首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Presynaptic A2-adrenoceptors and neuropeptide Y Y2 receptors inhibit (3H)noradrenaline release from rat hypothalamic synaptosomes via different mechanisms.
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Presynaptic A2-adrenoceptors and neuropeptide Y Y2 receptors inhibit (3H)noradrenaline release from rat hypothalamic synaptosomes via different mechanisms.

机译:突触前A2肾上腺素受体和神经肽Y Y2受体通过不同机制抑制大鼠下丘脑突触小体中的(3H)去甲肾上腺素释放。

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摘要

Presynaptic receptors may reduce transmitter release with different mechanisms. Both the alpha 2-agonist, clonidine and the Y2-agonist, neuropeptide Y fragment 13-36 (NPY 13-36), induce a concentration-dependent inhibition of the 4-aminopyridine (4-AP)-evoked [3H]noradrenaline ([3H]NA) release from hypothalamic synaptosomes. Changes in alpha 2- and Y2-modulation of noradrenaline (NA) release were observed by lowering the calcium influx with the use of omega-conotoxin (omega-CgTx), a calcium-channel blocking agent. In these experimental conditions, clonidine was less active, whereas NPY 13-36 preserved its efficacy. It therefore seems possible that presynaptic alpha 2-adrenoceptors can primarily inhibit NA release by reducing calcium influx via voltage-sensitive calcium channels (VSCC), while Y2-receptors may inhibit the intracellular release process with a mechanism independent of the calcium entry.
机译:突触前受体可以通过不同的机制减少递质的释放。 α2-激动剂可乐定和Y 2激动剂神经肽Y片段13-36(NPY 13-36)都对4-氨基吡啶(4-AP)诱发的[3H]去甲肾上腺素( [3H] NA)从下丘脑突触小体释放。通过使用钙通道阻滞剂ω-芋螺毒素(omega-CgTx)降低钙流入,可以观察到去甲肾上腺素(NA)释放的α2和Y 2调节发生变化。在这些实验条件下,可乐定活性较低,而NPY 13-36保留了其功效。因此,突触前α2肾上腺素受体似乎可以通过减少经由电压敏感钙通道(VSCC)的钙流入而主要抑制NA释放,而Y2受体可能以与钙进入无关的机制抑制细胞内释放过程。

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