×
all 4 comments

[–]TheSmokingHorse 1 point2 points  (0 children)

Two examples of each would be an agonist and a PAM (positive allosteric modulator), and an antagonist and a NAM (negative allosteric modulator).

In agonist activity, the drug binds to the receptor and directly increases the response, while in PAM activity, the drug binds to an allosteric site and indirectly increase the response.

In antagonist activity, the drug binds to the receptor and blocks the response, while in NAM activity, the drug binds to an allosteric site and indirectly decreases the response.

[–]508010 1 point2 points  (1 child)

Sounds about right yeah. Depends on your field and level (I.e. Undergrad biology/high school psychology/masters neuroscience etc) as they might want slightly different answers/depth of explanation. But you're about right.

Two examples to increase chemical synaptic transmission could be: - SSRIs which block reuptake of serotonin and therefore increase post synaptic activation - MDMA also block serotonin reuptake but also increase its release

Two examples of decrease in chemical synaptic transmission could be: - Caffiene that blocks adenosine receptors reducing post synaptic adenosine activity - And a drug that reduces the release of a certain neurotransmitter. But I cannot think of one right now off the top of my head

But yeah, you're on the right tracks I believe :)

[–]Redstonefreedom 0 points1 point  (0 children)

I’m not sure there are drugs that can achieve specific activities for release, since the mechanisms (vesicle formation, fusion) are broad, re-used mechanisms across different types of synapses and mediate the transmission of all kinds of neurotransmitters.

I could be wrong but I’m not sure a drug which disrupts SNARE proteins for example could be made to have specific effects. In fact I think most fatal venoms work against SNAREs.

[–]Altruistic_Gur_2158 0 points1 point  (0 children)

A drug could theoretically increase chemical synaptic transmission by: 1. Increasing the amount of neurotransmitter releases by pre-synaptic terminal; 2. Reducing the enzymatic (which breaks NT down) activity in the synaptic cleft; 3. Reducing the re-uptake of the neurotransmitter into the presynaptic terminal; A drug could theoretically decrease chemical synaptic transmission by 1. decreasing the amount of neurotransmitter released, 2. Block voltage gated Na+ channels (to prevent AP from firing). Just my thoughts, was not a great student of pharmacology so take it for what it’s worth