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

Stress-induced cortical alertness is maintained by a heightened excitability of noradrenergic neurons innervating, notably, the prefrontal cortex. However, neither the signaling axis linking hypothalamic activation to delayed and lasting noradrenergic excitability nor the molecular cascade gating noradrenaline synthesis is defined. Here, we show that hypothalamic corticotropin-releasing hormone-releasing neurons innervate ependymal cells of the 3rd ventricle to induce ciliary neurotrophic factor (CNTF) release for transport through the brain's aqueductal system. CNTF binding to its cognate receptors on norepinephrinergic neurons in the locus coeruleus then initiates sequential phosphorylation of extracellular signal-regulated kinase 1 and tyrosine hydroxylase with the Ca2+-sensor secretagogin ensuring activity dependence in both rodent and human brains. Both CNTF and secretagogin ablation occlude stress-induced cortical norepinephrine synthesis, ensuing neuronal excitation and behavioral stereotypes. Cumulatively, we identify a multimodal pathway that is rate-limited by CNTF volume transmission and poised to directly convert hypothalamic activation into long-lasting cortical excitability following acute stress.
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PMID:Hypothalamic CNTF volume transmission shapes cortical noradrenergic excitability upon acute stress. 3036 65