Opposing effects of an atypical glycinergic and substance P transmission on interpeduncular nucleus plasticity.

Authors:
Riccardo Melani
Riccardo Melani
and Institute of Anatomy and Molecular Neurobiology
Italy
Deqiang Jing
Deqiang Jing
Weill Cornell Medical College
United States
Peter Koppensteiner
Peter Koppensteiner
Columbia University
United States
Ipe Ninan
Ipe Ninan
New York University School of Medicine
United States

Neuropsychopharmacology 2019 Apr 20. Epub 2019 Apr 20.

Department of Psychiatry and NYU Neuroscience Institute, NYU Langone Medical Center, New York, NY, USA.

The medial habenula-interpeduncular nucleus (MHb-IPN) pathway has recently been implicated in the suppression of fear memory. A notable feature of this pathway is the corelease of neurotransmitters and neuropeptides from MHb neurons. Our studies in mice reveal that an activation of substance P-positive dorsomedial habenula (dMHb) neurons results in simultaneous release of glutamate and glycine in the lateral interpeduncular nucleus (LIPN). This glycine receptor activity inhibits an activity-dependent long-lasting potentiation of glutamatergic synapses in LIPN neurons, while substance P enhances this plasticity. An endocannabinoid CB1 receptor-mediated suppression of GABA receptor activity allows substance P to induce a long-lasting increase in glutamate release in LIPN neurons. Consistent with the substance P-dependent synaptic potentiation in the LIPN, the NK1R in the IPN is involved in fear extinction but not fear conditioning. Thus, our study describes a novel plasticity mechanism in the LIPN and a region-specific role of substance P in fear extinction.

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Source
http://www.nature.com/articles/s41386-019-0396-6
Publisher Site
http://dx.doi.org/10.1038/s41386-019-0396-6DOI Listing
April 2019
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