| A majority of strokes are ischemic strokes. It is of great significance to know how to lighten the brain damage induced by ischemic stroke. The sensitivities of neurons of central nervous system(CNS) to ischemia are different. Neurons of some special regions of brain are more sensitive to ischemia than others, and transient ischemia can cause neuronal death on these regions, which is called "selective sensitivity". Neurons in the CAl subfield of hippocampus happen to be such special neurons, and these neurons are very important in the memory of mammalian and human being, so the CAl subfield of hippocampus become a typical region in the research of ischemic brain injury. At present, the study of molecular mechanism of ischemic brain injury has been becoming a hotspot, and people advanced a lot of theories on it, but till now we still do not understand the mechanism exactly. Monoamine neurotransmitters participate in lots of physiological metabolism including sleep, thermoregulation, mental activity, emotion, and so on. Abundant experiments showed that the metabolism ofmonoamine neurotransmitters is in disorder when the brain is in the state of ischemia. We are not very clear about how the monoamine neurotransmitters take part in the ischemic brain injury, when compared to excitatory amino acid and y -aminobutyric acid, but we can affirm that they do have harm effects.In 1978, Havrankova and his group first found that there is insulin in rat's brain. A subsequent series of experiments showed that insulin receptors distribute widely in CNS. People have proved that insulin has a remarkable neuro-protective effect in brain ischemic models.To study on the mechanism of the neuroprotective effect of insulin and provide experimental base of insulin in the treatment of brain ischemic disease, two researches were carried out in our experiment. (1) To observe the appropriate time and dose of insulin treatment for cerebral ischemic-reperfusion injury in rat; (2) To investigate the changes of monoamine neurotransmitters, tyrosine hydroxylase(TH) and dopamine-p-hydroxylase(DpH) in rat's hippocampus .Major methods and results of the experiment are as follow.1. Research on time-effect relations and dose-effect relations of insulin injected into lateral ventricle post cerebral ischemiaDifferent doses of insulin are injected directly into the lateral ventricle in improved rat 4-VO model in different time after reperfusion. The results demonstrate that insulin has an effect in mitigating neuronal necrosis when it is injected within 6 hours after ischemia, and the best dose is l.OU2. Effects of insulin on monoamine neurotransmitters in hippocampus post cerebral ischemiaMonoamine neurotransmitters in rat's hippocampus are determined by HPLC-ED. In ischemic group, dramatic increases of the transmitters are apparentby 6 hours postischemia. Thereafter, they decline rapidly at 1 day and significant lower than their control values at 3 day. At 5 day postischemia, they rise again to normal. In insulin treated group, the transmitters begin to rise 6 hours postischemia, but they are lower than that in ischemic group. They decline at 1 day and reach their control values at 3 day. Homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) are formed from monoamine neurotrans-mitters. In ischemic group, the levels of HVA and 5-HIAA begin to rise 6 hours postischemia, at 1 day they still retain a high level. They decline at 3 day and reach their control values at 5 day. In insulin treated group, the levels begin to rise 6 hours postischemia, but they are lower than that in ischemic group. They declined at 1 day and reach their control values at 3 day.TH and Dî–Ž in hippocampus CAT region are detected by immunohistochemistry method. No TH and D P H positive neurons are detected in hippocampus CA1 region in control,Id and 3d post-ischemia group. In 5d post-ischemic group, the TH and D P H positive neurons are detected. While in all insulin treated group, no TH and D P H positive neurons a... |
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