Expression Of Synaptophysin In Hippocampus Research Articles

Beneficial effects of environmental enrichment on behavior, stress reactivity and synaptophysin/BDNF expression in hippocampus following early life stress

Exposure to environmental enrichment can beneficially influence the behavior and enhance synaptic plasticity. The aim of the present study was to investigate the mediated effects of environmental enrichment on postnatal stress-associated impact with regard to behavior, stress reactivity as well as synaptic plasticity changes in the dorsal hippocampus. Wistar rat pups were submitted to a 3 h maternal separation (MS) protocol during postnatal days 1–21, while another group was left undisturbed. On postnatal day 23, a subgroup from each rearing condition (maternal separation, no-maternal separation) was housed in enriched environmental conditions until postnatal day 65 (6 weeks duration). At approximately three months of age, adult rats underwent behavioral testing to evaluate anxiety (Elevated Plus Maze), locomotion (Open Field Test), spatial learning and memory (Morris Water Maze) as well as non-spatial recognition memory (Novel Object Recognition Test). After completion of behavioral testing, blood samples were taken for evaluation of stress-induced plasma corticosterone using an enzyme-linked immunosorbent assay (ELISA), while immunofluorescence was applied to evaluate hippocampal BDNF and synaptophysin expression in dorsal hippocampus. We found that environmental enrichment protected against the effects of maternal separation as indicated by the lower anxiety levels and the reversal of spatial memory deficits compared to animals housed in standard conditions. These changes were associated with increased BDNF and synaptophysin expression in the hippocampus. Regarding the neuroendocrine response to stress, while exposure to an acute stressor potentiated corticosterone increases in maternally-separated rats, environmental enrichment of these rats prevented this effect. The current study aimed at investigating the compensatory role of enriched environment against the negative outcomes of adverse experiences early in life concurrently on emotional and cognitive behaviors, HPA function and neuroplasticity markers.

The effects of early life lead exposure on the expression of P2X7 receptor and synaptophysin in the hippocampus of mouse pups

The present study was undertaken to investigate the effects of maternal lead exposure on expression of P2X7 receptor and synaptophysin in the hippocampus of mice offspring. Lead exposure initiated from beginning of gestation to weaning. Lead acetate administered in drinking solutions was dissolved in distilled deionized water at the concentrations of 0.1%, 0.5% and 1% groups, respectively. On the 21st postnatal day, the Pb levels were also determined by graphite furnace atomic absorption spectrometry. The expression of P2X7 receptor and synaptophysin in hippocampus was examined by immunohistochemistry and Western blotting. The lead levels in blood and hippocampus of all lead exposure groups were significantly higher than that of the control group (P<0.05). Compared with the control group, the expression of P2X7 receptor was increased in lead exposed groups (P<0.05), but the expression of synaptophysin was decreased (P<0.05). The high expression of P2X7 receptor and low expression of synaptophysin in the hippocampus of pups may contribute to the neurotoxicity associated with maternal Pb exposure.

Effects of polydatin on learning memory and the expression of synaptophysin in hippocampus induced by hypoxic-ischemic brain injury in neonatal rats

Objective To explore the protective effects and possible mechanisms of Polydatin (PD)on hypoxic-ischemia brain injury(HIBD) in neonatal rat by means of spatial learning memory and the expression of synaptophysin in hippocampal CA1. Methods Thirty-seven neonatal SD rats were divided into 3 groups at random: normal sham-operated group( no hypoxia and ischemia); HIBD group( no medication) ;PD treatment group. 7-old-day rat' s model of HIBD was established by left carotid artery ligation and 2 h hypoxia. Morris water maze test was used to evaluate cognitive function in the rats after 28-day-old( 21-day later after HI). Immunohistochemical method was used to measure the expression of synaptophysin after the end of Morris water maze test. Results Morris water maze results showed that the mean escape latency of the shamgroup (SG) ,HIBD group (HIBD) and PD treatment group (PD) were (39. 55 ±8. 08) s, (52. 37 ±8.03) s and (43.29 ± 7. 63 ) s respectirely. For PD and SG, the mean escape latency was significantly shorter than the HIBD (P ＜0.05). After training,the mean escape latency in the three groups of rats was shortened gradually. The frequency of platform crossings were 5. 29 ±2.62、2. 36 ± 1.80、4. 25 ± 1. 66 in the SG,HIBD and PD respectirely. The frequency of platform crossings in PD was higher than that of HIBD ( P ＜ 0. 05 ). The swimming time in target quadrant were ( 15.74 ± 3.85) s, ( 10. 63 ± 3.66) s and ( 14. 32 ± 2. 52 ) s in SG, HIBD and PD respectirely. For HIBD ,the swimming time in target quadrant was significantly shorter comparing to SG and PD ( P ＜ 0. 05 ). The expression of synaptophys in hippocampal CA1 in PD ( 0. 295 2 ± 0. 044 3 )were evidently higher than that in the HIBD group (0.261 2 ±0.032 3) at 3 week after operation (P ＜0. 05). Conclusion Spatial learning memory deficits and the decrease of synaptophys in hippocampal CA1 could be induced by hypoxic-ischemia. Polydatin could improve the learning and memory ability in neonatal rats following hypoxic-ischemia brain damage. The mechanisms of improvement with Polydatin treatment is associated with the enhancement of expression of synaptophys. Key words: Polydatin ; Hypoxic-ischemic brain injury ; Spatial learning memory ; Synaptophysin ; Rat

Effect of different doses of propofol on synaptophysin level in hippocampus of mentally depressed rats after electroconvulsive therapy

Objective To investigate the effects of different doses of propofol on expression of synaptophysin (SYP) mRNA and protein in the hippocampus of mentally depressed rats after electroconvulsive therapy (ECT) .Methods Fifty adult male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 10 each): group Ⅰ control (group C); group D mental depression (group D) ; group Ⅲ , Ⅳ , Ⅴ propofol 90, 110, 130 mg/kg + ECT (group M_1, M_2, M_3). Mental depression was induced by isolation and chronic unpredictable mild stress (CUMS) in group Ⅱ-Ⅴ . Group M_1 , M_2 and M_3 received intraperitoneal (IP) propofol 90, 110 and 130 mg/kg respectively + ECT once a day ×7 consecutive days while group C and D received IP normal saline instead of propofol. The rats underwent open field test and sucrose liquid consumption test the day before and after mental depression was established and one day after treatment. The rats were killed after the last test for determination of expression of SYP mRNA (by RT-PCR) and protein (by immuno-histochemistry) in the hippocampus. Results The ambulation scores, rearing scores, grooming time and sucrose consumption percentage were significantly decreased while the center,grid detention time (CDT) was significantly increased in group Ⅱ-Ⅴ as compared with control group indicating mental depression was successfully induced. The ambulation scores, rearing scores, grooming time, sucrose consumption percentage, SYP mRNA and protein expression were significantly increased while CDT was significantly decreased after treatment in group M_1 and M_2 as compared with group D indicating that propofol 90 or 110 mg/kg combined with ECT was effective for the treatment of mental depression.Conclusion Propofol 90 or 110 mg/kg combined with ECT is effective in treating mental depression while proprofol 130 mg/kg combined with ECT is not. Excessive inhibition of SYP expression in hippocampus by large dose of propofol may explain the mechanism.` Key words: Propofol; Electroconvulsive therapy; Depression; Synaptophysin

Mutant Presenilin 1 Alters Synaptic Transmission in Cultured Hippocampal Neurons

Mutations in presenilins are the major cause of familial Alzheimer disease, but the precise pathogenic mechanism by which presenilin (PS) mutations cause synaptic dysfunction leading to memory loss and neurodegeneration remains unclear. Using autaptic hippocampal cultures from transgenic mice expressing human PS1 with the A246E mutation, we demonstrate that mutant PS1 significantly depressed the amplitude of evoked alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and N-methyl-D-aspartate receptor-mediated synaptic currents. Analysis of the spontaneous miniature synaptic activity revealed a lower frequency of miniature currents but normal miniature amplitude. Both alterations could be rescued by the application of a gamma-secretase blocker. On the other hand, the application of synthetic soluble Abeta42 in wild-type neurons induced the PS1 mutant phenotype on synaptic strength. Together, these findings strongly suggest that the expression of mutant PS1 in cultured neurons depresses synaptic transmission by causing a physical reduction in the number of synapses. This hypothesis is consistent with morphometic and semiquantitative immunohistochemical analysis, revealing a decrease in synaptophysin-positive puncta in PS1 mutant hippocampal neurons.