PMID- 28167137
OWN - NLM
STAT- MEDLINE
DCOM- 20170829
LR  - 20211204
IS  - 1873-7064 (Electronic)
IS  - 0028-3908 (Print)
IS  - 0028-3908 (Linking)
VI  - 117
DP  - 2017 May 1
TI  - Deletion of Rictor in catecholaminergic neurons alters locomotor activity and 
      ingestive behavior.
PG  - 158-170
LID - S0028-3908(17)30042-4 [pii]
LID - 10.1016/j.neuropharm.2017.02.001 [doi]
AB  - While the etiology of depression is not fully understood, increasing evidence 
      from animal models suggests a role for the ventral tegmental area (VTA) in 
      pathogenesis. In this paper, we investigate the potential role of VTA mechanistic 
      target of rapamycin 2 (TORC2) signaling in mediating susceptibility to chronic 
      social defeat stress (CSDS), a well-established mouse model of depression. 
      Utilizing genetic and viral knockout of Rictor (rapamycin-insensitive companion 
      of target of rapamycin), a requisite component of TORC2, we demonstrate that 
      decreasing Rictor-dependent TORC2 signaling in catecholaminergic neurons, or 
      within the VTA specifically, does not alter susceptibility to CSDS. Opiate abuse 
      and mood disorders are often comorbid, and previous data demonstrate a role for 
      VTA TORC2 in mediating opiate reward. Thus, we also investigated its potential 
      role in mediating changes in opiate reward following CSDS. Catecholaminergic 
      deletion of Rictor increases water, sucrose, and morphine intake but not 
      preference in a two-bottle choice assay in stress-naive mice, and these effects 
      are maintained after stress. VTA-specific knockout of Rictor increases water and 
      sucrose intake after physical CSDS, but does not alter consummatory behavior in 
      the absence of stress. These findings suggest a novel role for TORC2 in mediating 
      stress-induced changes in consummatory behaviors that may contribute to some 
      aspects of mood disorders.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Kaska, Sophia
AU  - Kaska S
AD  - Dept. of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 
      48824, United States.
FAU - Brunk, Rebecca
AU  - Brunk R
AD  - Neuroscience Program, Michigan State University, East Lansing, MI 48824, United 
      States.
FAU - Bali, Vedrana
AU  - Bali V
AD  - Dept. of Physiology, Michigan State University, East Lansing, MI 48824, United 
      States.
FAU - Kechner, Megan
AU  - Kechner M
AD  - Neuroscience Program, Michigan State University, East Lansing, MI 48824, United 
      States.
FAU - Mazei-Robison, Michelle S
AU  - Mazei-Robison MS
AD  - Neuroscience Program, Michigan State University, East Lansing, MI 48824, United 
      States; Dept. of Physiology, Michigan State University, East Lansing, MI 48824, 
      United States. Electronic address: mazeirob@msu.edu.
LA  - eng
GR  - R01 DA039895/DA/NIDA NIH HHS/United States
GR  - R03 DA037426/DA/NIDA NIH HHS/United States
GR  - T32 GM092715/GM/NIGMS NIH HHS/United States
PT  - Journal Article
DEP - 20170203
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Carrier Proteins)
RN  - 0 (Multiprotein Complexes)
RN  - 0 (Rapamycin-Insensitive Companion of mTOR Protein)
RN  - 0 (rictor protein, mouse)
RN  - 57-50-1 (Sucrose)
RN  - 76I7G6D29C (Morphine)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Carrier Proteins/genetics/*physiology
MH  - Choice Behavior/drug effects
MH  - Drinking/*drug effects
MH  - Feeding Behavior/drug effects/*physiology
MH  - Female
MH  - Locomotion/*physiology
MH  - Male
MH  - Mechanistic Target of Rapamycin Complex 2
MH  - Mice
MH  - Mice, Knockout
MH  - Morphine/pharmacology
MH  - Multiprotein Complexes/*physiology
MH  - Neurons/*physiology
MH  - Rapamycin-Insensitive Companion of mTOR Protein
MH  - Social Behavior
MH  - Stress, Psychological/metabolism/psychology
MH  - Sucrose/*pharmacology
MH  - TOR Serine-Threonine Kinases/*physiology
MH  - Tyrosine 3-Monooxygenase/*metabolism
MH  - Ventral Tegmental Area/metabolism/*physiology
PMC - PMC5386799
MID - NIHMS851372
OTO - NOTNLM
OT  - Catecholamine
OT  - Consummatory
OT  - Drinking
OT  - Locomotor activity
OT  - Stress
OT  - Ventral tegmental area
COIS- Disclosure: The authors have no financial interests or conflicts of interest to 
      disclose.
EDAT- 2017/02/09 06:00
MHDA- 2017/08/30 06:00
PMCR- 2018/05/01
CRDT- 2017/02/08 06:00
PHST- 2016/12/21 00:00 [received]
PHST- 2017/01/31 00:00 [revised]
PHST- 2017/02/02 00:00 [accepted]
PHST- 2017/02/09 06:00 [pubmed]
PHST- 2017/08/30 06:00 [medline]
PHST- 2017/02/08 06:00 [entrez]
PHST- 2018/05/01 00:00 [pmc-release]
AID - S0028-3908(17)30042-4 [pii]
AID - 10.1016/j.neuropharm.2017.02.001 [doi]
PST - ppublish
SO  - Neuropharmacology. 2017 May 1;117:158-170. doi: 10.1016/j.neuropharm.2017.02.001. 
      Epub 2017 Feb 3.