Calcium channel signalling at neuronal endoplasmic reticulum-plasma membrane junctions.

Neurons are highly specialised cells that need to relay information over long distances and integrate signals from thousands of synaptic inputs. The complexity of neuronal function is evident in the morphology of their plasma membrane (PM), by far the most intricate of all cell types. Yet, within the neuron lies an organelle whose architecture adds another level to this morphological sophistication - the endoplasmic reticulum (ER).

The Effect of Electrophoretic Deposition Parameters on the Microstructure and Adhesion of Zein Coatings to Titanium Substrates.

Zein coatings were obtained by electrophoretic deposition (EPD) on commercially pure titanium substrates in an as-received state and after various chemical treatments. The properties of the zein solution, zeta potential and conductivity, at varying pH values were investigated. It was found that the zein content and the ratio of water to ethanol of the solution used for EPD, as well as the process voltage value and time, significantly influence the morphology of coatings.

Transgenic Mice Overexpressing Human and in Neurons Exhibit Changes in Behavior and Calcium Homeostasis but Show No Signs of Neurodegeneration.

The maintenance of proper cytosolic Ca level is crucial for neuronal survival, and dysregulation of Ca homeostasis is found in a variety of neurological disorders, including Alzheimer's disease. According to the "Ca hypothesis of aging", Ca disturbances precede the onset of AD symptoms and lead to neurodegeneration. STIM and ORAI proteins are involved in neuronal physiological and pathological processes as essential components of the store-operated Ca entry.

STIM Protein-NMDA2 Receptor Interaction Decreases NMDA-Dependent Calcium Levels in Cortical Neurons.

Neuronal Store-Operated Ca Entry (nSOCE) plays an essential role in refilling endoplasmic reticulum Ca stores and is critical for Ca-dependent neuronal processes. SOCE sensors, STIM1 and STIM2, can activate Orai, TRP channels and AMPA receptors, and inhibit voltage-gated channels in the plasma membrane. However, the link between STIM, SOCE, and NMDA receptors, another key cellular entry point for Ca contributing to synaptic plasticity and excitotoxicity, remains unclear.

Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing .

Previously, we showed that the overexpression of calcium channel in neurons of murine brain led to spontaneous occurrence of seizure-like events in aged animals of transgenic line FVB/NJ-Tg(ORAI1)Ibd (Nencki Institute of Experimental Biology). We aimed to identify the mechanism that is responsible for this phenomenon. Using a modified Ca-addback assay in the CA1 region of acute hippocampal slices and FURA-2 acetomethyl ester (AM) Ca indicator, we found that overexpression of in neurons led to altered Ca response.

Behavioral and electrophysiological changes in female mice overexpressing ORAI1 in neurons.

Orai proteins form highly selective Ca release-activated channels (CRACs). They play a critical role in store-operated Ca entry (SOCE; i.e.

Overexpression of STIM1 in neurons in mouse brain improves contextual learning and impairs long-term depression.

STIM1 is an endoplasmic reticulum calcium sensor that is involved in several processes in neurons, including store-operated calcium entry. STIM1 also inhibits voltage-gated calcium channels, such as Ca1.2 and Ca3.

Tetrahydrocarbazoles decrease elevated SOCE in medium spiny neurons from transgenic YAC128 mice, a model of Huntington's disease.

Huntington's disease (HD) is a hereditary neurodegenerative disease caused by a polyglutamine expansion within the huntingtin (HTT) gene. One of the cellular functions that is dysregulated in HD is store-operated calcium entry (SOCE), a process in which the depletion of Ca from the endoplasmic reticulum (ER) induces Ca influx from the extracellular space. We detected an enhanced activity of SOC channels in medium spiny neurons (MSNs) from YAC128 mice, a transgenic model of HD, and investigated whether this could be reverted by tetrahydrocarbazoles.