کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5549064 1556600 2017 13 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Deletion of Rictor in catecholaminergic neurons alters locomotor activity and ingestive behavior
ترجمه فارسی عنوان
حذف ریکتور در نورونهای کاتچولامینرژیک باعث تغییر رفتار فعالیت حرکتی و رفتار جسمی
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب رفتاری
چکیده انگلیسی


- Rictor knockout in TH neurons alters voluntary fluid intake and locomotor activity.
- Rictor knockout in VTA does not alter baseline activity or fluid intake.
- Rictor knockout in TH neurons or VTA alters fluid intake after chronic stress.
- Rictor knockout increases locomotor activity in males but not females.

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-naïve 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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuropharmacology - Volume 117, 1 May 2017, Pages 158-170
نویسندگان
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