ABSTRACT
<p><b>AIM</b>To study the mechanism of protective effect of GABA against hypoxic injury in rat hippocampal slices.</p><p><b>METHODS</b>The hippocampal slices from adult rats and extracellular recording technique were used to observe the effect of GABA on the evoked population spikes in rat hippocampal slices after hypoxia in vitro.</p><p><b>RESULTS</b>GABA can significantly delay the disappearance of PV, but have no effect on PS. When the receptor antagonist of GABA (bicuculline) and the inhibitor of Cl- channel (NPPB) were given, the protect effect could be suppressed.</p><p><b>CONCLUSION</b>GABA increases hypoxic tolerance of hippocampal slices. The mechanism of the effect of GABA may be involved in the elevation of chloride influx through GABA receptor.</p>
Subject(s)
Animals , Male , Rats , Chloride Channels , Physiology , Evoked Potentials , Hippocampus , Hypoxia , Drug Therapy , In Vitro Techniques , Neuroprotective Agents , Therapeutic Uses , Rats, Wistar , gamma-Aminobutyric Acid , Therapeutic UsesABSTRACT
<p><b>AIM</b>To study effect of CoCl2 pretreatment on the voltage-gated Na+ and K+ currents of the rat hippocampal neurons after acute hypoxia.</p><p><b>METHODS</b>Primarily cultured hippocampal neurons were divided into CoCl2 pretreated and non-pretreated groups. Patch clamp whole cell recording technique was used to examine Na+ and K+ currents of the hippocampal neurons.</p><p><b>RESULTS</b>After acute hypoxia, I(Na) and I(K) of the hippocampal neurons were significantly decreased and the threshold of I(Na) was right-shifted. Pretreatment of the neurons with CoCl2 inhibited the reduction of I(Na) and I(K).</p><p><b>CONCLUSION</b>CcCl2 pretreatment alleviates the acute hypoxia-induced changes of I(Na) and I(K), which may be one of the mechanisms for the protective effect of CoCl2 on neurons.</p>
Subject(s)
Animals , Rats , Animals, Newborn , Cell Hypoxia , Cobalt , Pharmacology , Hippocampus , Cell Biology , Neurons , Patch-Clamp Techniques , Potassium Channels , Metabolism , Rats, Wistar , Sodium Channels , MetabolismABSTRACT
The purpose of the present study was to determine the effects of recombinant human interleukin-6 (rhIL-6) on the Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons. The control and rhIL-6 treated hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2+10% CO2) for 2 and 4 h and then were reoxygenated for 24 and 72 h. The expression of Bcl-2 and Bax was revealed immunocytochemically using the antiserum against Bcl-2 and Bax. The apoptosis was examined by the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method and flow cytometric analysis. The results showed that in cultured hippocampal neurons the Bcl-2 expression decreased while Bax expression and the percentage of apoptotic neurons increased after anoxia-reoxygenation compared with those before anoxia. In comparison with the control, after anoxia-reoxygenation the Bcl-2 expression in hippocampal neurons was higher than that in rhIL-6 group; however the Bax expression and the percentage of the apoptosis were decreased in rhIL-6 group. It is suggested that rhIL-6 may play a role in protecting neurons from the damage induced by anoxia-reoxygenation.
Subject(s)
Animals , Rats , Apoptosis , Cell Hypoxia , Physiology , Cells, Cultured , Hippocampus , Cell Biology , Interleukin-6 , Pharmacology , Neurons , Physiology , Proto-Oncogene Proteins , Proto-Oncogene Proteins c-bcl-2 , Rats, Wistar , Recombinant Proteins , Pharmacology , bcl-2-Associated X ProteinABSTRACT
The effect of CoCl(2) pretreatment on glucose transport activity of cultured newborn rat hippocampal neurons and its role in neuronal hypoxic tolerance were observed. The results showed that the 2-deoxy-D-[1-(3)H ]glucose uptake rate and the mRNA expressions of glucose transporters (GLUT1 and GLUT3) in the hippocampal neurons were significantly increased after a 24-hour pretreatment with CoCl(2). The cell injury induced by 6-hour or 8-hour hypoxic exposure was also greatly reduced by CoCl(2) pretreatment. The protective effect of CoCl(2) on the neurons was largely abolished by cytochalasin B, a specific inhibitor of glucose transporters. The results suggest that CoCl(2) can increase mRNA expressions of GLUT1 and GLUT3 and glucose transporter activity of the neurons, which may be an important mechanism for the increased tolerance of the neurons to hypoxia.
Subject(s)
Animals , Rats , Animals, Newborn , Cell Hypoxia , Cell Survival , Cells, Cultured , Cobalt , Pharmacology , Glucose Transporter Type 1 , Metabolism , Glucose Transporter Type 3 , Metabolism , Hippocampus , Cell Biology , Hypoxia , Metabolism , Neurons , Metabolism , Organometallic Compounds , Pharmacology , RNA, Messenger , Genetics , Rats, WistarABSTRACT
<p><b>AIM</b>To study the effects of hypoxic preconditioning on anoxic tolerance and Jun expression in cultured rat hippocampal neurons after anoxia/reoxygenation.</p><p><b>METHODS</b>12 day cultured hippocampal neurons in control and hypoxic preconditioning group were exposed to anoxic environment (0.90L/L N2 + 0.10 L/L CO2) for 4 h, and then reoxygenated for either 24 h or 72 h. The neurons were immunocytochemically stained using the antiserum against Jun. The number of survival neurons and the percentage of Jun expressing neurons were investigated.</p><p><b>RESULTS</b>The percentage of Jun expressing neurons induced by anoxia in hypoxic-preconditioning group was significantly less than that in control group. The number of survival neurons was more in the hypoxic-preconditioning group than that in control group after anoxic reoxygenation.</p><p><b>CONCLUSION</b>Hypoxic-preconditioning can induce the development of anoxic-tolerance in cultured hippocampal neurons. The decrease in Jun expressing neurons in hippocampus may be an adaptive reaction to acute anoxia.</p>
Subject(s)
Animals , Rats , Animals, Newborn , Cell Hypoxia , Cells, Cultured , Genes, jun , Hippocampus , Metabolism , Neurons , Metabolism , Oxygen , Metabolism , Rats, WistarABSTRACT
<p><b>AIM</b>To investigate the relationship between enhanced anoxic tolerance induced by hypoxic preconditioning and Na+, K+ currents.</p><p><b>METHODS</b>After hypoxic preconditioning and acute anoxia the I(Na), I(K) were measured in cultured hypothalamic cells by patch-clamp whole cell recording technique.</p><p><b>RESULTS</b>The amplification of Na+ currents did not been significantly changed, but the amplification of K+ currents was in hypoxic preconditioning neurons; acute anoxia lead to the inhibition of Na+, K+ currents in the two groups, while Na+, K+ currents in non-preconditioned control group were inhibited severity than hypoxic preconditioning group.</p><p><b>CONCLUSION</b>It is presumed enhanced anoxia tolerance induced by hypoxic preconditioning may be related to the opening of K+ channels.</p>
Subject(s)
Animals , Rats , Cell Hypoxia , Cells, Cultured , Hypothalamus , Cell Biology , Neurons , Physiology , Oxygen , Physiology , Patch-Clamp Techniques , Potassium , Physiology , Rats, Wistar , Sodium , PhysiologyABSTRACT
<p><b>AIM</b>To investigate the effects of anoxia/reoxygenation on Fos and Jun expression and apoptosis in cultured rat hippocampal neurons.</p><p><b>METHODS</b>The hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2 + 10% CO2) for 4 h and then reoxygenated for 24 h and 72 h. The neurons were immunocytochemically stained using the antiserum against Fos and Jun, and the apoptosis were detected by using the terminal deoxynucleotidyl transferase mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method and flow cytometric analysis.</p><p><b>RESULTS</b>The percentage of Fos and Jun positive neurons and apoptosis neurons in cultured hippocampal neurons after anoxia/reoxygenation increased than those in control.</p><p><b>CONCLUSION</b>The occurrence of neurons apoptosis is related to the increase in Fos and Jun expression in cultured hippocampal neurons after anoxia/reoxygenation.</p>