BACKGROUND:Animal experiments and clinical studies have shown that, functional deprivation at the early development stage may possibly cause nerve and cognition dysfunction at adulthood. However, no research focuses on the effect of olfactory function on the neurogenesis in piriform cortex of adult guinea pigs.
OBJECTIVE:To establish olfactory deprivation models and explore the effect of olfactory experience on the distribution of doublecortin, parvalbumin, glutamic acid decarboxylase 67 and the co-localization of doublecortin with neuron-specific nuclear-binding protein in piriform cortex of adult guinea pigs.
METHODS:Twenty guinea pigs were randomly divided into two groups. Olfactory deprivation models were established through unilateral naris-occlusion and the occluded animals were al owed to survive 3 and 6 weeks, then the specimens were harvested. The distribution of doublecortin, parvalbumin, glutamic acid decarboxylase 67 was detected with immunohistochemistry. The co-localization of doublecortin with neuron-specific nuclear-binding protein in piriform cortex of adult guinea pigs was determined with immunofluorescence method.
RESULTS AND CONCLUSION:The number of doublecortin, parvalbumin, glutamic acid decarboxylase 67 positive cel s in piriform cortex at the undeprived side was significantly higher than that at the deprived side at 3 and 6 weeks (P<0.05). There was no significant difference in the co-localization of doublecortin with neuron-specific nuclear-binding protein in piriform cortex at 3 weeks group and 6 weeks group (P>0.05). The findings suggest that olfactory experience promotes the maturation and differentiation of neurons in piriform cortex of adult guinea pigs.

Objective To observe the effects of Buyang Huanwu decoction(BYHW) on the expression of Cyclin D1 and Cdk2 in rats with post-stroke depression(PSD).Methods The rats model of focal cerebral ischemia was established by means of middle cerebral artery occlusion(MCAO).Then three weeks of salute-living and chronic unpredictable mild stress(CUMS) was given to the animal after cerebral stroke to induce the post-stoke depression animal model.The rats were divided into 5 groups:the sham operated group,the midge cerebral artery occlusion(MCAO) group,the PSD group,the fluoxetine group and the BYHWD group.The rats were subjected to left MCAO rebuilding in consistent focal cerebral ischemia,followed by an 21-day exposure to chronic mild stress (CMS)and single housing to induce PSD animal model.All rats were killed in 7,14 and 21 day after operation.The expressions of Cyclin D1 and Cdk2 were measured by immunohistochemical staining.Results Pathological changes such as hippocampal nerve cell regression,degeneration and necrosis were observed in the model rats compare with the sham operated group.The expression of Cyclin D1 in normal hippocampus in 7,14 or 21 day after operation was (1.16±0.34)％,(1.62±0.29)％ and (1.60±0.24)％ respectively,and Cdk2 was (1.52±0.26)％,(1.85±0.23)％ and (1.97±0.10)％.After PSD the expression of Cyclin D1 was (49.69±5.68)％,(58.17± 2.89) ％ and (50.87 ± 2.48) ％ respectively,and Cdk2 was (50.63 ± 2.93) ％,(70.34± 1.47) ％ and (61.35 ± 3.04) ％.Compared with model group,Fluoxetine and BYHW significantly reduced the numbers of Cyclin D1 and Cdk2 positive cells,the expression of Cyclin D1 was (16.62±4.27)％,(29.66±5.24)％ and (26.71±1.32)％ at fluoxetine group,and Cdk2 was (18.05±2.26) ％,(33.84±3.12) ％ and (24.51±2.66) ％.The expression of Cvclin D1 was (14.62±2.06)％,(26.89±3.41)％ and (23.68±2.01)％ at BYHWD group,and Cdk2 was (16.60± 2.42) ％,(20.09±3.45) ％ and (22.19± 1.70) ％.Conclusion The abnormal expression of Cyclin D1 and Cdk2 at the PSD rats indicate that they may be involved in the mechanism of neuronal death.Buyang Huanwu decoction may reduce the neuronal apoptosis through down-regulating the expression of Cyclin D1 and Cdk2.