Anorectic factor modulates synaptic transmission in the insular cortex

瘦素和胰岛素是抑制食欲的激素。岛叶皮质 (IC) 表达高密度的这些受体。然而，几乎没有关于瘦素和胰岛素在 IC 中的功能作用的信息。为了探索这一点，我在 IC 切片制备中进行了多次全细胞膜片钳记录。我发现瘦素降低了兴奋性突触后电流（EPSC）的幅度。与 EPSC 相比，瘦素通过磷酸肌醇 3 激酶 (PI3-K) 以及信号转导器和转录因子 3 (STAT3) 级联激活子，增加了快速尖峰神经元 (FS) 与锥体细胞 (Pry) 连接中抑制性突触后电流 (IPSC) 的幅度。瘦素对 IPSC 的促进作用呈剂量依赖性。这些结果表明瘦素可能在抑制味觉信息处理中发挥作用。

Leptin and insulin are hormone that suppress appetite. The insular cortex (IC) expresses high density of these receptors. However almost no information is about the functional roles of leptin and insulin in the IC. To explore this, I performed multiple whole-cell patch clamp recording in the IC slice preparation. I found that the amplitude of excitatory postsynaptic current (EPSC) was decreased by leptin. In contrast to EPSC, leptin increased the amplitude of inhibitory postsynaptic current (IPSC) in fast-spiking neuron (FS) to pyramidal cell (Pry) connections via phosphoinositid 3-kinase (PI3-K) and signal transducers and activators of transcription factors 3 (STAT3) cascade. The facilitative effect of leptin on the IPSC were dose dependent. These results suggest leptin is likely to play a role in suppression of gustatory information processing.