PMID- 18234244 OWN - NLM STAT- MEDLINE DCOM- 20080709 LR - 20211020 IS - 0031-9384 (Print) IS - 0031-9384 (Linking) VI - 94 IP - 1 DP - 2008 Apr 22 TI - Factors regulating vagal sensory development: potential role in obesities of developmental origin. PG - 90-104 LID - 10.1016/j.physbeh.2007.11.024 [doi] AB - Contributors to increased obesity in children may include perinatal under- or overnutrition. Humans and rodents raised under these conditions develop obesity, which like obesities of other etiologies has been associated with increased meal size. Since vagal sensory innervation of the gastrointestinal (GI) tract transmits satiation signals that regulate meal size, one mechanism through which abnormal perinatal nutrition could increase meal size is by altering vagal development, possibly by causing changes in the expression of factors that control it. Therefore, we have begun to characterize development of vagal innervation of the GI tract and the expression patterns and functions of the genes involved in this process. Important events in development of mouse vagal GI innervation occurred between midgestation and the second postnatal week, suggesting they could be vulnerable to effects of abnormal nutrition pre- or postnatally. One gene investigated was brain- derived neurotrophic factor (BDNF), which regulates survival of a subpopulation of vagal sensory neurons. BDNF was expressed in some developing stomach wall tissues innervated by vagal afferents. At birth, mice deficient in BDNF exhibited a 50% reduction of putative intraganglionic laminar ending mechanoreceptor precursors, and a 50% increase in axons that had exited fiber bundles. Additionally, BDNF was required for patterning of individual axons and fiber bundles in the antrum and differentiation of intramuscular array mechanoreceptors in the forestomach. It will be important to determine whether abnormal perinatal environments alter development of vagal sensory innervation of the GI tract, involving effects on expression of BDNF, or other factors regulating vagal development. FAU - Fox, Edward A AU - Fox EA AD - Behavioral Neurogenetics Laboratory, Ingestive Behavior Research Center, Department of Psychological Sciences, Purdue University, West Lafayette, IN 47907, USA. au_gc@psych.purdue.edu FAU - Murphy, Michelle C AU - Murphy MC LA - eng GR - R01 NS046716/NS/NINDS NIH HHS/United States GR - R01 NS046716-03/NS/NINDS NIH HHS/United States GR - NS046716/NS/NINDS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20071122 PL - United States TA - Physiol Behav JT - Physiology & behavior JID - 0151504 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Carbocyanines) RN - 84109-08-0 (carbocyanine dye DiIC12(3)) RN - EC 2.7.10.1 (Receptor, trkB) RN - EC 3.2.1.23 (beta-Galactosidase) SB - IM MH - Animals MH - Animals, Newborn MH - Axons/physiology/ultrastructure MH - Brain-Derived Neurotrophic Factor/biosynthesis/genetics/*physiology MH - Carbocyanines MH - Female MH - Gastric Mucosa/metabolism MH - Mice MH - Mice, Knockout MH - Mutation/physiology MH - Neurons, Afferent/physiology MH - Neurons, Efferent/physiology MH - Obesity/*physiopathology MH - Pregnancy MH - Receptor, trkB/physiology MH - Stomach/embryology/innervation MH - Vagus Nerve/*growth & development/*physiology/physiopathology MH - beta-Galactosidase/metabolism PMC - PMC2399896 MID - NIHMS49980 EDAT- 2008/02/01 09:00 MHDA- 2008/07/10 09:00 PMCR- 2009/04/22 CRDT- 2008/02/01 09:00 PHST- 2007/10/31 00:00 [received] PHST- 2007/11/15 00:00 [accepted] PHST- 2008/02/01 09:00 [pubmed] PHST- 2008/07/10 09:00 [medline] PHST- 2008/02/01 09:00 [entrez] PHST- 2009/04/22 00:00 [pmc-release] AID - S0031-9384(07)00466-0 [pii] AID - 10.1016/j.physbeh.2007.11.024 [doi] PST - ppublish SO - Physiol Behav. 2008 Apr 22;94(1):90-104. doi: 10.1016/j.physbeh.2007.11.024. Epub 2007 Nov 22.