Research Achievments
2002-2005. Evidence that appropriate neural activity is important to the development of synapses and neurons
Using a mouse model for congenital deafness, I have studied the effect of lack of activity to the development of synapses and neurons from the auditory neural system. Using electrophysiology, immunohistochemistry and mathematical modeling, I have demonstrated that inhibitory synapses of the medial nucleus of the trapezoid body (MNTB) preserve embryonic features throughout developed stages, causing inhibitory currents to be slower than currents in normal littermates. MNTB neurons also display greater excitability due to a decrease in potassium currents and an increase in hyperpolarization-activated currents. These results are published in mainstream journals. Activity is also critical to the development of intrinsic rhythms in spontaneous synaptic release. I have shown that the determinism found in miniature inhibitory postsynaptic currents (mIPSC) is not found in deaf mice cells.
2002-2005. Study of basic synapse mechanisms and the application of nonlinear techniques to the analysis of synaptic events
Issues regarding the contribution of internal calcium stores in the modulation of spontaneous synaptic release are controversial. I have investigated the relationship between ryanodine Ca2+ stores and mIPSC using pharmacology and nonlinear mathematical techniques. The blockage of ryanodine stores did not change mIPSC amplitude, frequency or kinetics. However, the deterministic nature of spontaneous release vanished and mIPSC appeared to be random with the blocking of ryanodine stores [4]. These results suggested that spontaneous events and ryanodine stores interact as loosely coupled oscillators.
2001. Involvement of stretch reflex in spasticity and development of computational tools to improve electromyographic signal analysis
I have studied stretch reflex in humans using surface electromyography (sEMG) while an external device provokes mechanical perturbations in a given joint. By extracting torque responses at different perturbation frequencies, a computer model was able to predict the contributions of passive (no muscle contraction) and active (muscle contraction) components in joint stiffness. Using these techniques, my results indicated that the effect of passive factors were more important to the development of spasticity (in stroke patients) than active factors (i.e. stretch reflex). During this period I have also tried to contribute to the analyses and parameterisation of sEMG signals. sEMG is a robust, non-invasive tool for the analyses of electrical activity of nerves and muscles. However, the complexity of sEMG caused by unpredictable interactions of excitable tissues with non-excitable structures impairs the interpretation of these signals. I have developed a technique based on wavelet transform that improves the temporal resolution and normalise sEMG to be compared between different subjects. This technique is published in.
1998-1999. Development of a computational model to study the effect of non-neural structures to the electrical stimulation of the cochlea
Electrical stimulation of the auditory nerve through cochlear implants is one of the most important achievements of biomedical engineering aiding patients. Yet, little is known about the electrical potentials that a given stimulus provoke along different cochlea regions, thus, the prediction of which neural fibres are being stimulated by a given electrode. I have worked in conjunction with Prof. F. Rattay, from the Vienna University of Technology, in the development of a comprehensive model of the electrically stimulated cochlea using finite element. Our model predicts important aspects of nerve stimulation and helps to develop stimulation strategies.
