TLS interaction with NMDA R1 splice variant in retinal ganglion cell line RGC-5.

Translocated in liposarcoma (TLS or FUS) is a multifunctional protein component of the heterogenous ribonuclear complex involved in the splicing of pre-mRNA and the export of fully processed mRNA from the nucleus to the cytoplasm. As we determined that TLS was substantially expressed in the adult retina, we investigated the functions of TLS in a rat retinal ganglion cell (RGC) line RGC-5. TLS was found to be associated with N-methyl-d-aspartate (NMDA) receptor 1 (NR1) and myosinVa (MyoVa) in a calcium-dependent manner.

TLS-GFP cannot rescue mRNP formation near spines and spine phenotype in TLS-KO.

RNA-binding protein TLS transports Nd1-L mRNA, which encodes an actin-stabilizing protein, to the neuronal dendrites. TLS-null mouse (TLS-KO) hippocampal neurons display abnormal spine morphology, and thus could be attributed to actin destabilization by the improper supply of Nd1-L mRNA to the dendrites. In this study, we showed that the exogenous expression of TLS in TLS-KO neurons did not rescue the abnormal spine phenotypes.

Imaging of molecular dynamics regulated by electrical activities in neural circuits and in synapses.

One of the major challenges in brain research is to unravel a network of molecules, neurons, circuits and systems that are responsible for dynamic and hierarchical brain functions. To understand molecular events that occur in synapses could be an important key to exploring the mechanism of information processing. A spatiotemporal recording method is required to observe neuronal activities in a particular local circuit and to resolve single synaptic potential with high resolution.

beta-Adrenoceptor-mediated long-term up-regulation of the release machinery at rat cerebellar GABAergic synapses.

Properly regulated interactions among excitatory and inhibitory synapses are critical for brain function. Compared to excitatory synapses, much less is known about the gain control mechanisms at inhibitory synapses. Herein we report a mechanism of noradrenergic long-term potentiation (LTP) at inhibitory synapses following presynaptic beta-adrenoceptor activation.