| First Author | Lecca S | Year | 2017 |
| Journal | Elife | Volume | 6 |
| PubMed ID | 28871962 | Mgi Jnum | J:248309 |
| Mgi Id | MGI:5919737 | Doi | 10.7554/eLife.30697 |
| Citation | Lecca S, et al. (2017) Aversive stimuli drive hypothalamus-to-habenula excitation to promote escape behavior. Elife 6:e30697 |
| abstractText | A sudden aversive event produces escape behaviors, an innate response essential for survival in virtually all-animal species. Nuclei including the lateral habenula (LHb), the lateral hypothalamus (LH), and the midbrain are not only reciprocally connected, but also respond to negative events contributing to goal-directed behaviors. However, whether aversion encoding requires these neural circuits to ultimately prompt escape behaviors remains unclear. We observe that aversive stimuli, including foot-shocks, excite LHb neurons and promote escape behaviors in mice. The foot-shock-driven excitation within the LHb requires glutamatergic signaling from the LH, but not from the midbrain. This hypothalamic excitatory projection predominates over LHb neurons monosynaptically innervating aversion-encoding midbrain GABA cells. Finally, the selective chemogenetic silencing of the LH-to-LHb pathway impairs aversion-driven escape behaviors. These findings unveil a habenular neurocircuitry devoted to encode external threats and the consequent escape; a process that, if disrupted, may compromise the animal's survival. |
