Electrical impedance myography method of measuring anisotropic tongue tissue.

Objective.To date, measurement of the conductivity and relative permittivity properties of anisotropic biological tissues using electrical impedance myography (EIM) has only been possible through an invasiveex vivobiopsy procedure. Here, we present a novel forward and inverse theoretical modeling framework to estimate these properties combining surface and needle EIM measurements.Methods. The framework here presented models the electrical potential distribution within a monodomain, homogeneous, and three-dimensional anisotropic tissue. Finite-element method (FEM) simulations and tongue experimental results verify the validity of our method to reverse-engineer three-dimensional conductivity and relative permittivity properties from EIM measurements.Results. FEM-based simulations confirm the validity of our analytical framework, with relative errors between analytical predictions and simulations smaller than 0.12% and 2.6% in a cuboid and tongue model, respectively. Experimental results confirm qualitative differences in the conductivity and the relative permittivity properties in thex,y, andzdirections.Conclusion. Our methodology enables EIM technology to reverse-engineer the anisotropic tongue tissue conductivity and relative permittivity properties, thus unfolding full forward and inverse EIM predictability capabilities.Significance. This new method of evaluating anisotropic tongue tissue will lead to a deeper understanding of the role of biology necessary for the development of new EIM tools and approaches for tongue health measurement and monitoring.

RTP801 regulates motor cortex synaptic transmission and learning.

BACKGROUND: RTP801/REDD1 is a stress-regulated protein whose upregulation is necessary and sufficient to trigger neuronal death in in vitro and in vivo models of Parkinson's and Huntington's diseases and is up regulated in compromised neurons in human postmortem brains of both neurodegenerative disorders. Indeed, in both Parkinson's and Huntington's disease mouse models, RTP801 knockdown alleviates motor-learning deficits. RESULTS: We investigated the physiological role of RTP801 in neuronal plasticity and we found RTP801 in rat, mouse and human synapses. The absence of RTP801 enhanced excitatory synaptic transmission in both neuronal cultures and brain slices from RTP801 knock-out (KO) mice. Indeed, RTP801 KO mice showed improved motor learning, which correlated with lower spine density but increased basal filopodia and mushroom spines in the motor cortex layer V. This paralleled with higher levels of synaptosomal GluA1 and TrkB receptors in homogenates derived from KO mice motor cortex, proteins that are associated with synaptic strengthening. CONCLUSIONS: Altogether, these results indicate that RTP801 has an important role modulating neuronal plasticity and motor learning. They will help to understand its role in neurodegenerative disorders where RTP801 levels are detrimentally upregulated.