Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effect of ciliary neurotrophic factor (CNTF) on behavior and morphology of hippocampal neurons were observed and its mechanisms in rats were explored by Nissl staining, Bielschowsky-Gros-Lawrentjew staining, transmission electron microscopy, behavior determination, primary culture of hippocampal neuron, running photography of living cell, whole-cell patch clamp recording, detection of intracellular free Ca2+ and immunohistochemical detection of P53 protein. The results showed that there was no statistically significant change in the morphology of hippocampal neurons as a result of acute stress. The behavioral activity was increased during acute stress stage, which was not affected by CNTF. In chronic stress stage, neuronal damage in hippocampus was significant, and behavioral activity was significantly decreased under basal line. Administration of CNTF into bilateral hippocampus prevented neurons from damage and improved behavior. In vitro, CNTF could significantly suppress channel current, intracellular Ca2+ content and the expression of P53 protein in the nucleus induced by glutamate. The results suggested that the protective effect of CNTF may involve rapid effects on cell membrane and cytoplasma, and delayed effects on nucleus, thereby improve behavioral defects.
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PMID:[Protective effect of ciliary neurotrophic factor on the hippocampal neuronal damage induced by stress and its mechanisms in rats]. 1254 30

Previously we reported delayed cell death, defined by clear-cut cell loss 60 days after a nitrite-induced hypoxic episode. The loss of cells was not apparent two weeks after the treatment, although some changes in cellular appearance were observed at that time. A similar delayed loss of neurons in the hippocampus after hypoxia induced by blood vessel occlusion has also been found. In addition, we reported that the amount of methemoglobinemia induced by the sodium nitrite can be reduced by the stress produced by handling and the injection of saline 2 or 24 h before the nitrite administration. The degree of methemoglobin formed is directly related to cell death in certain areas of the brain, including regions within the hippocampus. Considering the many effects that can be produced by chronic and acute stress of several kinds and the length of time during which these effects manifest themselves, we undertook to determine the histologic effects of the stresses of transport on the neuroanatomic effects of sodium nitrite administration 60 days post administration. Comparisons were made of the effects of two methods of transport from the laboratory in which the animals (male CD-1 mice) were injected with the sodium nitrite or saline (Tufts Medical School) to the laboratory in which the histologic evaluations were made (Binghamton University). The animals began their travel several hours after the injections. One transport method was by commuter airline and the other was by automobile. All animals had the same transport from the supplier to the Boston location (truck). Thus, the stress of experimental interest occurred after the nitrite administration. Upon arrival at Binghamton University, the animals were housed at the University in their own colony room for 60 days before sacrifice. After sacrifice, sections from their brains were subjected to a number of histologic staining procedures, including PTAH, the Bielschowsky silver method, GFAP, and the standard Nissl procedure. Although special attention was paid to hippocampal areas, changes in cells in the habenulae and the linings of ventricular areas were also prominent. Surprisingly, the nitrite treatment before transport to Binghamton offered partial protection against the very substantial and lasting effects of the injections, transport, and handling found in the control animals. Differential effects caused by the two methods of transport were also noted.
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PMID:Environmental conditions unexpectedly affect the long-term extent of cell death following an hypoxic episode. 1285 12