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This thesis describes experiments designed to investigate the effects of neuromuscular electrical stimulation (NMES) on corticospinal (CS) excitability in humans. NMES delivered at 100 Hz was more effective for increasing CS excitability than 10-, 50-, or 200-Hz NMES. CS excitability increases occurred after 24 min of 100-Hz NMES, were strongest in the stimulated muscle, and were mediated primarily at a supraspinal level. NMES of the common peroneal nerve of the leg increased CS excitability in multiple leg muscles, whereas NMES of the median nerve of the hand increased CS excitability in only the muscle innervated by that nerve. Additionally, CS excitability for the hand increased after 40 min of relatively high intensity and frequency NMES but not after 2 h of lower intensity and frequency NMES. These results have implications for identifying optimal NMES parameters to augment CS excitability for rehabilitation after central nervous system injury.

Listeners with severe-sloping losses often don’t perceive high-frequency sound cues. Conventional amplification fails to provide these cues due to loudness discomfort experienced by the listener, and/or acoustic feedback. Alternative signal-processing solutions include shifting higher frequencies down to lower frequencies, or providing electrical stimulation via a speech processor. Three experiments were carried out on adult hearing-impaired listeners to determine the best way of providing high-frequency information: conventional amplification, frequency compression or cochlear implantation.

This diploma thesis deals with study of the rate-dependence of the magnitude of a current through the heart channel that conducts slowly activating component of delayed rectifier outward current (IKs). This property is very important for the IKs channel function. When other repolarizing currents are insufficient, but also when the heart rate accelerates, especially during elevated sympathetic tone, IKs provides so-called repolarization reserve, which prevents excessive lengthening of cardiac action potential repolarization. The IKs channel structure is encoded by the KCNQ1 (pore-forming -subunit) and KCNE1 (modulatory -subunit) genes. Mutations in these genes disrupt the physiological function of the IKs channel and cause inherited arrhythmogenic syndromes, especially long QT syndrome (LQTS). Such mutations include the c.926C>T (p.T309I) mutation in the KCNQ1 gene, which results in LQTS type 1 in heterozygous carriers. The theoretical part of the thesis provides basic information about the IKs channel and the patch clamp technique, this knowledge is necessary for the practical part. The experimental part is focused on cultivation of the CHO cell line and its transient transfection for subsequent electrophysiological measurements by whole-cell patch clamp technique to study the dependence of the IKs magnitude on stimulation frequency, both in the wild type channels (i.e. without mutation) and in those with cotransfected wild type and T309I subunits.