Prolonged ethanol abuse has been associated with brain injury. In rodents, postnatal exposure to ethanol has been shown to be a major contributing factor to neurodegeneration in the hippocampus and cortex, leading to deficits in synaptic function and memory. Among the potential mechanisms involved in ethanol-induced brain damage, oxidative stress is considered a primary factor. However, the molecular mechanisms underlying ethanol-induced neurotoxicity remain incompletely understood. Evidence suggests that ethanol impairs the functions of both the cytoskeleton and cellular membranes, resulting in alterations to neuronal physiology. The plasma membrane of eukaryotic cells contains microdomains enriched in specific glycosphingolipids, gangliosides, and cholesterol, collectively forming membrane/lipid rafts (MLRs). As demonstrated in previous studies, MLRs function as scaffolds for a variety of molecular entities, including signaling receptors and ion channels. In addition, they mediate the organisation of the cytoskeleton. Indeed, numerous cytoskeletal components, their binding partners, and enzymes that regulate cytoskeletal dynamics localise to MLRs and contribute to the regulation of the lateral diffusion of membrane proteins and lipids in response to extracellular stimuli. The objective of the present research was to examine the effects of ethanol on the cytoskeleton, specifically actin and tubulin, in C6 glioma cells.

Detecting moving objects is crucial in the animal kingdom and is fundamental to vision. In the vertebrate retina, starburst amacrine cells (SACs) are directionally selective in terms of their calcium responses to stimuli that move centrifugally from the soma. The mechanism by which starburst amacrine cells show calcium bias for centrifugal motion is still to be determined. Recent morphological studies using fluorescent microscopy and immunostaining have shown that the endoplasmic reticulum is omnipresent in the soma, extending to the distal processes of starburst amacrine cells. Electron microscopy for ChAT SAC in adult rat retina unequivocally proves the presence of local endoplasmic reticulum (ER) extending through the dendritic branches of SAC and the submicron diameter of the ER in SAC dendrites suggests that the ER is not luminally connected between the soma and the distal tips. We construct a computational model of a SAC dendrite with an ER to simulate the Ca2+-induced Ca2+ release (CICR)-based calcium waves in the presence of an unsaturated buffer to test the hypothesis a CICR mechanism can sustain constant calcium wave propagation in the centrifugal direction. Here, we focus on a working hypothesis, in which a CICR mechanism in the presence of local ER underlies the preference for directionality in the centrifugal direction and rather than the centripetal direction. Modeling the heterogeneity of calcium ER in simulated SACs sheds light on a possible explanation for the cause of speed tuning of direction-selective Ca2+ responses in dendrites of SACs. A simulation of the calcium-induced-calcium release-based Ca2+ waves in the presence of an unsaturated buffer is presented using an analytically derived solution of the two-pool model for cytosolic calcium. We find the conditions that support the calcium-induced calcium-release-based propagating Ca2+ wavefront in the centrifugal direction and its relation to where measurements are made. This suggests CICR from the ER can provide an initial seed underlying directionality in SAC.

​Epileptic seizures are often described as transitions into hypersynchrony, disorder or increased entropy. Prior neurotopological work argued that epileptic pathology may also be interpreted as breakdown of network geometry rather than entropy increase alone (Salazar Chon & Kadhim, 2025). Here, I report an expanded exploratory reconstruction of transition structure in a public HUP intracranial EEG cohort. The analysis used 85 derived ictal runs from 22 subjects and expanded the interictal control layer to 42 interictal pseudo-onset runs from 21 subjects. Markers were organized into algorithm-defined transition families, temporal first-crossing sequences, circular time-shift null controls and expanded ictal-versus-interictal screening. Across the expanded control, ictal runs showed stronger transition-risk escalation than interictal pseudo-onset segments at run level, subject level and matched-subject level. Early risk gain was higher in ictal runs at run level (median 0.4573 versus -0.0932, p