I show new idea how mu-opioids and high prenatal nicotine cause respiratory slowdown linked toslow wave sleep. A high dose of mu-opioids overstimulates the medial habenula whichactivates the interpeduncular nucleus. The IPN causes respiratory depression via its output toPAG, DRN, MRN, or LPO-RMTg.SWS is linked to a natural slowdown of respiration and heart rate. The MHb and rostromedial tegmental nucleus are known for high amount of mu-opioid receptors. Both MHb and RMTg were proposed to be activated in the neural circuit that promotes SWS, rest, immune defense and recovery (Vadovičová, 2015). That work showed how the MHb→IPN→MRN circuit activates serotonin release and inhibits the theta states, alert, wakefulness, consciousness and REM sleep linked circuits, to promote slow wave oscillations, sharp wave ripples, replay of relationally bound memories, rest, restoration and BDNF linked growth. Possible effectors, through which MHb-IPN system decreases respiration are DRN, PAG and MRN (MRN→caudal raphe).The same MHb-IPN circuit that causes respiratory slowdown likely causes ventilatory deficits in mammalian neonates, known as sudden infant death syndrome (SIDS), linked to high fetal nicotine intake. My circuit model explains the role of the MHb→IPN→MRN→claustrum + hippocampus circuit in anesthesia, memory replay, cortical slow wave oscillations and SWS. I propose that ketamine acts via serotonin receptors on vACC/infralimbic, IPN and maybe medial LHb. And activates the IPN and MRN's serotonin, leading to SWA, anesthesia, SWS and theta states suppression. I explain why are ketamine and hallucinogens antianxiogenic and antidepressant.