AIM: To observe the effects of IBMX on cGMP production in gerbil hippocampus after recirculation following ischemia. METHODS: Bilateral occlusion of common carotid arteries and immunofluorescent staining methods in gerbil hippocampal tissue slice were used. RESULTS: Recirculation following ischemia caused a rise in hippocampus cGMP concentration. IBMX increased cGMP production. cGMP positive cells mainly distributed in rediatum layer and molecular layer in the CA_1 subfield. CONCLUSION: IBMX increased cGMP production in gerbil hippocampus after recirculation following ischemia.

Pathological pain or clinical pain is caused by tissue and nerve injuries, and is usually chronic and mainly divided into inflammatory pain and neuropathic pain. Pathological pain is typically characterized by hyperalgesia (increased responsiveness to noxious stimuli) and allodynia (painful responses to normally innocuous stimuli). The mitogen-activated proteins kinases (MAPKs) are a family of evolutionally conserved molecules that play a critical role in cell signaling, consisting of extracellular signal regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), which play an important role in neural plasticity of pathological pain. Inhibition of MAPKs alleviates inflammatory pain and neuropathic pain in different animal models. It is very important to study the inhibition of MAPKs as a therapeutic approach to treat pathological pain.

Brain ischemia/hypoxia preconditioning(I/HPC) is one kind of endocardial protective phenomenon by organism against blood and oxygen deficit.Researches discovered various proteins such as hypoxic inducible factor-1(HIF-1),heat shock proteins(HSPs),erythropoietin(EPO),Bcl-2 family,calcitoningene related peptide(CGRP) and so on participated in brain I/HPC.This essay explains function and participating I/HPC mechanism of these proteins.

The MAPKs activation pathway consists of three protein kinases in activation sequence:MAPKs kinase kinases (MKKKs)→,MAPKs kinases (MKKs)→MAPKs and four pathways:extracellular signal-regulated kinase (MAPK~(ERK)),C-JUN N-terminal kinase (MAPK~(JNK)),MAPK~(P38) and MKKS/MAPK~(ERK5) activation pathways.It has been proved that MAPKs(ERK,JNK and P38) are acvtivated in the progress of morphine tolerance.Inhibitors of any element of MAPKs activation pathway may function as a potential clinical medicine for morphine tolerance.

Objective To investigate the effects of hypoxic preconditioning on learning and memory and the possible protective mechanism in mice with cerebral ischemia-reperfusion injury.Methods Healthy adult male Kunming mice were randomly divided into five groups by Random number table:normal group( N group),hypoxic preconditioning group (HPC group),sham operation group (C group),ischemia-reperfusion group(O group),hypoxic preconditioning and ischemia-reperfusion group(HPC+O group).HPC+O group were given hypoxic preconditioning before 24h of ischemia-reperfusion.The escape latency was detected by Morris water maze and the neuron apoptosis of CA 1 area of hippocampal was determined by immunofluores-cence techniqueR.e sults The escape latency in HPC+O group on the second,third and fourth day of MWM was (39.92±4.52)s,(30.98±2.44)s,(19.69±4.27)s,and significantly lower than that in O group((54.35± 3.66)s,(46.31±4.81)s,(36.81±3.86)s).Mice in HPC+O spent longer time in the target quadrant than that in O group((36.44±5.33)%and(24.5±2.59)%,respectively, P<0.05).Immunofluorescence showed that the apoptotic ration of nerve cells in hippocampal CA 1 was significantly lower than that in O group ( 11.7 ± 0.14 and 1.35±0.14, P<0.05).Conclusion Hypoxic preconditioning can increase hippocampal CA1 neurons hypoxia tolerance of ischemia reperfusion injury in mice,and reduce the incidence of neural cell apoptosis.