is atropine?
What does it do?
Where are many of the metabotropic receptors?
What does a high dose do?
ACh antagonist.
Binds and blocks muscarinic receptors- blocks its effects.
In the brain.
Disrupt memory.
Continuation from the seventh:
What is curare?
What does it do?
What does it cause?
ACh antagonist- it is naturally occurring + derived from plants.
Bind and block nicotinic receptors, the ionotropic receptors at the neuromuscular junction.
Paralysis.
What is eigth?
Explain it.
Drugs bind to autoreceptor- may mimic effects of NTs at its presynaptic autoreceptors.
Presynaptic cell releases synapses- diffuse across synapse- acts as a postsynaptic receptors on its membrane- some NTs act as autoreceptors that exist on the presynaptic cell- form negative feedback mechanism.
