Noradrenergic regulation of plasticity marker expression in the adult rodent piriform cortex.
Noradrenergic regulation of plasticity marker expression in the adult rodent piriform cortex.
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DOI：
10.1016/j.neulet.2017.02.060
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发表时间：
2017-03-22
影响因子：
2.5
通讯作者：
Vaidya VA
中科院分区：
文献类型：
--
作者：
Vadodaria KC;Yanpallewar SU;Vadhvani M;Toshniwal D;Liles LC;Rommelfanger KS;Weinshenker D;Vaidya VA
据报道，成年啮齿动物梨状皮质含有未成熟神经元，表达与神经发育和可塑性相关的标志，即多唾液酸神经细胞黏附分子(PSA-NCAM)和双皮质激素(DCX)。我们研究了PSA-NCAM和DCX在大鼠梨状皮质吻尾轴上的表达，并观察到PSA-NCAM和DCX在后部的阳性细胞数量较多。正如在大鼠梨状皮质观察到的那样，Nestin-GFP报告小鼠也显示出类似的GFP阳性细胞梯度，表达的吻端-尾端梯度增加。鉴于梨状皮质广泛的去甲肾上腺素能神经支配及其在调节梨状皮质功能和突触可塑性中的作用，我们探讨去甲肾上腺素(NE)对梨状皮质可塑性标志物表达的影响。用去甲肾上腺素能神经毒素DSP-4处理去甲肾上腺素可显著增加成年大鼠梨状皮质DCX和PSA-NCAM免疫阳性细胞的数量。类似地，经dsp-4处理的Nestin-GFP报告鼠在NE耗竭后，梨状皮质内GFP阳性细胞的诱导也很强。多巴胺β-羟基酶基因敲除小鼠去甲肾上腺素的遗传缺失与−/−-4的作用相似，梨状皮质中PSA-NCAM和Dcx阳性细胞增多。此外，用受体激动剂Ganabenz刺激成年大鼠梨状皮质中的α-NCAM和Dcx阳性细胞，以及巢蛋白-绿色荧光蛋白小鼠梨状皮质中的GFP阳性细胞。相反，用育亨宾拮抗剂慢性阻断PSA2-肾上腺素能受体使成年大鼠梨状皮质α-NCAM和Dcx阳性细胞减少。我们的结果为去甲肾上腺素在成年小鼠和大鼠梨状皮质中调节可塑性标记物，包括PSA-NCAM、DCX和Nestin的表达提供了新的证据。
The adult rodent piriform cortex has been reported to harbor immature neurons that express markers associated with neurodevelopment and plasticity, namely polysialylated neural cell adhesion molecule (PSA-NCAM) and doublecortin (DCX). We characterized the expression of PSA-NCAM and DCX across the rostrocaudal axis of the rat piriform cortex and observed higher numbers of PSA-NCAM and DCX positive cells in the posterior subdivision. As observed in the rat piriform cortex, Nestin-GFP reporter mice also revealed a similar gradient of GFP-positive cells with an increasing rostro-caudal gradient of expression. Given the extensive noradrenergic innervation of the piriform cortex and its role in regulating piriform cortex function and synaptic plasticity, we addressed the influence of norepinephrine (NE) on piriform cortex plasticity marker expression. Depletion of NE by treatment with the noradrenergic neurotoxin DSP-4 significantly increased the number of DCX and PSA-NCAM immunopositive cells in the piriform cortex of adult rats. Similarly, DSP-4 treated Nestin-GFP reporter mice revealed a robust induction of GFP-positive cells within the piriform cortex following NE depletion. Genetic loss of NE in dopamine β-hydroxylase knockout (Dbh −/−) mice phenocopied the effects of DSP-4, with an increase noted in PSA-NCAM and DCX positive cells in the piriform cortex. Further, chronic α2-adrenergic receptor stimulation with the agonist guanabenz increased PSA-NCAM and DCX positive cells in the piriform cortex of adult rats and GFP-positive cells in the piriform cortex of Nestin-GFP mice. By contrast, chronic α2-adrenergic receptor blockade with the antagonist yohimbine reduced PSA-NCAM and DCX positive cells in the piriform cortex of adult rats. Our results provide novel evidence for a role of NE in regulating the expression of plasticity markers, including PSA-NCAM, DCX, and nestin, within the adult mouse and rat piriform cortex.
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影响因子：
5.6
作者：
Freund, M.;Walther, T.;Halbach, O. von Bohlem Und
通讯作者：
Halbach, O. von Bohlem Und
影响因子：
5.6
作者：
Giorgi, Filippo S.;Mauceli, Giuseppe;Fornai, Francesco
通讯作者：
Fornai, Francesco
影响因子：
7.2
作者：
Bonaguidi, Michael A.;Stadel, Ryan P.;Song, Hongjun
通讯作者：
Song, Hongjun
影响因子：
3.3
作者：
Nacher, J;Pham, K;McEwen, BS
通讯作者：
McEwen, BS
影响因子：
3.7
作者：
Klempin F;Kronenberg G;Cheung G;Kettenmann H;Kempermann G
通讯作者：
Kempermann G