In vivo brain-derived neurotrophic factor release and tyrosine kinase B receptor expression in the supraoptic nucleus after osmotic stress stimulus in rats

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.