It seems that there is a huge variety of mind-altering drugs with unique mental characteristics in terms of qualitative experience, yet the action of drugs is frequently explained as being the result of influencing the amount of key neurotransmitters in the brain, often dopamine, serotonin and neuroepinephrine.

Is this an overly reductionistic view of how drugs change brain activity? Why should the effect of drugs so often be explained just in terms of these common neurotransmitters?


The brief answer to your question is that:

  • Serotonin to be clear is not a primary neurotransmitter, as it is not a primary driver or inhibitor of action potential generation --- the core signal by which we understand our brain encodes information --- but rather a neuromodulator that tends to indeed 'modulate' the effect of glutamate and GABA among other classical neurotransmitters.
  • So, serotonin is likely best thought of as a mechanism akin to the effect of weather or social pressure on human conversations.
  • Thus, as serotonin levels change, they affect the tone, the tempo, and the general intensity of the signaling without distorting the signals at their core level - this is part of the reason why they work without causing substantial dysfunction which is what can happen if you cause significant changes in the effect of primary neurotransmitters (e.g., Ketamine for glutamate, EtOh for GABA).

The somewhat longer answer to your question has to do with coding. In computer chips, you just have one encoding signal, that is electrons. The 1s or 0s of digital circuitry are stored simply on whether the number of electrons at a certain physical location is below or above a certain intensity threshold. Reframing your question, one could ask, how is it that computer chips can do so much with just one 'encoding signal?' Is such a viewpoint overly reductionist? We know it is not overly reductionistic because we know that is actually how computers work. Rather, digital 1s and 0s vary in significance and effect depending on where they are stored.

As it relates to neural signals, the same neurotransmitter means 'different things' not just depending on where it is released in relation to a particular neuron, but also depending on the following:

  1. timing
  2. duration
  3. intensity
  4. dendritic location (closest equivalent to the "where")
  5. neuronal map location
  6. coincidence of signals
  7. presynaptic neuromodulation
  8. postsynaptic neuromodulation
  9. intracellular 2nd messenger
  10. transcriptional activity
  11. post-transcriptional effects
  12. methylation effects
  13. cross-brain synchrony
  14. interactions with supporting cells (e.g., astrocytes)
  15. mirror neurons incl. language-speaking more broadly
  16. transaxonal transport mechanisms
  17. retrograde signaling
  • $\begingroup$ Can you elaborate on how mirror neurons are relevant to the question asked? $\endgroup$ Nov 22 at 7:12
  • $\begingroup$ Brief review of mirror neurons and link to language: link. Mirror neurons, and their neurotransmitter release, become active whether you perform an action or witness someone else doing it, and may be behind our capacity for empathy (feeling someone else's emotion as our own) and language (ditto for cognition). $\endgroup$ Nov 24 at 17:45
  • $\begingroup$ thank you, to be more clear, I'm confused about the function of mirror neurons concerning the impact of drugs. $\endgroup$ Nov 24 at 17:55
  • $\begingroup$ Now, let's take it to a computer analogy: if a digital '1' was represented in one computer, it has one meaning, but if that '1' is represented is in 2 computers, suddenly you have the possibility of the Internet. Now let's switch back to the brain: the humble neurotransmitter that represented my answer to this question on StackExchange, when I posted it, suddenly had a companion release in your brain, and so that initial neurotransmitter release gained new meaning and effect. It could go on to support your follow-up question, people now reading these words, and all that may come from it. $\endgroup$ Nov 24 at 17:56
  • 1
    $\begingroup$ Well, your question is vast, and to answer it in detail could take a 1000s Wikipedias in length. But here's a simple example: it's been seen that before SSRIs have their effect in mood, which can take more than a month, even within the first weeks, people already start to experience others as being less angry, less scary, and more friendly. In other words, their ability to read others (or what is called "theory of mind" in fancier circles), and is believed to be in part mediated by mirror neurons, has already shifted towards the positive. $\endgroup$ Nov 24 at 17:58

Put simply, this is because many "mind-altering drugs" work by changing levels of neurotransmitters at the synapse. The most common example perhaps is the use of SSRIs (Selective Serotonin Reuptake Inhibitors) for depression, like Paxil or Prozac. These drugs increase the amount of serotonin by blocking the reabsorption of the neurotransmitter at the pre-synapse. Thus, increasing the amount of serotonin for the post-synaptic neuron, and increasing the amount of serotonin absorbed there.

LSD (the psychedelic drug) also binds to receptors of neurons to influence the way serotonin is absorbed (more specifically acts as a receptor agonist). This is what induces the psychedelic effect, such as changes in auditory and visual processing.


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