Wnt activation promotes β-catenin accumulation upon inhibition of β-catenin degradation. Stabilized β-catenin translocates to the nucleus where it triggers transcription of the Lef1/Tcf target genes. Wnt/β-catenin signaling is essential for nervous system development as well as division and maturation of neuronal progenitors in adult brain. We showed recently that nuclear β-catenin is abundant in vivo in non-dividing neurons of adult thalamus, where it is involved in gene transcription of CACNA1G gene (Wisniewska et al, J Neurosci, 2010). Here we demonstrate spontaneous accumulation of β-catenin in 40% of cultured thalamic neurons and lack of such accumulation in cortical neurons. This phenomenon does not depend on soluble factors produced by glia or cortical neurons, since neither conditioned medium of cortical cells nor glial cells co-culture affect the number of β-catenin positive cells. This suggests that nuclear localization of β-catenin in thalamic neurons is not a consequence of paracrine stimulation. We also observed that Wnt signaling inhibitor DKK1 had no major effect on the number of β-catenin positive thalamic neurons. Thus, autocrine Wnt stimulation is not responsible for nuclear β-catenin accumulation in these neurons. We analyzed expression of APC, AXIN1 and GSK3β that are involved in degradation of β-catenin and detected lower level of APC and GSK3β in thalamus when compared to other brain regions. Our observations support an idea that β-catenin accumulation is an intrinsic feature of thalamic neurons, independent on cellular environment of thalamic neurons and on Wnt stimulation. We propose that accumulation of β-catenin in thalamus is a result of reduced β-catenin degradation rate. This work is supported by “Health-Prot” Grant no 229676 and Polish MNiSW Grant no 4252/B/P01/2010/38.
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