Topic: medial habenula

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).

The habenula (Hb) is a diencephalic brain region implicated in adaptive behaviors and neuropsychiatric disorders. Two main Hb subdivisions, the lateral habenula and medial habenula, have been shown to play different roles in diverse behaviors, ranging from classical and operant learning to the prediction of outcomes, fear, addiction, and social interactions. However, our understanding of cytoarchitecture and topography of the vertebrate Hb, as well as how different Hb microcircuits are organized across species, remains limited. In this study, we utilized a combination of single-cell and spatia

The habenula is a phylogenetically conserved bilateral brain structure known to modulate negative emotions. Hemispheric asymmetry in cortical areas plays a key role in behavior and cognition. Although habenular asymmetry is prominent in several vertebrate species, there is little evidence for left-right asymmetry in the mammalian habenula. To investigate the asymmetry in synaptic transmission in the medial habenula (MHb) to the interpeduncular nucleus (IPN) pathway in mice, we performed targeted electrical stimulation of left or right MHb-derived axons in acute slices. We discovered that the p

GABAB receptor (GBR) activation inhibits neurotransmitter release in axon terminals in the brain, except in medial habenula (MHb) terminals, which show robust potentiation. However, mechanisms underlying this enigmatic potentiation remain elusive. Here, we report that GBR activation on MHb terminals induces an activity-dependent transition from a facilitating, tonic to a depressing, phasic neurotransmitter release mode. This transition is accompanied by a 4.1-fold increase in readily releasable vesicle pool (RRP) size and a 3.5-fold increase of docked synaptic vesicles at the presynaptic activ