Cooperative activation of cultured vagal afferent neurons by leptin and cholecystokinin
Cooperative activation of cultured vagal afferent neurons by leptin and cholecystokinin
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DOI：
10.1210/en.2004-0221
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发表时间：
2004-08-01
期刊：
影响因子：
4.8
通讯作者：
Simasko, SM
中科院分区：
文献类型：
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作者：
Peters, JH;Karpiel, AB;Simasko, SM
为了验证瘦素可以直接激活迷走神经传入神经元的假设，我们使用荧光成像检测急性变化后，瘦素应用于从成年大鼠结状神经节分离的迷走神经传入神经元的原代培养物的胞浆钙。我们发现，大约40%的迷走神经传入神经元暴露于瘦素（40 ng/ml）的反应与细胞溶质钙的快速和可逆的增加。这些反应依赖于细胞外钙。如前所述，约35%的迷走神经传入神经对肠肽胆囊收缩素（CCK）的反应是增加胞浆钙。大多数（74%）对CCK有反应的神经元也表现出对瘦素有反应的胞浆钙增加。此外，当瘦素和CCK联合应用时，观察到细胞溶质钙的协同增加。这些结果表明，瘦素直接作用于迷走神经传入神经元，触发细胞外钙的急性流入。我们的研究结果还表明瘦素和CCK之间的合作，在一些迷走神经传入神经元的激活。瘦素单独或与CCK联合急性激活迷走神经传入可能有助于内脏反射的调节和食物摄入的控制。
To test the hypothesis that leptin can directly activate vagal afferent neurons, we used fluorescence imaging to detect acute changes in cytosolic calcium after leptin application to primary cultures of vagal afferent neurons dissociated from adult rat nodose ganglia. We found that approximately 40% of vagal afferent neurons exposed to leptin (40 ng/ml) responded with rapid and reversible increases in cytosolic calcium. These responses were dependent upon extracellular calcium. As previously reported, about 35% of vagal afferents increase cytosolic calcium in response to the gut-peptide cholecystokinin (CCK). A majority (74%) of neurons that responded to CCK also exhibited increases in cytosolic calcium in response to leptin. In addition, synergistic increases in cytosolic calcium were observed when leptin and CCK were applied in combination. These results demonstrate that leptin acts directly on vagal afferent neurons to trigger acute influxes of extracellular calcium. Our results also suggest cooperation between leptin and CCK in the activation of some vagal afferent neurons. Acute activation of vagal afferents by leptin alone and in combination with CCK may contribute to modulation of visceral reflexes and control of food intake.