| ObjectiveCentral glutamate function is important in the pathogenesis of schizophrenia, glutamate is the cerebral cortex neurons of the important neurotransmitter, it is considered to be the brain’s "master switch", because it can be excitedand start the brain excitatory neurons. N-methyl-D-aspartate (NMDA) glutamate in the brain-specific receptors, if antagonists of this receptor can cause increased glutamate and cause similar symptoms of schizophrenia. Phencyclidine (PCP) the main pharmacological mechanism is the antagonism of NMDA glutamate receptor, resulting in the symptoms of schizophrenia, the virtual PCP to build a virtual model of schizophrenia in use in macaques, in order to study the pathogenesis of schizophrenia, while the establishment of this model also provides the possibility for mental surgery the experimental operation.MethodsWe use four macaque monkeys to try to establish the model, the experiment was divided into two parts:a constant dose and administration of a daily dose increment, constant dose to give the monkeys PCP is constant, increasing dose of every three days to rhesus PCP will increase the dose. The administration process lasted for14days, to the medicine two times a day, morning and afternoon10:00injection,16:00injection. Constant dose, were working memory, in the before and after administration detection activity and blood cortisol, through these three indicators of the model evaluation. Evaluation of increasing dose part before and after drug administration were also working memory and activity to model.ResultsThe end of the experiment, we get the following results:four monkeys in the administration section of the constant amount of working memory after administration damaged can be restored after treatment, but the the female monkeys Data changes are inconsistent with the male monkeys. In the detection of activity, we found that compared to the same before the administration of macaque activities excitement, this the excitement is consistent continued until about three weeks after the withdrawal, female monkeys administered both before and after the activity, the activity no significant difference. In the detection of blood cortisol before and after administration, we found no difference in changes in the macaques blood cortisol. Three male macaques in the administration section of the working memory increment after administration appeared damaged, but the female monkeys working memory performance but increased after administration. Active detection of four monkeys found no significant difference before and after administration.ConclusionThese results suggest that the experimental from macaque working memory, the active use of PCP in macaques intends to schizophrenia model is feasible. Of course, the PCP-induced macaques to be the ultimate success of the establishment of the schizophrenia model also has a long way to go, we need more experiments to evaluate the model, to understand the characteristics of the model, in order to establish a comprehensive and stable to be schizophrenic disease model.2, monkeys may be the presence of PCP resistance, may fail in the same group of macaques secondary modeling, the macaque cognitive and behavioral changes due to secondary administration becomes schizophrenia with classic behavioral and cognitivechanges inconsistent.3, through changes PCP induced macaques intends to schizophrenia experiments, we found that gender factors that may affect the model, female monkeys PCP after the intervention on the behavioral and cognitive performance is inconsistent with the male monkeys, and three male monkeys consistent. |