Elzbieta Rebas has completed her PhD and DSc from Medical University of Lodz. Currently she is an Associate Professor of Department of Molecular Neurochemistry at Medical University of Lodz. She has published a number of papers related to brain function in reputed international journals and participated in many international conferences, congresses and symposia. She has more than 20 years of teaching experience in the field of Biochemistry. She is a Member of FEBS and Council of Polish Biochemical Society.

Many neurodegenerative and affective diseases are related to disturbed metabolism of - aminobutyric acid (GABA) and GABA-shunt enzymes: glutamate decarboxylase (GAD), GABA aminotransferase (GABA-T) and succinate-semialdehyde dehydrogenase (SSADH). Neurological diseases are also often accompanied by impaired calcium conditions. Traditional drugs are not always efficient and may evoke adverse side effects. Chemicals naturally occurring in plants can provide an attractive alternative target in modulating of neurotransmission via affecting of GABA-shunt enzymes activity. The aim of this study was to investigate an effect of selected phytochemicals: genistein and zeaxanthin on activity of GABA-shunt enzymes. In our study we used stably transfected pseudoneuronal PC12 cells with reduced expression of neuron-specific isoforms of calcium membrane pumps: PMCA2 or PMCA3 and increased intracellular calcium concentration. Cells were incubated with 10 M and 20 M of tested compounds during 10 and 20 minutes, a short time precluding genomic action or during 4 and 12 hours. Enzymes activity was determined with fluorimetric and spectrophotometric methods. Additionaly, during GAD activity determination we used vigabatrin, inhibitor of GABA-T. Our results indicate that genistein and zeaxhantin can modulate activity of GABA-shunt, especially glutamate decarboxylase and this way change balance between to oppositely acting neurotransmitters. Genistein decreases GAD activity in all studied lines, but cells with reduced expression of PMCA are more sensitive to genistein. Zeaxhantin inhibits GAD under disturbed calcium homeostasis but increases GAD activity in normal cells. Due to short time of incubation we suggest non-genomic action of studied phytochemicals.

Hannah Palmer has completed her MS in Biomedical Sciences from Duke University School of Medicine. She is currently a Clinical Trials Specialist at Duke University in the Department of Psychiatry and Behavioral Sciences. She conducts research within the division of Brain Stimulation and Neurophysiology using various brain stimulation techniques such as Transcranial Magnetic Stimulation (TMS) and Transcranial Direct Current Stimulation (tDCS) with both clinical populations and healthy volunteers.

Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique that delivers constant, low voltage electrical current to the cortex. This approach has been shown to create changes in cortical excitability leading to greater learning when paired with manual skill training. Laparoscopic surgery requires mastery of bimanual motor skills in order to obtain board certification. Training to proficiency can take extensive time and practice. Therefore, use of tDCS in laparoscopic technical skill training could lead to accelerated motor learning in less time. To test this hypothesis, sixty participants were randomized to active or sham tDCS between two different stimulation configurations: bilateral motor cortex (bM1) and supplementary motor area (SMA). Training included repetition of the Fundamentals of Laparoscopic Surgery (FLS) peg-transfer task over six, 20-min sessions and completion of pre- and post testing sessions of one repetition each. Videos were recorded and scored accounting for errors such as bad transfers and dropping the object outside the field-of-view. Linear mixed effects models were tested comparing the active configurations to sham. A significant main effect of session was observed with increased learning in all groups. Moreover, bM1 stimulation demonstrated significantly greater learning than sham (p<0.03) leading to faster skill acquisition. SMA stimulation produced greater average learning though this condition did not differ significantly from sham. In conclusion, laparoscopic technical skills were enhanced using active bM1 stimulation, demonstrating the potential for noninvasive brain stimulation to aid in learning of manual technical skills in surgery.

Ludmila Zylinska PhD, DSc, is a Full Professor and Head of the Department of Molecular Neurochemistry, Medical University of Lodz, Poland. Her scientific interests are related to regulation of neuronal calcium homeostasis with particular attention brought on plasma membrane calcium pumps in the CNS, as well as on molecular mechanisms of calcium-dependent processes that regulate neuronal transmission in physiological and pathological conditions. She has published more than 60 papers in the areas of Biochemistry, Neuroscience and Cell Biology.

Neurodegeneration is a critical process observed in the ageing brain as well as in neuroinflammatory diseases induced by some chemokines. They constitute a large family of structurally-related small molecules that act by G-protein coupled receptors. Chemokine CCL5 can bind CCR1, CCR3 and CCR5 with downstream activation of PLC/IP3R pathway, thereby mobilizes Ca2+ from endoplasmic reticulum (ER). A low basal cytosolic Ca2+ level is maintained predominantly by plasma membrane Ca2+-ATPase (PMCA) existing in 4 isoforms. In our lab the unique function of PMCA has been studied using a suitable model of pseudo-neuronal differentiated PC12 cells. Since PMCA decreases with age, we have also developed the lines with suppressed PMCA2 or PMCA3 isoform to mimic the aging neurons. In both PMCA-reduced lines CCL5 released more Ca2+ from ER and increased a time required for Ca2+ clearance, but reduction of PMCA2 appeared to be more detrimental for the cells than deficiency of PMCA3. Altered PMCAs composition induced some adaptive mechanisms by changes of CCR5 and IP3Rs expression level, which could provide some protection against calcium overload. However, in aging brain increased BBB permeability, augmented leukocytes infiltration, more severe CCL5 action and long-lasting Ca2+ dyshomeostasis may cause that these compensatory mechanisms could not be sufficient for full cells protection.

Marie-Soleil Houde completed a Master degree in Health Sciences at the University of Ottawa in 2004. She is currently the Lab Coordinator for the Auditory Neuroscience Laboratory of the University of Montreal and work as a Clinical Audiologist at a Rehabilitation Center in Quebec.

Postural control is a complex task that requires the integration of multiple sensory inputs. Long-term deprivation of a sensory modality can modify the relative importance of these inputs in a context of postural control. Indeed, reduced postural control has been reported in hearing-impaired individuals. These impacts on postural control are reflected by the increased risk of falls. If a strong relationship exists between an increased risk of falls and decreased auditory ability, auditory amplification through hearing aids may be an effective preventative tool. If only a few studies have investigated the effect of hearing aids on postural control, they clearly suggest that hearing aids do improve postural control. However, the large prevalence of vestibular impairment in hearing-impaired individuals could be an important confounding factor that was not taken into account by these previous studies. Thus, the aim of the present study was to evaluate the effect of hearing aids on postural control in deaf individuals with and without vestibular impairment. 14 controls and 18 hearing-impaired participants were evaluated while performing a static postural task with and without hearing aids. Prior to postural control assessment, each participant underwent a complete vestibular evaluation. The results suggest that hearing aids improve postural control in challenging conditions but is only beneficial to deaf individuals with concomitant vestibular impairment. The reduced postural sway within this group may be linked to a reduced somatosensory dependence when participants wear hearing aids.

Qian-Quan Sun has completed his PhD from Andrews University and Postdoctoral studies from Stanford University School of Medicine. He is the Director of Wyoming Sensory Biology Center, a NIH funded center of biomedicla excellence. He has published 40 papers in peer reviewed journals.

Malformation of cortical development underlies a significant portion of intellectual and cognitive deficits and intractable epilepsy in human patients. How aberrant synapses of cortical elements contribute to sensory and cognitive deficits remains unclear. Our recent results demonstrate inputs and layer, and cell type specific features of E/I balance. Building on this study, the goal of this study is to understand how canonical cortical circuits in the barrel cortex are maladaptively wired and if the knowledge of this maladaptive wiring helps the understanding of sensory deficits, cognitive problems and epileptiform activities in vivo. Our comprehensive mapping studies identified a hot spot: the L2/3 but not L5B excitatory pyramidal cells (PCs), located far away (~1 mm) from the microgyrus, form maladaptive hyperexcitable circuits that involves de novo inter-laminar and intercolumnar but not intracolumnar excitatory inputs. Functions of somatostatin interneurons were impaired in a layer-specific fashion, consistent with its contribution to the altered excitabilities. Second, combining optogenetic manipulation and multi-electrode array and EEG recordings, we found that this ‘hot spot’ are responsible for the up-state and epileptiform activities under both optogenetic, and whisker-stimulation under light anesthesia. We conclude that sensory and cognitive deficits in this model results from overabundant excitatory innervation in a layer, region and cell-type specific fashion, leading to imbalanced excitation and inhibition. The imbalanced cortical activities may be triggered by the thalamocortical inputs during normal sensory process, and slow wave sleep period, resulting in sensory deficits during awake and spike-wave-discharges during sleep.