I propose new roles for the medial habenula (MHb) and interpeduncular nucleus circuits: MHb promotes slow wave sleep (SWS or NREM sleep), hippocampo-cortical memory replay and consolidation, unawareness, anesthesia, respiratory slowdown (also OIRD, opiate crisis), synaptogenesis and neural growth by activating the IPN and its effectors (Vadovičová, 2015). This MHb-IPN circuit interacts also with immune response, directly at MHb, and disynaptically by inducing the median raphe nucleus (MRN) serotonin release, that activates also the brain-derived neurotrophic factor (BDNF) and dentate gyrus (DG) neurogenesis. MHb activates melatonin release in pineal gland which is inhibited by light (Ronnekleiv et al., 1980; Ronnekleiv and Moller, 1979). Medial septum and diagonal band of Broca (MS/DBB) inhibit MHb, while stress, fear, worries, danger, noradrenaline, corticotropine releasing hormone (CRH), and dopamine inhibit the IPN. Theta states and arousal promoting regions inhibit the IPN, MRN or both (Vadovičová, 2015). The MHb is activated by safety, mBNST, posterior septum, mu-opioids, endocannabinoids (they inhibit gabaergic MS/DBB input, Vickstrom et al., 2021), glutamate, acetylcholine and nicotine. I propose that IPN and claustrum are activated by ketamine, psychedelics and serotonin via 5-HT2a receptors, causing loss of awareness by inducing slow wave activity in cortex, basal ganglia and amygdala.
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Karin Vadovičová (2024) studied this question.
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