Abstract

Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family involved in plasticity and neuroprotective processes. In recent years, we have reported the presence of BDNF mRNA in the supraoptic nucleus (SON) as well its sensitivity to osmotic stress. The rat SON is a relatively homogenous nucleus mainly consisting of magnocellular soma with their dendritic processes. BDNF may be released from dendrites to the extracellular space to stimulate tyrosine kinase (Trk) B receptors which are hypothetically present on these subcellular SON compartments. The main goal of this work was thus to study the presence and the in vivo BDNF-IR release from SON using the push-pull perfusion technique following systemic (i.p.) or local (within the SON) osmotic stimulation. BDNF was detected by immunocytochemistry and its release was measured by immunological assay (ELISA). Likewise, TrkB receptor localization in the SON-mRNA and their respective proteins-were studied by in situ hybridization and immunohistofluorescence techniques, respectively. Phosphorylation of CREB was detected by immunohistofluorescence. We present here direct evidence of in vivo dendritic BDNF release from SON which is highly sensitive to osmotic stress. The osmotic response latency period clearly depends on the mode of stimulus application (210 min for i.p. route vs. 15 min for intra-SON administration). The fact that BDNF is released as a very rapid peak when osmotic stimulation is locally applied is strong evidence in favor of an intra-SON origin of this secretion. Osmotic stress also increased phosphorylated cAMP response element binding protein immunoreactivity in the SON. In addition, we show in control rats that truncated forms of tyrosine kinase B receptor 2 mRNA represent the most abundant messenger in the SON as compared with brain-derived neurotrophic factor full-length catalytic receptor or truncated forms of tyrosine kinase B receptor 1 mRNA. In conclusion, it is likely that BDNF and their receptors are involved in neuronal plasticity changes induced by osmotic stress in the SON. © 2007 IBRO.