Differential expression of neurotrophins in postnatal C57BL/6 mice striatum

Abstract

Neurotrophin expression in early stages of development is crucial for brain assembly and function. In particular, postnatal expression of neurotrophins has not been well documented in the neostriatum and in general neurotrophins or their receptor mRNA's are normally reported, but not protein expression. In the present study, immunocytochemical expression of BDNF, NT-3 and NT-4/5 was characterized in striatal tissue of C57BL/6 mice at postnatal days 10 th (P10), 21 st (P21), 42 nd (P42) and 80 th (P80). We found that the expression of BDNF diminished along the postnatal time course we evaluated, while staining for NT-4 increased up to age P42 and remained constant, thereafter in the cell's soma. In contrast, NT-3 was first expressed in the neostriatal bundles and later on, in neostriatal cell somas. These results provide information about differences in the spatial and temporal expression of each neurotrophin in the neostriatum during the first 80 th postnatal days. RT-PCR procedures were also carried out to further determine whether protein levels of neurotrophins observed in the neostriatum were under control of gene expression. All neurotrophin mRNAs were expressed and only mRNA BDNF was reduced during the postnatal evaluated days. Differences in temporal expression of neurotrophins may be related to the heterochronic development of neostriatal cell populations, but also with the specificity of each neurotrophin modulating different neuronal targets.

3-Nitropropionic acid modifies neurotrophin mRNA expression in the mouse striatum: 18S-rRNA is a reliable control gene for studies of the striatum

“…In this regard, we did not find a significant change in proposed that NT-4/5 can replace BDNF deficiency to promote the survival [43] of specific striatal neuronal populations [44] . We have demonstrated that NT-4/5 becomes detectable in striatal cells after BDNF during postnatal development [45] , and since there is no evidence that it comes from the cortex, it is possible that NT-4/5 is produced by cells that are not as sensitive to 3-NP as those that respond to BDNF. administration.…”

“…This increase suggests that NT-3 plays an important trophic role in striatal function. NT-3 may be released into the striatum from corticostriatal afferents [45] and protect striatal cells [46] by activating the TrkC receptor and MAPK/ERK and PI-3K/Ark signaling pathways [41] .…”

Reduced Intestinal Brain-Derived Neurotrophic Factor Increases Vagal Sensory Innervation of the Intestine and Enhances Satiation

“…To visualize vagal afferent axons and terminals in the GI tract of control, INT-BDNF ϩ/Ϫ , and INT-BDNF Ϫ/Ϫ mice, the nerve tracer horseradish peroxidase conjugated to wheat-germ agglutinin (WGA-HRP) was injected into the left nodose ganglion (controls, n ϭ 15; INT-BDNF ϩ/Ϫ , n ϭ 11; and INT-BDNF Ϫ/Ϫ , n ϭ 12). This method was used because, to date, it has been the most successful for labeling consistent, large numbers of vagal sensory elements supplying the GI wall and, therefore, has been the most useful for quantification of vagal sensory axons and their terminal endings, as well as for making quantitative comparisons of these elements between groups of mutant and control animals (Fox et al, , 2001a(Fox et al, ,b, 2002Wang and Powley, 2000). The left nodose was chosen for injections because it was known to provide much greater innervation to the proximal intestine compared with the right nodose ganglion in mice and rats (Fox et al, , 2001bWang and Powley, 2000).…”

“…One of these pathways, vagal afferents, expresses trkB during development and maturity (Ernfors et al, 1992;Wetmore and Olson, 1995), and BDNF knock-out (KO) results in substantial loss of vagal afferents and disrupts survival or formation of vagal mechanoreceptors that supply the neonatal stomach wall (Jones et al, 1994;Erickson et al, 1996;Fox and Murphy, 2008;Murphy and Fox, 2010). These findings suggest that some vagal afferents may depend on GI BDNF for survival or other aspects of development.…”

“…Additionally, BDNF loss from mature GI tissues could alter vagal GI afferents by perturbing their maintenance as demonstrated for vagal baroreceptors or by disrupting their sensory transduction as shown for some cutaneous mechanoreceptors (Carroll et al, 1998;Postigo et al, 2002). Among vagal GI afferents, intraganglionic laminar endings (IGLEs) are the predominant vagal mechanoreceptor innervating GI smooth muscle (SM) and are concentrated in the region of the upper GI tract in which most food collects during consumption of a meal Wang and Powley, 2000). They consist of plates of densely packed terminal puncta that innervate myenteric ganglia and are activated by muscle wall tension or stretch and possibly by satiation hormones, such as CCK (Rodrigo et al, 1982;Schwartz and Moran, 1994;Zagorodnyuk et al, 2001).…”