PMID- 22717678
OWN - NLM
STAT- MEDLINE
DCOM- 20130724
LR  - 20211021
IS  - 1619-1560 (Electronic)
IS  - 0959-9851 (Linking)
VI  - 23
IP  - 1
DP  - 2013 Feb
TI  - Vagal afferent controls of feeding: a possible role for gastrointestinal BDNF.
PG  - 15-31
LID - 10.1007/s10286-012-0170-x [doi]
AB  - INTRODUCTION: Vagal gastrointestinal (GI) afferents do not appear to contribute 
      to long-term controls of feeding, despite downstream connections that could 
      support such a role. This view is largely attributable to a lack of evidence for 
      long-term effects, especially the failure of vagal afferent lesions to produce 
      hyperphagia or obesity. AIMS: Here, the possibility is evaluated that "side 
      effects" of vagal lesion methods resulting largely from complexities of vagal 
      organization would probably suppress long-term effects. Criteria based on 
      knowledge of vagal organization were utilized to critique and compare vagal 
      lesion methods and to interpret their effects on GI function, feeding and body 
      weight. RESULTS AND CONCLUSIONS: This analysis suggested that it was premature to 
      eliminate a long-term vagal GI afferent role based on the effects of these 
      lesions and highlighted aspects of vagal organization that must be addressed to 
      reduce the problematic side effects of vagal lesions. The potential of "genetic" 
      lesions that alter vagal sensory development to address these aspects, 
      examination of the feasibility of this approach, and the properties of 
      brain-derived neurotrophic factor (BDNF) that made it an attractive candidate for 
      application of this approach are described. BDNF knockout from GI smooth muscle 
      unexpectedly demonstrated substantial overeating and weight gain associated with 
      increased meal size and frequency. The decay of eating rate during a scheduled 
      meal was also reduced. However, meal-induced c-Fos activation was increased in 
      the dorsal motor nucleus of the vagus, suggesting that the effect on eating rate 
      was due to augmentation of GI reflexes by vagal afferents or other neural 
      systems.
FAU - Fox, Edward A
AU  - Fox EA
AD  - Behavioral Neurogenetics Laboratory and Ingestive Behavior Research Center, 
      Department of Psychological Sciences, Purdue University, West Lafayette, IN 
      47907, USA. au_gc@psych.purdue.edu
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20120621
PL  - Germany
TA  - Clin Auton Res
JT  - Clinical autonomic research : official journal of the Clinical Autonomic Research 
      Society
JID - 9106549
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Feeding Behavior/*physiology
MH  - Gastrointestinal Tract/*innervation/*metabolism
MH  - Humans
MH  - Neurons, Afferent/metabolism
MH  - Vagus Nerve/*physiology
EDAT- 2012/06/22 06:00
MHDA- 2013/07/25 06:00
CRDT- 2012/06/22 06:00
PHST- 2012/03/12 00:00 [received]
PHST- 2012/05/24 00:00 [accepted]
PHST- 2012/06/22 06:00 [entrez]
PHST- 2012/06/22 06:00 [pubmed]
PHST- 2013/07/25 06:00 [medline]
AID - 10.1007/s10286-012-0170-x [doi]
PST - ppublish
SO  - Clin Auton Res. 2013 Feb;23(1):15-31. doi: 10.1007/s10286-012-0170-x. Epub 2012 
      Jun 21.