The present study was conducted to evaluate the effect of different salt concentrations (50 and 200 mM NaCl) on growth, permeability properties (electrolyte leakage, cell viability) and activity of glutamine synthetase (GS) and glutamate dehydrogenase (GDH) in roots of maize seedlings. Both salt concentrations significantly affected growth and permeability properties of maize seedling roots and this negative effect increased with concentration of salt and duration of experiments. On the other hand salinity induced only small changes in the activities of GS and GDH, usually small increase in the activity was observed. To characterise the possible protective effect of silicon (Si) on maize roots exposed to saline stress, different concentrations of Si were simultaneously applied to both, low (50 mM) and high (200 mM) salt concentrations. Possible protective effects of Si on studied parameters were analysed in time range of 3 days treatment with the most positive effect on salt-induced root growth inhibition at high salt concentration and electrolyte leakage. The results show significant increase in GDH activity under all the tested conditions, although the mechanisms underlying this increase have not been elucidated. The results indicate that silicon may ameliorate the salt-induced root growth inhibition and increase the plant vigour at stressful conditions.

Neuronal growth factor (NGF) induces neurodifferentiation of PC12 cells into cholinergic neurons-like cells. It was shown that intracellular Ca 2+ ions participate in regulation of the differentiation of PC12 cells. We tested whether L-type calcium channels contribute to Ca 2+ entry which supports neurite outgrowth accompanying NGF-activated differentiation process. Development of morphological changes did correlate with increase of functional expression of L-type calcium channels. However, inhibition of L-type calcium channels by 1 μM of isradipine did not affect significantly an NGF-activated neurite outgrowth.

Acute injury to central nervous system (CNS) triggers neurodegenerative processes that can result in serious damage or complete loss of function. After injury, production of transforming growth factor β1 (TGFβ1) increases and initiates creation of a fibrotic scar that prevents normal growth, plasticity, and recovery of damaged neurons. Administration of TGFβ1 antagonists can prevent its pathological effects. To define consequences of increased TGFβ1 release on calcium signaling, neuronal plasticity, excitability, and mitochondrial dynamics in CNS neurons we directly exposed a rat primary culture of cerebellar granule neurons to TGFβ1. We focused on changes in expression of intracellular calcium transporters, especially inositol-1,4,5-trisphosphate receptor (IP3R) type 1, mitochondrial dynamics, and membrane excitability. TGFβ1 significantly decreased the gene and protein expression of inositol-1,4,5-trisphosphate receptor type 1 and the gene expression of additional intracellular Ca transporters such as IP3R2, ryanodine receptor type 1 (RyR1), RyR2, and SERCA2. Altered calcium signaling suppressed neurite outgrowth and significantly decreased the length of the mitochondria and the frequency of mitochondrial fusion. The resting membrane potential of cerebellar granule neurons was hyperpolarized and slow after depolarization of single action potential was suppressed. LY364947, a blocker of TGFβ1 receptor I, prevented these effects, and IP3 receptor blocker 2-aminoethoxydiphenyl borate (2APB) mimicked them. After CNS injury TGFβ1 downregulates intracellular Ca levels and alters Ca signaling within injured neurons. We suggest that in our model TGFβ1 may trigger both neurodegenerative and neuroprotective events through IP3-induced Ca signaling.

Low-voltage-activated CaV3 channels are distinguished among other voltage-activated calcium channels by the most negative voltage activation threshold. The voltage dependence of current activation is virtually identical in all three CaV3 channels while the current kinetics of the CaV3.3 current is one order slower than that of the CaV3.1 and CaV3.2 channels. We have analyzed the voltage dependence and kinetics of charge (Q) movement in human recombinant CaV3.3 and CaV3.1 channels. The voltage dependence of voltage sensor activation (Qon-V) of the CaV3.3 channel was significantly shifted with respect to that of the CaV3.1 channel by +18.6 mV and the kinetic of Qon activation in the CaV3.3 channel was significantly slower than that of the CaV3.1 channel. Removal of the gating brake in the intracellular loop connecting repeats I and II in the CaV3.3 channel in the ID12 mutant channel shifted the Qon-V relation to a value even more negative than that for the CaV3.1 channel. The kinetic of Qon activation was not significantly different between ID12 and CaV3.1 channels. Deletion of the gating brake in the CaV3.1 channel resulted in a GD12 channel with the voltage dependence of the gating current activation significantly shifted toward more negative potentials. The Qon kinetic was not significantly altered. ID12 and GD12 mutants did not differ significantly in voltage dependence nor in the kinetic of voltage sensor activation. In conclusion, the putative gating brake in the intracellular loop connecting repeats I and II controls the gating current of the CaV3 channels. We suggest that activation of the voltage sensor in domain I is limiting both the voltage dependence and the kinetics of CaV3 channel activation.

Abstract. Neurodegeneration comprises assembly of pathophysiological events that gives rise to a progressive loss of neuronal structure and function including cellular damage, diseases development or cellular death. Neurons respond by adjusting signaling pathways, from gene expression to morphological changes. In most of these processes, Ca 2+ signaling plays a pivotal role. By increasing the Ca 2+ concentration, the cell responds to neuronal, neurotrophic and other growth factor stimuli, however, the molecular mechanism of Ca 2+ -dependent neurite outgrowth and development yet requires further elucidation.Here we focus on the role of Ca 2+ and selected Ca 2+ transporters involved in processes of CNS neurodegeneration -inositol 1,4,5-trisphosphate (IP 3 Rs) and ryanodine receptors (RyRs), considering the fact that these receptors may be important "sensors" of disturbed intracellular calcium homeostasis. We propose that in vitro cellular models could serve as suitable experimental systems for the determination of the role that these receptors play in neuropathological conditions.Recognition of the principles, key players and regulatory processes may elucidate the role of Ca 2+ in the regulation of neuronal proliferation, development and differentiation, growth and axon navigation in neurodegenerative and regenerative processes. This may provide a new insight and also discovery of novel therapeutic-targeting possibilities for severe neurological disorders and pathophysiological changes.

No abstract

In the present study the impact of beauvericin (BEA) on the cell membrane properties and respiration of young initial leaves of maize were studied using two maize cultivars differing in their susceptibility to Fusarium sp. BEA significantly depolarized E M of leaf parenchymal cells and this depolarization showed time and dose dependency regardless on the sensitivity of maize cultivars to Fusarium. However, the extent of BEA-induced depolarization was 2-5 times higher in sensitive cv. Pavla than in tolerant cv. Lucia. Membrane permeability and K + leakage from leaves cells treated with BEA was higher in sensitive cv. Pavla but the differences were not so considerable than the depolarization of E M . Treatment of maize young initial leaves with 40 μmol BEA significantly inhibited respiration. In accord with electrophysiological measurements inhibition of respiration was higher in sensitive cv. Pavla showing 70% inhibition already after 90 min of BEA treatment while in tolerant cv. Lucia inhibition represented only 27%. The biological activity of BEA seems to be mediated by the ability of BEA to affect membrane permeability and ion transport. This is probably the initial effect of BEA on plant cell leading to subsequent effect on other cell organelles (mitochondria) and cell metabolism.

Effects of fusaproliferin (FUS) on membrane potential (EM), electrolyte leakage, enzymes activity and respiration of roots, were studied in two maize cultivars (Zea mays L.), differing in their susceptibility to this toxin. In short-term experiments (≤ 6 h), EM has been rapidly and significantly depolarized by FUS. The rapidity of EM depolarization in tolerant cv. Lucia was more expressive in comparison with susceptible cv. Pavla, but the extent of EM depolarization was higher in cv. Pavla. In both maize cultivars, higher depolarization of EM was registered in cells of root zone I. In long-term experiments after the first EM depolarization, which occurred during the first 6 h of FUS treatment, gradual depolarization continued up to 24 h and was represented not only by the active component (EP) but also by the passive component (ED) of EM. The decrease in EM and ED was followed by a loss of K + ions from FUS treated roots of both cultivars. The leak of K + ions from the root cells of both root zones as well as both maize cultivars increased with the time of FUS treatment and was significantly higher in susceptible cv. Pavla than in tolerant cv. Lucia. FUS treatment of maize roots resulted in a significant decrease of root respiration which was higher in susceptible cv. Pavla than in tolerant cv. Lucia. The analysis of enzyme activities revealed that FUS significantly stimulated POD activity in both maize cultivars. SOD activity was significantly increased only in susceptible cv. Pavla, while APX activity was not affected by the presence of FUS. GST activity was specifically induced by FUS only in tolerant cv. Lucia. Due to the observed correlation between the extent of depolarization and the sensitivity of the studied maize cultivars to fusaproliferin, the EM parameters should be used for rapid screening of FUS-resistant cultivars for agricultural practice.