Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of neuropeptides and their analogs on anoxia-induced amnesia was examined using one-trial passive avoidance task in mice. Anoxia, produced by the exposure to CO2 immediately after the acquisition of avoidance response, induced amnesia which is shown by a short latency to enter from the safety compartment into the shocked compartment in the retention test conducted 24 hr later. In these anoxia-treated animals, thyrotropin-releasing hormone (TRH: 10-20 mg/kg), its analog DN-1417 (10-20 mg/kg) and ACTH 4-10 (66 micrograms/body), which were given sc 15-60 min before the retention test, markedly prolonged the latency in a dose-dependent manner, indicating a reversal of the amnesia. Arginine- and lysine-vasopressin also reversed the amnesia at a dose of 100 micrograms/body. These results suggest that TRH and DN-1417, known to reverse the amnesia produced by the protein synthesis inhibitor cycloheximide, have ameliorating effects on the retrieval process of memory.
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PMID:[Effect of TRH and its analog DN-1417 on anoxia-induced amnesia in mice]. 299 54

We have investigated the relationship between energy metabolism, NMDA-receptor antagonism, and anoxic damage in vitro. Anoxic damage was assessed by measuring protein synthesis, defined as the incorporation of [14C]lysine into perchloric acid-insoluble tissue extracts. The concentrations of energy metabolites were measured by ion-exchange HPLC. Anoxia caused an inhibition of protein synthesis, a reduction in phosphocreatine and adenosine triphosphate, and extensive neuronal damage. The reduction of protein synthesis depended on the duration of anoxia and the time allowed for recovery. Preincubation with the creatine dose-dependently (0.03-3 mmol/L) increased baseline levels of phosphocreatine, reduced the anoxia-induced decline in phosphocreatine and adenosine triphosphate, prevented the impairment of protein synthesis, and reduced neuronal death. Incubation with (R,S)-3-guanidinobutyric acid, a synthetic analogue of creatine that cannot be phosphorylated, did not prevent the anoxia-induced impairment of protein synthesis and did not enhance the levels of phosphocreatine and adenosine triphosphate. Incubation with a combination of both creatine and the noncompetitive NMDA antagonist MK-801 provided complete protection. These results indicate that energy status is a major factor controlling anoxic damage in the rat hippocampal slice.
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PMID:Preincubation with creatine enhances levels of creatine phosphate and prevents anoxic damage in rat hippocampal slices. 776 49