Structural plasticity of synaptic interface structure and expression of synaptophysin in hippocampus in anxious rats suffered from morphine withdrawal
Su-yuan Luo, Jialin Gao, Gang Qian, Mingsong Wu
Abstract
Su-yuan Luo, Jialin Gao, Gang Qian, Mingsong Wu
Abstract
Objective For the hippocampal CA1 and CA3 regions,the possible relationship between structural plasticity of synaptic interface structure and expression of synaptophysin and their functional roles were explored in anxiety-behavioral rats.Methods The escalating doses of morphine and the elevated plus maze were applied to validate anxiety-like behavior in rats.Both electron microscopy and immunohistochemitry were applied to detect parameters,including structural plasticity of synaptic interface structure and expression of synaptophysin(P38),in the hippocampal fields CA1 and CA3 in control group,morphine-withdrawal group and cured group(n=6).Results (1)Anxiety-like behavioral symptoms were observed in the rats suffering from the escalating morphine doses(t,least significant difference test,P<0.01 or P<0.05).(2)Compared with control group and cured group,higher values of postsynaptic density (10.7±0.9)nm,length of postsynaptic thickening(45±4)nm,widths in synaptic interface structure on junctions(3.80±0.30)nm and curvature of the cleft region(1.37±0.12)nm were notably observed in hippocampal CA1 region in anxious rats(P<0.01 or P<0.05).Similarly,higher scores of postsynaptic density(12.9±1.1)nm,length of postsynaptic thickening(53±8)nm,widths in synaptic interface structure on junctions(3.81±0.59)nm and curvature of the cleft region(1.39±0.30)nm were detected in hippocampal field CA3 in anxious rats(P<0.01 or P<0.05).(3)Higher accumulated levels of synaptophysin were found in the hippocampal CA1 and CA3 regions in anxiety-behavioral rats(0.42±0.06and 0.43±0.05).Conclusion Our results suggested that structural plasticity of synaptic interface structure and expression of synaptophysin in the hippocampus could be contributed to development of drug addiction in rats. Key words: Morphine; Substance withdrawal syndrome; Anxiety; Hippocampus; Synapses; Synaptophysin
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Objective For the hippocampal CA1 and CA3 regions,the possible relationship between structural plasticity of synaptic interface structure and expression of synaptophysin and their functional roles were explored in anxiety-behavioral rats.Methods The escalating doses of morphine and the elevated plus maze were applied to validate anxiety-like behavior in rats.Both electron microscopy and immunohistochemitry were applied to detect parameters,including structural plasticity of synaptic interface structure and expression of synaptophysin(P38),in the hippocampal fields CA1 and CA3 in control group,morphine-withdrawal group and cured group(n=6).Results (1)Anxiety-like behavioral symptoms were observed in the rats suffering from the escalating morphine doses(t,least significant difference test,P<0.01 or P<0.05).(2)Compared with control group and cured group,higher values of postsynaptic density (10.7±0.9)nm,length of postsynaptic thickening(45±4)nm,widths in synaptic interface structure on junctions(3.80±0.30)nm and curvature of the cleft region(1.37±0.12)nm were notably observed in hippocampal CA1 region in anxious rats(P<0.01 or P<0.05).Similarly,higher scores of postsynaptic density(12.9±1.1)nm,length of postsynaptic thickening(53±8)nm,widths in synaptic interface structure on junctions(3.81±0.59)nm and curvature of the cleft region(1.39±0.30)nm were detected in hippocampal field CA3 in anxious rats(P<0.01 or P<0.05).(3)Higher accumulated levels of synaptophysin were found in the hippocampal CA1 and CA3 regions in anxiety-behavioral rats(0.42±0.06and 0.43±0.05).Conclusion Our results suggested that structural plasticity of synaptic interface structure and expression of synaptophysin in the hippocampus could be contributed to development of drug addiction in rats. Key words: Morphine; Substance withdrawal syndrome; Anxiety; Hippocampus; Synapses; Synaptophysin
Key concepts: Synaptophysin, Postsynaptic density, Hippocampal formation, Synaptic plasticity, Hippocampus, Postsynaptic potential, Neuroscience, Endocrinology