| Literature DB >> 31104950 |
Mazahir T Hasan1, Ferdinand Althammer2, Miriam Silva da Gouveia2, Stephanie Goyon3, Marina Eliava2, Arthur Lefevre2, Damien Kerspern3, Jonas Schimmer2, Androniki Raftogianni2, Jerome Wahis3, H Sophie Knobloch-Bollmann2, Yan Tang2, Xinying Liu2, Apar Jain2, Virginie Chavant3, Yannick Goumon3, Jan-Marek Weislogel4, René Hurlemann5, Sabine C Herpertz6, Claudia Pitzer7, Pascal Darbon3, Godwin K Dogbevia8, Ilaria Bertocchi9, Matthew E Larkum10, Rolf Sprengel9, Hilmar Bading4, Alexandre Charlet11, Valery Grinevich12.
Abstract
Oxytocin (OT) release by axonal terminals onto the central nucleus of the amygdala exerts anxiolysis. To investigate which subpopulation of OT neurons contributes to this effect, we developed a novel method: virus-delivered genetic activity-induced tagging of cell ensembles (vGATE). With the vGATE method, we identified and permanently tagged a small subpopulation of OT cells, which, by optogenetic stimulation, strongly attenuated contextual fear-induced freezing, and pharmacogenetic silencing of tagged OT neurons impaired context-specific fear extinction, demonstrating that the tagged OT neurons are sufficient and necessary, respectively, to control contextual fear. Intriguingly, OT cell terminals of fear-experienced rats displayed enhanced glutamate release in the amygdala. Furthermore, rats exposed to another round of fear conditioning displayed 5-fold more activated magnocellular OT neurons in a novel environment than a familiar one, possibly for a generalized fear response. Thus, our results provide first evidence that hypothalamic OT neurons represent a fear memory engram.Entities:
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Year: 2019 PMID： 31104950 DOI： 10.1016/j.neuron.2019.04.029
Source DB: PubMed Journal: Neuron ISSN： 0896-6273 Impact factor: 17.173