The effects of exercise-induced fatigue on acetylcholinesterase expression and activity at rat neuromuscular junctions.

Acetylcholinesterase is the enzyme that terminates neurotransmission by hydrolyzing the acetylcholine released by the motoneurons at the neuromuscular junctions. Although acetylcholinesterase has been studied for almost a century, the underlying relationship between exercise-induced fatigue and acetylcholinesterase activity at the synaptic cleft is not clear. The purpose of this study was to assess the effects of exercise-induced fatigue on the expression and activity of acetylcholinesterase at the neuromuscular junctions. The expression and activity of acetylcholinesterase at the gastrocnemius neuromuscular junctions was decreased transiently by exercise-induced fatigue and then gradually increased over 24 hr. The expression of acetylcholinesterase in the 24 hr recovery group returned to the level of the control (non-exercised) group, but the activity of acetylcholinesterase remained significantly lower. These data suggest that the decrease of acetylcholinesterase expression and activity may be involved in the production and/or maintenance of exercise-induced fatigue.

Astrocyte activation and Bcl-2 protein expression induced by lipopolysaccharide in mouse brain / 中南大学学报(医学版)

OBJECTIVE@#To investigate the changes of anti-apoptotic protein Bcl-2 expression in neurons and activation of brain astroglial cells, and the relationship between astrocytes and neurons in mice after a single intracerebroventricular (ICV) stereotaxic injection of lipopolysaccharide (LPS).@*METHODS@#C57BL/6J mice of different ages were divided into a control group and an experiment group. Immunohistochemistry to Bcl-2 and that to GFAP were conducted to observe the expression of Bcl-2 protein in neurons and GFAP in astrocytes in the brain at different time-points after the LPS injection. The glial cell type expressing Bcl-2 was characterized with immunofluorescence double labeling.@*RESULTS@#GFAP-immunoreactive cells in the control mice were observed mainly within hippocampal formation, piriform, entorhinal cortex, septum, striatum, amygdaloid nucleus, subcortical white matter, as well as in the main fiber tracts. At 24 h after the LPS treatment there was no obvious difference in GFAP immunoreactivity compared with the controls. Astrocytes were markedly activated in periventricular brain regions such as hippocampus, the hypothalamic parenchyma surrounding the third ventricle, with larger cell body and hypertrophic processes 2 days after the endotoxin treatment. After the LPS injection, Bcl-2 positive cells were distributed widely in the brain, such as in the cortex (primary and secondary motor cortex, somatosensory cortex), hypothalamic parenchyma surrounding the third ventricle, diagonal band, hippocampus, septum and the red nucleus of the midbrain. At these sites, Bcl-2 induction increased significantly 2 days after the ICV LPS injection, with some subregional differences, peaking on 4th day. No immunofluorescent double labeling cells for GFAP and Bcl-2 were observed in the brain of the mice after the LPS administration, but merging GFAP positive astrocytes and Bcl-2 positive neurons were seen. Double staining for Bcl-2 and GFAP also showed that the projections of activated astrocytes were found in the sheath of Bcl-2 positive neurons 4 days after the ICV LPS administration.@*CONCLUSION@#LPS can activate astroglial cells and upregulate of Bcl-2 expression in the neurons in the mouse brain, which may participate in the administration of central nervous system to central-immunity stimulated regulation and the protective response to the inflammatory stimulus. The projections of activated astrocytes are found in the sheath of Bcl-2 positive neurons, indicating that there is close relationship between astrocytes and neurons.

Effect of chronic stress on PKA and P-CREB expression in hippocampus of rats and the antagonism of antidepressors / 中南大学学报(医学版)

OBJECTIVE@#To observe the effect of chronic unpredicted sequence of mild stress on the expression of cAMP-dependent protein kinase A(PKA) and phosphorylated cAMP-responsive element binding protein (P-CREB) in hippocampus of rats and the antagonism of antidepressors (fluoxetine).@*METHODS@#Thirty-six male Sprague Dawley rats were randomly and equally allocated to 3 groups: A normal control group, a model group, and a fluoxetine group. All rats except the control group were singly housed and exposed to an unpredicted sequence of mild stressors. The different distribution and expression of PKA and P-CREB in the hippocampus of rats in different groups were investigated with immunohistochemistry and Westernblot technique.@*RESULTS@#The positive PKA and P-CREB cells in the hippocampus of normal controls were the pyramidal cells and the granule cells. The PKA and P-CREB protein expression levels in the hippocampus of model rats were significantly lower than those of the normal controls (P<0.05). The PKA and P-CREB protein expression levels in the hippocampus of the fluoxetine group were significantly higher than those of the model group (P<0.05).@*CONCLUSION@#Chronic unpredicted mild stress can affect the PKA and P-CREB expression in hippocampus of rats and fluoxetine has antagonism against it.