synaptic transitions details

• An action potential triggers the vesicles in the pre-synaptic dendrites to burst and release their neurotransmitters into the synaptic gap where they diffuse across and bind with receptors on the post-synaptic dendrite. ​​
• Any excess that doesn't bind gets taken back up into the vesicles to await the next action potential. ​​
• Excitation / inhibition depends on the neurotransmitter that is released: adrenaline and dopamine are excitatory neurotransmitters, so when they are released, diffuse across the gap and bind to receptors, they excite the next axon and so messages get passed on.
• However, serotonin and GABA are inhibitory neurotransmitters, so when they are released, diffuse across the gap and bind to the receptors, they inhibit the next action potential so messages slow down. ​​
• This explains why a lack of serotonin at the post-synaptic membrane (perhaps due to excessive reuptake) is associated with the high brain activity of repetitive, intrusive thoughts in anxiety, depression and OCD. ​
• ​Using SSRIs to inhibit (reduce) reuptake allows more serotonin to bind to receptors, and can alleviate the symptoms and slow the thoughts, calming the brain.