A rat G protein-coupled receptor (rTAR1) stimulates cAMP production when exposed to trace amines such as p-tyramine, beta-phenethylamine, tryptamine, and octopamine. Psychostimulant and hallucinogenic amphetamines, ergoline derivatives, adrenergic ligands, and 3-methylated metabolites of catecholamine neurotransmitters also act as potent agonists at this receptor. These findings indicate that trace amines and catecholamine metabolites may be endogenous ligands for a novel intercellular signaling system in the vertebrate brain and periphery. The potency of amphetamines, including MDMA (ecstasy), as rTAR1 agonists suggests that some effects of these drugs may be mediated through this receptor in addition to neurotransmitter transporter proteins.
The default-mode network (DMN) in rats contains three coactive micropattern (CAMP) networks that show greater functional connectivity and efficiency than the original DMN structure across all states of consciousness. In the waking state, these three networks do not differ significantly in connectivity or network properties, but in two sleep states they exhibit distinct characteristics, suggesting each plays a specific role. Changes in the CAMP networks' connectivity and properties mirror those of the original DMN, indicating that different states of consciousness intrinsically affect DMN dynamics. These findings deepen understanding of how DMN functional connectivity alters during the sleep-wake cycle.