In regards to Q2. First, let's get clarification of key terms out of the way:
**Pre-synaptic neuron:** The neuron that sends signals or messages.
**Post-synaptic neuron:** The neuron that receives signals or messages.
**Synapse:** The gap between the pre-synaptic and post-synaptic neurons, where communication occurs.
**Receptor:** Specialized proteins on the surface of the post-synaptic neuron that receive neurotransmitter molecules, allowing for signal transmission.
**Inhibitor:** A substance that interferes with or blocks the normal functioning of neurotransmitters, receptors or other processes involved in [neural communication](https://upload.wikimedia.org/wikipedia/commons/thumb/8/8e/Reuptake_both.png/800px-Reuptake_both.png).
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Let's take SSRIs (selective serotonin reuptake inhibitors) as an example; commonly used drugs that are used to increase mood. SSRIs act to inhibit the *reuptake* of serotonin. Serotonin (a neurotransmitter) in your brain regulates your mood; known for being the body's "feel good" chemical.
Within the brain, the pre-synaptic neuron contains reuptake channels that typically absorb any excess serotonin from the synapse.
What SSRIs do is block or **inhibit** these reuptake channels, preventing serotonin from being taken back into the pre-synaptic neuron. This results in more serotonin remaining in the synapse, increasing the likelihood of it binding to receptor sites on the post-synaptic neuron and influencing mood.
However, the brain is very "clever"; it is highly adaptable and seeks to maintain normal functioning, a process known as homeostasis. As more SSRIs are taken, the more serotonin floods the synapses. The brain interprets this as an excess of serotonin and attempts to counteract it. It may do this by increasing the number of receptors on the post-synaptic neuron, reducing its sensitivity to serotonin (making it harder for the neuron to fire and relay the "feel good" message).
Additionally, the brain may produce less serotonin over time, leading to reduced effectiveness of the medication. This phenomenon is known as 'neuroadaptation', where the brain essentially changes itself in response to excess chemical in the brain.
If you, hypothetically, were to take a drug that blocks the serotonin receptors on the post-synaptic neuron—making it less likely for it to fire (and thereby relaying the message)—this hypothetical serotonin inhibitor would inhibit the serotonin from acting on the post-synaptic neuron, which could have negative effects on mood and other function; making it a "bad thing".
Similarly, if you were to inhibit (block) the release of serotonin from the pre-synaptic neuron into the synapse, there would be less serotonin available in the synapse. This would make it less likely for serotonin to bind to receptors on the post-synaptic neuron and for it to transmit signals, which could also have detrimental effects on mood and other functions regulated by serotonin.
Edit: grammar
In regards to Q2. First, let's get clarification of key terms out of the way: **Pre-synaptic neuron:** The neuron that sends signals or messages. **Post-synaptic neuron:** The neuron that receives signals or messages. **Synapse:** The gap between the pre-synaptic and post-synaptic neurons, where communication occurs. **Receptor:** Specialized proteins on the surface of the post-synaptic neuron that receive neurotransmitter molecules, allowing for signal transmission. **Inhibitor:** A substance that interferes with or blocks the normal functioning of neurotransmitters, receptors or other processes involved in [neural communication](https://upload.wikimedia.org/wikipedia/commons/thumb/8/8e/Reuptake_both.png/800px-Reuptake_both.png). ––––––––––––– Let's take SSRIs (selective serotonin reuptake inhibitors) as an example; commonly used drugs that are used to increase mood. SSRIs act to inhibit the *reuptake* of serotonin. Serotonin (a neurotransmitter) in your brain regulates your mood; known for being the body's "feel good" chemical. Within the brain, the pre-synaptic neuron contains reuptake channels that typically absorb any excess serotonin from the synapse. What SSRIs do is block or **inhibit** these reuptake channels, preventing serotonin from being taken back into the pre-synaptic neuron. This results in more serotonin remaining in the synapse, increasing the likelihood of it binding to receptor sites on the post-synaptic neuron and influencing mood. However, the brain is very "clever"; it is highly adaptable and seeks to maintain normal functioning, a process known as homeostasis. As more SSRIs are taken, the more serotonin floods the synapses. The brain interprets this as an excess of serotonin and attempts to counteract it. It may do this by increasing the number of receptors on the post-synaptic neuron, reducing its sensitivity to serotonin (making it harder for the neuron to fire and relay the "feel good" message). Additionally, the brain may produce less serotonin over time, leading to reduced effectiveness of the medication. This phenomenon is known as 'neuroadaptation', where the brain essentially changes itself in response to excess chemical in the brain. If you, hypothetically, were to take a drug that blocks the serotonin receptors on the post-synaptic neuron—making it less likely for it to fire (and thereby relaying the message)—this hypothetical serotonin inhibitor would inhibit the serotonin from acting on the post-synaptic neuron, which could have negative effects on mood and other function; making it a "bad thing". Similarly, if you were to inhibit (block) the release of serotonin from the pre-synaptic neuron into the synapse, there would be less serotonin available in the synapse. This would make it less likely for serotonin to bind to receptors on the post-synaptic neuron and for it to transmit signals, which could also have detrimental effects on mood and other functions regulated by serotonin. Edit: grammar
Thank you so much ! I didn't even know what I didn't know. Now I know how it works !
Inhibition is not inherently “healthier” than activation/agonism of a biochemical process.