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SUMMARY:SLC6A15\, a novel stress vulnerability candidate\, regulates anxie
 ty and depressive like behavior through the glutamatergic system.
DTSTART:20170925T090000
DTEND:20170925T100000
DTSTAMP:20260609T214958Z
UID:a651e9662a46054d183a04cb7afefe34ddb8c41e85b8fbffe3ad2b7d
CATEGORIES:Conferences - Seminars
DESCRIPTION:Prof. Mathias V. Schmidt\, Max Planck Institute of Psychiatry\
 , Department of Stress Neurobiology and Neurogenetics\, DE\nSLC6A15\, a ne
 utral amino acid transporter predominantly expressed in neurons\, has been
  recently suggested to play a role in the aetiology of major depressive di
 sorder. The purpose of this study was to explore a putative mechanism of a
 ction of the transporter in the brain and to characterize behavioural and 
 molecular changes following manipulation of SLC6A15 in mice. Therefore\, w
 e analysed hippocampal neurochemistry and behaviour in animals with reduce
 d\, i.e. full knockout or acute pharmacological inhibition\, or increased 
 levels of SLC6A15\, i.e. targeted overexpression in the hippocampus. We fu
 rthermore investigated the effects of reduced SLC6A15 levels on glutamate 
 synthesis\, mitochondrial function and electrophysiology in primary hippoc
 ampal cell culture. Ablation of SLC6A15 reduced tissue levels of several s
 ubstrate amino acids such as proline and leucine as well as glutamate leve
 ls in the hippocampus\, while overexpression increased hippocampal glutama
 te levels. We observed an anxiolytic effect of SLC6A15 KO after chronic st
 ress exposure and of SLC6A15 antagonist treatment under control conditions
 \, an effect that was reversed by hippocampal overexpression of the transp
 orter. Lack of the transporter was furthermore associated with alterations
  in sensorimotor gating. In neuronal culture\, lack or inhibition of SLC6A
 15 affected neuronal transmission as well as mitochondrial respiration. In
  summary\, our results implement SLC6A15 as a modulating factor for emotio
 nal behaviour and stress vulnerability. Our data thereby provide a mechani
 stic basis for the genetic associations of SLC6A15 polymorphisms with ment
 al disorders and suggest SLC6A15 antagonists as a promising therapeutic in
 tervention strategy.\n 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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