[Effects of chronic alcohol exposure on hippocampus and cerebral cortex neurons in mice].

This study was performed to investigate the changes of the number, morphology and ultrastructure of the central nervous system of mice during the long-term alcohol exposure. Mice at 60 days in age were used to establish the long-term alcohol exposure model. The structure of the central nervous system, such as nuclear antigen, dendritic spines and synapses, were labeled by the methods of immunocytochemistry and DiI (1,1'- dioctadecyl-3,3,3',3'-tetramethy lindocarbocyanine perchlorate) scattering. The results showed that prolonged alcohol exposure could promote apoptosis of nerve cells in the central nervous system, and inhibit the proliferation of neural stem cells, which reduced the number of nerve cells in the central nervous system. Long-term ethanol exposure can also lead to a decrease in the density of dendritic spines of neuron, a smaller number of synapses(connections between nerve cells), and some changes in synaptic ultrastructure. The density of nerve cells and their dendritic spines, as well as the changes of synaptic ultrastructure, suggest that the function of nerve cells may be low.

Effects of chronic cold exposure on murine central nervous system.

Recently, cold-adaptation medicine has gotten more and more attention because of its specific significance to health care, military activities, sports performance, and so on. Although numerous studies have focused on respiratory, immune, and circulatory systems as well as skin damage upon cold exposure, the impacts on central nervous system are not well understood. This study explores the effects of chronic cold exposure on the murine central nervous system. To establish a chronic cold-exposure animal model, adult male mice from postnatal days 40-50 (P40-50) were housed at 0-4°C for 20 days. During the study period, estrogen receptors were labeled via immunohistochemistry, the dendritic spines of visual cortical pyramidal cells were labeled with DiI diolistic assay, and synaptic ultrastructure was observed by transmission electron microscopy. The results showed that cold exposure could inhibit neural proliferation significantly, with an increase of G-protein-coupled receptor 30 (GPR30) expression. Chronic cold exposure could also induce a decrease in the dendritic spines of pyramidal cells in visual cortex, along with a decrease in the number of synaptic formations. The ultrastructure of synapses after cold exposure was observed. It was found that pre- and postsynaptic membranes were fused, with a vague synaptic cleft. Furthermore, neuronal cytoplasmic and organelle swellings were also observed, along with microtubule disintegration. In conclusion, chronic cold exposure can cause structural and functional changes in the mouse central nervous system, possibly by direct participation of estrogen and its receptor, GPR30, in response to chronic cold exposure.

Prenatal alcohol exposure induces long-term changes in dendritic spines and synapses in the mouse visual cortex.

AIMS: To study the long-term changes of dendritic spine and synapse taking place in a mouse model of fetal alcohol spectrum disorders (FASDs). METHODS: Pregnant mice were intubated daily with ethanol (EtOH) from E5 to parturition. A DiI diolistic method was used to label dendritic spines of pyramidal cells in the visual cortex of EtOH-exposed and control pups over the period from postnatal (P) day P0 to P30; synaptic ultrastructure was also analyzed using transmission electron microscopy. RESULTS: Prenatal alcohol exposure was associated with a significant decrease in the number of dendritic spines of pyramidal neurons in the visual cortex and an increase in their mean length. The changes were dose dependent and persisted to P30. Ultrastructural changes were also observed, with decreased numbers of synaptic vesicles, narrowing of the synaptic cleft and thickening of the postsynaptic density compared to controls; ultrastructural changes also persisted to P30. CONCLUSIONS: Prenatal alcohol exposure is associated with long-term changes in dendritic spines and synaptic ultrastructure; these alterations probably reflect the developmental retardation of dendritic spines and synapses in visual cortex. These long-term changes are likely to contribute to lifelong mental retardation associated with childhood FASDs.

[Effects of alcohol exposure during pregnancy on dendritic spine and synapse of visual cortex in filial mice].

The prenatal ethanol exposure induced the alterations of dendritic spine and synapse in visual cortex and their long-term effect would be investigated in mice from P0 to P30. Pregnant mice were intubated ethanol daily from E5 through the pup's birth to establish mode of prenatal alcohol abuse. The dendritic spines of pyramidal cells in visual cortex of pups were labeled with DiI diolistic assay, and the synaptic ultrastructure was observed under transmission electron microscope. Prenatal alcohol exposure was associated with a significant decrease in the number of dendritic spines of pyramidal neurons in the visual cortex and an increase in their mean length; ultrastructural changes were also observed, with decreased numbers of synaptic vesicles, narrowing of the synaptic cleft and thickening of the postsynaptic density compared to controls. Prenatal alcohol exposure is associated with long-term changes in dendritic spines and synaptic ultrastructure. The changes were dose-dependent with long term effect even at postnatal 30.