If amphetamines exert their effects via G-Protein Coupled Receptors (GPCRs) like TAARs, then doesn’t their use optimize homeostatic mechanisms involved in dopaminergic signaling?

Amphetamines signal through intracellular TAAR1 receptors coupled to Gα13 and GαS in discrete subcellular domains

Link to direct file

Underhill, Suzanne M., et al. “Amphetamines signal through intracellular TAAR1 receptors coupled to Gα13 and GαS in discrete subcellular domains.” Molecular psychiatry 26.4 (2021): 1208-1223.

Significance of this work

My goal here is to convey the extremely paired down version of tis explanation for two reasons:

  1. Some of the nuances of the technical structures and interactions at the biomolecular level is beyond my knowledge and skill.
  2. You don’t need to memorize the “players” in this system in order to understand the cross-cutting mechanics and logic.

Quick History

It is common to interact with information and other people who might suggest that deficits in attention, sensory-motor integration, etc. is related to “low levels of dopamine”. It’s usually not specified where, specifically, or what kinds of neurons are specifically implicated here, but the as the story goes:

Administration of amphetamine –> Attenuation of attention and motivational deficits –> Is associated with higher concentrations of extracellular dopamine

Anatomy of A Misperception

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