Conclusion In 24 h after treatment with ketamine, the expression of synaptophysin was decreased in hippocampl neural cells, the number of apoptotic neuronal cells were increased, which may be involved in neurotoxicity caused by ketamine.
After using naloxone the increase range of the Ca2+i under hypoxia and after giving oxygen condition significantly reduced compared with hypoxia group which suggests that naloxone has stable action on hypoxia neuron Ca2+i and can decrease the increase of neuron Ca2+I to play a protective action on neuron cells.
Methods The primary cultured neuron cell of l8-day-pregnan embryoid Sprague-Dawley rat's hippocampus has been selected as the experimental material. The experimental concentration of magnesium sulfate will be 0 mmol/L,1 mmol/L,2 mmol/L,4 mmol/L;
In Gansu zokor, the vomeronasal epidermis thickness in adult males, the zones width of accessory olfactory bulb granular cells and the mitral cells are remarkably wider than that of the females (P<0.05). But the length of vomeronasalmucous, the density of vomeronasal epidermis neuron cells, the diameter of neuron cell nucleus, the zones length of accessory olfactory bulb granular cells and the mitral cells in females and males are no significant difference (P>0.05).
Methods neurons were randomly divided into normal control(24 h,48 h) group,hydraulic impact injury(24 h,48 h) model group,taurine group(to hydraulic impact injury at 24 h,48 h),alteration in Ca2+ in SD rat's neuronal cell following hydraulic impact injury was measured by means of a confocal laser scanning microscope using Fluo-3/AM as a calcium indicator.
②Hippocampus neuronal cell activity: The cell activity was obviously higher in control group and Rg1 pretreatment groups of 2 and 4 μmol/L than in model group (P < 0.05), and the highest in Rg1 pretreatment group of 4 μmol/L;
The extracellular matrix molecules constitute the basement membrane underlying the vasculature and play a critical role in maintaining the integrity of the BBB. After stroke, there is a breakdown of the BBB by activated MMP -9 with an associated increase in vascular permeability, inflammatory cell influx, and neuronal cell death.
The expression of β-III tubulin, a marker protein of early neuronal cells, was studied by molecular genetic and immunochemical techniques.
β-Amyloid peptide (Aβ), a normal constituent of neuronal and non-neuronal cells, has been proved to be the major component of extracellular plaque of Alzheimer's disease (AD).
Role of Lipids in the Assembly of Endoplasmic Reticulum and Dictyosomes in Neuronal Cells from the Cerebral Cortex of Yakutian G
Since leukocytes are much more available than hepatocytes or neuronal cells in humans, we assume that CE in peripheral blood leukocytes (neutrophils and monocytes) can be used as markers for indication of pending liver damage by CPZ.
When Na/K-ATPase was inhibited by high ouabain concentrations (10-5-5·10-4 M), an increase in stationary ROS level in neuronal cells was noted, this effect being attenuated by NMDA antagonists, MK-801 and D-AP5.
Unlike skeletal muscles that can survive for hours without oxygen, neuron cells in the brain are easily subjected to an irreversible damage within minutes from the onset of oxygen deficiency.
Dactylorhin B reduces toxic effects of β-amyloid fragment (25-35) on neuron cells and isolated rat brain mitochondria
Indeed, foot and mantle mucocytes exhibited muramic acid in a terminal position, linked to (subterminal) N-acetylgalactosamine, whereas in neuron cells muramic acid was present in an internal position and linked to N-acetylglucosamine.
In bursting excitable cells such as pancreaticβ-cells and molluscanAplysia neuron cells, intracellular Ca2+ ion plays a central role in various cellular functions.
As shown by MTT test, PrP106-126 induced significant death of neuron cells and marked proliferation of astrocytes after 10 days of treatment.
Studies of mechanisms involved in neuronal cell death induced by chronic stress in rats
Mechanisms of peroxynitrite-induced [Ca2+]i increase in single neuronal cell
A proteomic analysis of the effect of mapk pathway activation on l-glutamate-induced neuronal cell death
In this study, we used proteomic analysis to investigate the role of the MAPK pathway in oxidative stress-induced neuronal cell death.
The results demonstrated that several proteins, including eukaryotic translation elongation factor 2 (eEF2) and enolase I, showed a differential expression pattern during the neuronal cell death process, and this was MAPK pathway dependent.