PMID- 27861553
OWN - NLM
STAT- MEDLINE
DCOM- 20170626
LR  - 20201215
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 11
IP  - 11
DP  - 2016
TI  - Activity-Based Anorexia Alters the Expression of BDNF Transcripts in the 
      Mesocorticolimbic Reward Circuit.
PG  - e0166756
LID - 10.1371/journal.pone.0166756 [doi]
LID - e0166756
AB  - Anorexia nervosa (AN) is a complex eating disorder with severe dysregulation of 
      appetitive behavior. The activity-based anorexia (ABA) paradigm is an animal 
      model in which rodents exposed to both running wheels and scheduled feeding 
      develop aspects of AN including paradoxical hypophagia, dramatic weight loss, and 
      hyperactivity, while animals exposed to only one condition maintain normal body 
      weight. Brain-derived neurotrophic factor (BDNF), an activity-dependent modulator 
      of neuronal plasticity, is reduced in the serum of AN patients, and is a known 
      regulator of feeding and weight maintenance. We assessed the effects of scheduled 
      feeding, running wheel access, or both on the expression of BDNF transcripts 
      within the mesocorticolimbic pathway. We also assessed the expression of neuronal 
      cell adhesion molecule 1 (NCAM1) to explore the specificity of effects on BDNF 
      within the mesocorticolimbic pathway. Scheduled feeding increased the levels of 
      both transcripts in the hippocampus (HPC), increased NCAM1 mRNA expression in the 
      ventral tegmental area (VTA), and decreased BDNF mRNA levels in the medial 
      prefrontal cortex (mPFC). In addition, wheel running increased BDNF mRNA 
      expression in the VTA. No changes in either transcript were observed in the 
      nucleus accumbens (NAc). Furthermore, no changes in either transcript were 
      induced by the combined scheduled feeding and wheel access condition. These data 
      indicate that scheduled feeding or wheel running alter BDNF and NCAM1 expression 
      levels in specific regions of the mesocorticolimbic pathway. These findings 
      contribute to our current knowledge of the molecular alterations induced by ABA 
      and may help elucidate possible mechanisms of AN pathology.
FAU - Ho, Emily V
AU  - Ho EV
AD  - Department of Psychiatry, University of California San Diego, La Jolla, 
      California, United States of America.
FAU - Klenotich, Stephanie J
AU  - Klenotich SJ
AD  - Department of Psychiatry, University of Chicago, Chicago, Illinois, United States 
      of America.
FAU - McMurray, Matthew S
AU  - McMurray MS
AD  - Department of Psychology, University of Illinois Chicago, Chicago, Illinois, 
      United States of America.
FAU - Dulawa, Stephanie C
AU  - Dulawa SC
AD  - Department of Psychiatry, University of California San Diego, La Jolla, 
      California, United States of America.
LA  - eng
GR  - R01 MH099248/MH/NIMH NIH HHS/United States
GR  - UL1 RR024999/RR/NCRR NIH HHS/United States
PT  - Journal Article
DEP - 20161118
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Anorexia/*etiology/*physiopathology
MH  - Behavior, Animal
MH  - Brain-Derived Neurotrophic Factor/*genetics
MH  - Disease Models, Animal
MH  - Female
MH  - *Gene Expression
MH  - Gene Expression Regulation
MH  - Mice
MH  - *Motor Activity
MH  - Physical Exertion
MH  - *Reward
PMC - PMC5115804
COIS- The authors have declared that no competing interests exist.
EDAT- 2016/11/20 06:00
MHDA- 2017/06/27 06:00
PMCR- 2016/11/18
CRDT- 2016/11/19 06:00
PHST- 2016/07/28 00:00 [received]
PHST- 2016/11/03 00:00 [accepted]
PHST- 2016/11/19 06:00 [entrez]
PHST- 2016/11/20 06:00 [pubmed]
PHST- 2017/06/27 06:00 [medline]
PHST- 2016/11/18 00:00 [pmc-release]
AID - PONE-D-16-30258 [pii]
AID - 10.1371/journal.pone.0166756 [doi]
PST - epublish
SO  - PLoS One. 2016 Nov 18;11(11):e0166756. doi: 10.1371/journal.pone.0166756. 
      eCollection 2016.