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突触释放的组胺增加视上核血管加压素能神经元之间的染料偶联:由H1受体和环核苷酸介导。

Synaptically released histamine increases dye coupling among vasopressinergic neurons of the supraoptic nucleus: mediation by H1 receptors and cyclic nucleotides.

作者信息

Hatton G I, Yang Q Z

机构信息

Department of Neuroscience, University of California, Riverside 92521, USA.

出版信息

J Neurosci. 1996 Jan;16(1):123-9. doi: 10.1523/JNEUROSCI.16-01-00123.1996.

Abstract

Activating direct olfactory (glutamatergic) inputs to supraoptic nucleus (SON) neurons increases interneuronal coupling in slices from lactating but from not virgin or male rats. Studied here were influences on coupling of another monosynaptic input to SON, the histaminergic tuberomammillary nucleus (TM) projection, activation of which selectively excites phasically firing (putative vasopressin) cells. Effects of TM stimulation and its possible downstream consequences on Lucifer yellow (LY) dye coupling among putative vasopressin cells were determined in male rat SONs. In unstimulated slices, 12 LY injections (1 cell/SON) yielded eight single and four pairs of coupled neurons. In slices in which TM was stimulated for 10 min at 10 Hz, 13 injections yielded 4 single and 28 coupled cells, with groups of 2 to 4 cells coupled to the injected neuron, a threefold increase in the number of coupled cells per injection (p < 0.02). Bathing slices in medium containing 10 microM pyrilamine (H1 antagonist) blocked this stimulation-induced coupling increase, suggesting mediation by activation of guanylate cyclase-cGMP to which H1 receptors often are linked . Bathing slices in medium containing 0.5-1 mM 8-bromo-cGMP yielded results similar to those of TM stimulation, a 2.5-fold increase over control in the number of coupled cells per injection. Effects of TM stimulation on coupling also were blocked by bathing slices in a guanylate cyclase inhibitor (10 microM LY83583). In contrast to cGMP, 1 mM 8-bromo-cAMP significantly reduced coupling. We conclude that synaptically released histamine increases coupling via cGMP-dependent mechanisms.

摘要

激活视上核(SON)神经元的直接嗅觉(谷氨酸能)输入会增加哺乳期大鼠而非未生育或雄性大鼠脑片内的神经元间耦合。本研究探讨了另一种对SON的单突触输入——组胺能结节乳头体核(TM)投射对耦合的影响,该投射的激活可选择性地兴奋阵发性放电(假定为血管加压素)细胞。在雄性大鼠的SON中,确定了TM刺激及其可能的下游后果对假定血管加压素细胞间荧光黄(LY)染料耦合的影响。在未刺激的脑片中,12次LY注射(每个SON 1个细胞)产生了8个单个神经元和4对耦合神经元。在以10 Hz频率刺激TM 10分钟的脑片中,13次注射产生了4个单个神经元和28个耦合细胞,有2至4个细胞的群体与注射的神经元耦合,每次注射耦合细胞数量增加了三倍(p < 0.02)。将脑片浸泡在含有10 μM吡咯胺(H1拮抗剂)的培养基中可阻断这种刺激诱导的耦合增加,提示其通过激活通常与H1受体相连的鸟苷酸环化酶 - cGMP介导。将脑片浸泡在含有0.5 - 1 mM 8 - 溴 - cGMP的培养基中产生的结果与TM刺激相似,每次注射耦合细胞数量比对照增加了2.5倍。在鸟苷酸环化酶抑制剂(10 μM LY83583)中浸泡脑片也可阻断TM刺激对耦合的影响。与cGMP相反,1 mM 8 - 溴 - cAMP显著降低了耦合。我们得出结论,突触释放的组胺通过cGMP依赖性机制增加耦合。

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