Objective Our aim was to observe the effects of prenatal nicotine exposure on development of cerebral cortex and hippocampus in the offsprings of pregnant mice and expressions of NCAM proteins. Methods We established prenatally nicotine exposed(PNE) animal models.We investigated the offspring's structural changes of cerebral cortex and hippocampus with HE staining.Using immunohistochemistry and Western blotting we observed the changes of expressions of NCAM proteins in the neonatal mice. Results Cerebral cortex and hippocampus as well as hippocampal cell layers of the PNE offsprings were thinner than that of the control group.The expressions of PSA-NCAM in cerebral cortex and hippocampus of the PNE offsprings were higher than the control group while the expressions of NCAM-180,140 and 120 weaker.Conclusion Prenatally nicotine exposure can prevent normal morphogenesis of cerebral cortex and hippocampus of mice and can change the expressions of NCAM proteins in cerebral cortex and hippocampus of neonatal mice.

Objective To investigate the effects of acute nicotine exposure on expression of Caspase-3 and apoptosis of neuron in adolescent rat's brain. Methods The Caspase-3 expression was detected with immunohistochemistry and Western blotting. Apoptosis cells were detected by TUNEL method. Results The Caspase-3 expression in cerebral cortex, hippocampal dentate gyrus, CA2 and CA3 of the experimental group was higher than that of the control group through immunohistiochemistry. The expression of Caspase-3 prototype and active fragments in cerebral cortex and hippocampus of the experimental group was higher than that of the control group with Western blotting. The TUNEL positive cells in cerebral cortex and hippocampal dentate gyrus of the experimental group were more than that of the control group.Conclusion Acute nicotine exposure can activate Caspase-3 and increase neuron apoptosis in cerebral cortex and hippocampal dentate gyrus of the adolescent rat's brain.

Objective To observe the regulation of ?-7 neuronal nicotinic acetylcholine receptors(?-7-nAChRs) by nicotine in the ventral tegmental area(VTA),the substantia nigra(SN) and the cortex of the rat. Methods Nicotine exposed animal models were established.The changes of ?-7-nAChRs proteins and mRNA were observed by immunohistochemistry and in situ hybridization in VTA,SN and cortex,and the expression of ?-7-nAChRs proteins by Western blotting in PC12 cells. Results The expression of ?-7-nAChRs proteins in cortex and mRNA in VTA and SN were upregulated by nicotine.The expressions of ?-7-nAChRs in PC12 cells were in proportion to and dependent on the time for nicotine to function and the dose.Conclusion Both ?-7-nAChRs mRNA in VTA and SN in transcriptional mechanism and ?-7-nAChRs protein in the cortex at the translation level were upregulated.

Objective To explore the effect of nicotine on the degeneration of dopaminergic neurons in PD rats. Methods Forty-five SD rats were randomly divided into three groups: PBS group (CON), normal saline + LPS ( NS ) group and nicotine +LPS ( NIC ) group. On 24 hours after LPS or PBS injection, inducible nitric oxide synthase ( iNOS ) protein expression was examined by immunoblotting. ON 14d after LPS or PBS injection, the numbers of tyrosine hydroxylase ( TH ) positive neurons and morphological changes of OX-42 positive cells in the substantia nigra(SN) were observed by immunohistochemistry. TH mRNA and TH protein expressions were examined by RT-PCR or immunoblotting. Results Compared with CON group, iNOS protein increased markedly 24 hours after LPS injection in NS group. TH positive neurons, TH mRNA and TH protein in the SN decreased remarkably 14 days after nigrainjiection. Most of microlglial showed big cell body with thicker and shorter processes. However, nicotine reversed the above changes, Compared with NS group, TH positive neurons, TH mRNA and TH protein in the SN increased remarkably in NIC. Besides, most microglia showed small cell body with slim and long processes. Conclusion Nicotine could prevent LPS-induced degeneration of DA neurons, probably because of that the pretreatment with nicotine blocks the activation of microglia and the expression iNOS protein.

Objective To observe the effect of nicotine(NIC) on the activation and resultant death of microglia induced by LPS. Methods The animal model that exposed to chronic nicotine treatment was established and LPS was injected intraperitoneally to induce the activation of microglia. Furthermore, the CD11b-positive microglia in cerebral cortex, hippocampal and substantia ngra were observed through immunohistochemical staining. BV2 cells(Microglial cell line of mouse) were subcultured, simultaneously the following kits were used including CCK-8 kit assay for cell activity, Nitric oxide assay kit assay for NO release, RT-PCR assay for the iNOS,TNF-α,IL-1β,IL-6,COX-2,IRF-1,Caspase-11 mRNA expression, Western blotting assay for the protein expression of P-I-κB and Caspase-3. Results Nicotine suppressed the CD11b-positive microglia expression in cerebral cortex,hippocampal and substantia ngra induced by LPS;Nicotine inhibited the activation-induced cell death (AICD), attenuated NO release, reduced iNOS,TNF-α,IL-1β,IL-6,COX-2,IRF-1,Caspase-11 mRNA expression, decreased the protein expression including P-I-κB and Caspase-3 of BV2 cells. Conclusion Nicotine pretreatment can suppress the activation and resultant death of microglial cells induced by LPS, which suggests that nicotine may play a neuroprotective role on inflammatory reaction of brain.;