PMID- 25080597 OWN - NLM STAT- MEDLINE DCOM- 20140929 LR - 20211021 IS - 1529-2401 (Electronic) IS - 0270-6474 (Print) IS - 0270-6474 (Linking) VI - 34 IP - 31 DP - 2014 Jul 30 TI - Reduced intestinal brain-derived neurotrophic factor increases vagal sensory innervation of the intestine and enhances satiation. PG - 10379-93 LID - 10.1523/JNEUROSCI.1042-14.2014 [doi] AB - Brain-derived neurotrophic factor (BDNF) is produced by developing and mature gastrointestinal (GI) tissues that are heavily innervated by autonomic neurons and may therefore control their development or function. To begin investigating this hypothesis, we compared the morphology, distribution, and density of intraganglionic laminar endings (IGLEs), the predominant vagal GI afferent, in mice with reduced intestinal BDNF (INT-BDNF(-/-)) and controls. Contrary to expectations of reduced development, IGLE density and longitudinal axon bundle number in the intestine of INT-BDNF(-/-) mice were increased, but stomach IGLEs were normal. INT-BDNF(-/-) mice also exhibited increased vagal sensory neuron numbers, suggesting that their survival was enhanced. To determine whether increased intestinal IGLE density or other changes to gut innervation in INT-BDNF(-/-) mice altered feeding behavior, meal pattern and microstructural analyses were performed. INT-BDNF(-/-) mice ate meals of much shorter duration than controls, resulting in reduced meal size. Increased suppression of feeding in INT-BDNF(-/-) mice during the late phase of a scheduled meal suggested that increased satiation signaling contributed to reduced meal duration and size. Furthermore, INT-BDNF(-/-) mice demonstrated increases in total daily intermeal interval and satiety ratio, suggesting that satiety signaling was augmented. Compensatory responses maintained normal daily food intake and body weight in INT-BDNF(-/-) mice. These findings suggest a target organ-derived neurotrophin suppresses development of that organ's sensory innervation and sensory neuron survival and demonstrate a role for BDNF produced by peripheral tissues in short-term controls of feeding, likely through its regulation of development or function of gut innervation, possibly including augmented intestinal IGLE innervation. CI - Copyright (c) 2014 the authors 0270-6474/14/3410379-15$15.00/0. FAU - Biddinger, Jessica E AU - Biddinger JE AD - Behavioral Neurogenetics Laboratory, Department of Psychological Sciences, Purdue University, West Lafayette, Indiana 47907. FAU - Fox, Edward A AU - Fox EA AD - Behavioral Neurogenetics Laboratory, Department of Psychological Sciences, Purdue University, West Lafayette, Indiana 47907 au_gc@psych.purdue.edu. LA - eng GR - R01 NS046716/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PL - United States TA - J Neurosci JT - The Journal of neuroscience : the official journal of the Society for Neuroscience JID - 8102140 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Microfilament Proteins) RN - 0 (Muscle Proteins) RN - 0 (RNA, Messenger) RN - 0 (Tagln protein, mouse) RN - 0 (Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate) SB - IM MH - Analysis of Variance MH - Animals MH - Axons/physiology MH - Body Composition/genetics MH - Body Weight/genetics MH - Brain-Derived Neurotrophic Factor/*deficiency/genetics MH - Eating/genetics MH - Feeding Behavior/physiology MH - Intestines/innervation/*physiology MH - Mice MH - Mice, Transgenic MH - Microfilament Proteins/*genetics MH - Muscle Proteins/*genetics MH - Neurons, Afferent/*physiology MH - Nodose Ganglion/cytology/metabolism MH - RNA, Messenger/metabolism MH - Satiation/*physiology MH - Vagus Nerve/*physiology MH - Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate/metabolism PMC - PMC4115142 OTO - NOTNLM OT - food intake OT - growth factor OT - ingestive behavior OT - meal patterns OT - nodose ganglion OT - vagus nerve EDAT- 2014/08/01 06:00 MHDA- 2014/09/30 06:00 PMCR- 2015/01/30 CRDT- 2014/08/01 06:00 PHST- 2014/08/01 06:00 [entrez] PHST- 2014/08/01 06:00 [pubmed] PHST- 2014/09/30 06:00 [medline] PHST- 2015/01/30 00:00 [pmc-release] AID - 34/31/10379 [pii] AID - 1042-14 [pii] AID - 10.1523/JNEUROSCI.1042-14.2014 [doi] PST - ppublish SO - J Neurosci. 2014 Jul 30;34(31):10379-93. doi: 10.1523/JNEUROSCI.1042-14.2014.