| PrefaceDepression is the most popular kind of psychical disease. It has a higher recurrent rate and lifetime mortality. For a long time, we due the depression to the abnormality of neurotransmitters 'quantity with the acknowledge and analysis of the depressional model, we find that there are a series of plasticity regulation of synapse depart in pathogenic mechanism besides the abnormality of quantity of neurotransmitters. The damage of hippocampus neuron is the key part in plasticity regulation of synapse and play a critical role in the mechanism of depression. Recent investigations have focused the mechanism of the stress injury to the hippocampus primary on the activated hormone glucoccor-ticoid ( GC). GC lead to the release of endogenous activated aminoac-id and mediate a series damages by N - methyl - D - aspartate( NMDA) receptor curriculum. The majority of NMDA receptor channel is Ca2 + channel. Calcium overload is the critical substance of damage. The free Ca2 + is one of the important part that lead to the apoptosis. Our purpose is to determine the content change of free Ca2 + in the hippocampus neuron of the depressional model rats and to evaluate whether Ca2+ is the majority injury factor of NMDA receptor channel . To determine whether application of NMDA receptor antagonist can protect the neuron . The result would be helpful to explicate the pathogen-esis of nervous damage of stress depression and quest the new treatment to depression.Experimental Materials1. Animals; Thirty -six male young wistar rats.2. Reagent: Fura - 2/AM, MK - 801, Nicaidipine.3. Apparatus :YSD -4 electronic stimulus instrument, spectro-pho tome trie instrument.Experimental MethodsAccording to Open - field , thirty - six male young Wistar rats are randomly divided into control (A, 6 rats) and three case groups; the depressional model rats(B, 10 rats) ; the depressional model rats with MK -801 preadmission(C, 10 rats) ; the depressional model rats with nicardipine preadmission( D, 10 rats). Chronic stresses were used on three case groups, to get depressional model rats, which then were decapitated rapidly and the hippocampus were removed immediately. The centigrade of free Ca2 + in the hippocampus synapse were evaluated with Fura -2/AM.Results:(1) Latency to leave the inner circle and the number of field segments entered of Group B, C, D were decreased compared to group A . ( 2) Compared to group A, the centigrade of free Ca + in the hippocampus synapse increased significantly ( P < 0. 05 ). Compared to group B , the centigrade of free Ca2 + in the hippocampus synapse of group C and D decreased significantly, (P <0.05).DiscussionTo evaluate the significance of open - field activity in the stress depressional model rats. Acute stresses increase the behaviors of rats and chronic stresses induce the contrary results with the persist of the stresses. The behaviors of the rats convert to the restraint station from excitement . In this experiment, we use chronic stresses to make model rats. Stresses decrease the activity of group B which demonstrate the distinctive reduction modified behaviors. The data of group B have profound differences from those of group A ( p < 0. 01 ) which prove the depressional model is successful.The activities of group C ( preadmission with MK - 801 - NMDA receptor antagonist) and group D ( preadmission with nicardipine -blocker of Ca2 + channel) are also decreased profoundly. Group C and group D have distinct differences from group A.These results suggest these two kinds of drugs can not reverse the restraint behaviors induced by chronic stresses. The restraint behaviors of depressional model rats are not relevant to the increase of free Ca2 + in hippocampus synapse . The behaviors of group C and D have more improvement than those of group B . Although these results do not have statistic significance, they suggest that these two kinds of drugs can prevent the occurrence of injury and help to improve the behaviors.The change and significance of free Ca2... |
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