I added a Figure 1 for the main interactions of the MHb-IPN circuit. Serotonin release from MRN was highlighted in Figure.

Opiates are fast pain relievers that can cause respiratory arrest. I show new mechanisms how mu-opioids and high prenatal nicotine cause respiratory slowdown linked to slow wave sleep. Mu-opioids activate the medial habenula which activates the interpeduncular nucleus. The MHb-IPN system decreases respiration and alarm/arousal response to hypercapnia by projections to PAG, DRN, MRN and MRN→LPO→RMTg→vPAG. 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. Natural slowdown of respiration and heart rate is caused by slow wave sleep, when body is not moving. The MHb and rostromedial tegmental nucleus are known for high amount of mu-opioid receptors. Both were claimed to be activated by the MHb→IPN→MRN circuit that activates serotonin release, promotes slow SWS, rest, immune defense, recovery, sharp wave ripples, cortical spindles, replay of temporaly, spatialy and relationally bound memories, synaptogenesis, BDNF linked growth and DG neurogenesis, but inhibits theta states, arousal, alert wakefulness, awareness and REM sleep linked circuits (Vadovičová, 2015).This updated circuit model explains role of the MHb→IPN→MRN→hippocampus + claustrum→cortical slow wave activity (SWA) in anesthesia, memory replay, loss of awareness, SWS and in theta states suppression. I proposed new mechanisms for anesthetic ketamine effect: activation of the IPN→MRN→claustrum→cortical SWA circuit by the 5-HT2a IPN and claustrum receptors. I show why are ketamine and hallucinogens anxiolytic and antidepressant, andhow activation of 5-HT2a receptors in vACC/infralimbic cortex increases the safety, well-beingsignal, and cognitive flexibility.