Dopaminergic- and cholinergic-inputs from substantia nigra and pedunculo-pontine tegmentum, respectively, converge in amygdala to modulate rapid eye movement sleep in rats.

Dreams appear intermittently during phasic rapid eye movement sleep (REMS). Although reasonable progress has been made about neuro-physio-pharmacological mechanism of appearance of REMS, appearance of dreams is a mystery. Isolated studies have reported that substantia nigra (SN) withdraws inhibition from pedunculo-pontine tegmentum (PPT) acetylcholine (ACh)-ergic REM-ON neurons to trigger REMS; some REM-ON neurons become phasically active during REMS; amygdala (Amyg), a limbic structure associated with emotions, may be related with dreaming like state; Amyg receives projections from both SN-Dopamine (DA)-ergic and PPT-ACh-ergic neurons. Collating these isolated findings, we proposed that on the background of REMS, SN-DA-ergic and PPT-ACh-ergic inputs phasically activate Amyg-neurons to manifest dreams. In the absence of better criteria, we recorded electrophysiological characteristics of REMS as the closest objective read-out for dreams in surgically prepared, chronic, freely moving rats. Microinjection of either DA-ergic or ACh-ergic agonist [Quinpirole (Qnp) or Carbachol (Carb)] bilaterally into Amyg increased, while antagonists [Haloperidol (Hal) or Scopolamine (Scop)] reduced REMS. Electrical stimulation of either bilateral SN or PPT increased REMS, which however, was prevented when stimulated in presence of Hal or Scop, respectively into the Amyg. These findings confirm and support our contention that SN-DA-ergic and PPT-ACh-ergic inputs integrate in Amyg for REMS regulation. Further, subject to confirmation in humans, we propose that on the background of REMS, some phasic PPT-ACh-ergic-REM-ON neurons intermittently trigger some neurons in Amyg, the area known to be associated with memory and emotions, causing intermittent appearance of REMS-associated dreams and in REMS behavior disorder.