Vagal sensory neurons are dependent on neurotrophins to survive programmed cell death during development. Here, the contribution of brain-derived neurotrophic factor (BDNF) to the survival of gastric vagal sensory afferents was investigated. Also, based on BDNF roles in other sensory systems, its effects on axon guidance and mechanoreceptor differentiation were examined. Postmortem anterograde tracing with 1, 1’-dioctadecyl-3,3,3’,3’-tetramethylindocarbocyanine perchlorate (DiI) was used to selectively label vagal projections to the stomach on postnatal day (P)0, 3, 4, and 6 in wild types and heterozygous or homozygous BDNF mutants. Sampling sites distributed throughout the ventral stomach wall were scanned with a confocal microscope and vagal axon bundles, single axons, putative mechanoreceptor precursors (intraganglionic laminar endings, IGLEs; intramuscular arrays, IMAs) and efferent terminals were quantified. Also, myenteric neurons, which are innervated by IGLEs, were stained with cuprolinic blue and quantified. In homozygous mutants, at P0, IGLE density was reduced by 50% without any effect on myenteric neurons or vagal efferents. Also, putative IMA precursors exhibited truncated telodendria, and antrum innervation was disorganized. At P3-P6, the effects on IGLEs and antrum innervation still occurred, but to a lesser degree, some IMA telodendria were still truncated, and there was a large, but non-significant trend toward decreased IMA density (42%). These results suggest BDNF contributes to the survival of subpopulations of gastric IGLEs and possibly IMAs (or to IMA differentiation) and to patterning of antral innervation. Additionally, it is possible that other growth factors expressed in the stomach wall compensated for BDNF deficiency and reduced the losses of mechanoreceptors.


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