Subcellular localization of m2 muscarinic receptors in GABAergic interneurons of the olfactory bulb

Subcellular localization of m2 muscarinic receptors in GABAergic interneurons of the olfactory bulb
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DOI:
10.1046/j.1460-9568.2000.00289.x
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发表时间:
2000-11-01
影响因子:
3.4
通讯作者:
Martínez-Guijarro, FJ
Martínez-Guijarro, FJ
中科院分区:
医学3区
文献类型:
--
作者:
Crespo, C;Blasco-Ibáñez, JM;Martínez-Guijarro, FJ

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应用免疫组织化学技术、光镜和电镜观察了大鼠嗅球M2受体的超微结构分布。在γ-氨基丁酸(GABA)能延髓中间神经元的细胞室中,m2 R的分布有差异。它位于芽的颗粒细胞和在突触位点的interneurons的外丛状层,表明m2 R激活可以调节释放GABA从这些interneurons到主细胞的突触前机制。相比之下,受体出现在位于二尖瓣下层的二级短轴突中间神经元的胞体和树突状干中,表明这些细胞中的突触后毒蕈碱激活可以引起颗粒细胞的抑制,导致主细胞的去抑制。我们还详细介绍了一个新的假定的毒蕈碱调制,以前没有描述的解剖基板,并可能影响嗅觉肾小球内的感觉信息的接收。m2 R出现在由嗅觉轴突支配的GABA能/多巴胺能肾小球细胞亚群中,但在不接受感觉输入的肾小球细胞中不存在。这一发现表明,m2 R激活可以修改,通过多巴胺能局部电路,嗅觉神经输入到主细胞的强度。毒蕈碱受体的激活可调节嗅球内的嗅觉信息编码,并可通过突触前和突触后机制促进延髓向上级中枢的传递,影响GABA的释放。两者合计,我们的数据提供了神经解剖学的基础上,一个复杂的行动m2 R在不同层次的哺乳动物OB。
We analysed the ultrastructural distribution of the m2 muscarinic receptor (m2R) in the rat olfactory bulb (OB) using immunohistochemical techniques and light and electron microscopy. m2R was differentially distributed within the cellular compartments of gamma -aminobutyric acid (GABA)ergic bulbar interneurons. It is located in the gemmules of granule cells and in the synaptic loci of the interneurons of the external plexiform layer, suggesting that m2R activation could modulate the release of GABA from these interneurons onto principal cells by a presynaptic mechanism. By contrast, the receptor appears in the somata and dendritic trunks of second-order short-axon interneurons located in the inframitral layers, suggesting that postsynaptic muscarinic activation in these cells could elicit the inhibition of granule cells, leading to a disinhibition of principal cells. We also detail the anatomical substrate for a new putative muscarinic modulation that has not been previously described, and that could influence the reception of sensory information within the olfactory glomeruli. m2R appears in a subset of GABAergic/dopaminergic juxtaglomerular cells innervated by olfactory axons but is absent in juxtaglomerular cells that do not receive sensory inputs. This finding suggests that m2R activation could modify, through dopaminergic local circuits, the strength of olfactory nerve inputs onto principal cells. Activation of the muscarinic receptor may modulate the olfactory information encoding within olfactory glomeruli and may facilitate the bulbar transmission to superior centres influencing the GABA release by presynaptic and postsynaptic mechanisms. Taken together, our data provide the neuroanatomical basis for a complex action of m2R at different levels in the mammalian OB.