Department of Pharmacology, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.
Synapse. 2010 Apr;64(4):323-34. doi: 10.1002/syn.20731.
Neural plasticity in the gustatory area of the insular cortex (IC) plays a critical role in detecting novel taste and taste memory formation, which require extracellular signal-regulated kinase 1-2 (ERK1-2) phosphorylation. However, the distribution patterns of phosphorylated ERK1-2 (pERK) responses to gustatory stimulation remain unknown. This study examined distribution patterns of gustatory stimulation-driven pERK expression in the IC of anesthetized and alert rats. In both pentobarbital-anesthetized and alert rats, gustatory stimulation (10% sucrose) induced pERK-like immunoreactivity in pyramidal cells of all IC subdivisions: agranular (AI), dysgranular (DI), and granular IC (GI). Alert naïve rats exhibited approximately 10-fold larger number of pERK-like immunopositive (pERK-LI) cells than anesthetized naïve rats in response to sucrose application. Most pERK-LI cells were located in layers II/III but not deeper layers and almost no parvalbumin/somatostatin-immunopositive cells expressed pERK. In the AI, rostral regions exhibited more pERK-LI cells than caudal regions, whereas most pERK-LI cells existed in the DI/GI around the intersection of the rhinal fissure and middle cerebral artery (MCA), where in vivo optical imaging revealed activation during sucrose application in addition to the ventral primary and secondary somatosensory cortices. Gustatory experience affected the number of pERK-LI cells in the IC: sucrose stimulation induced more pERK-LI cells in the DI/GI of alert naïve rats than sucrose-exposed rats, which had received sucrose solution for 1 week. These results suggest that pyramidal cells in the upper layers of the gustatory region are highly susceptible to ERK1-2 phosphorylation by gustatory stimulation, which may induce neuroplastic changes in the IC.
岛叶味觉区的神经可塑性在检测新味觉和味觉记忆形成中起着关键作用，这需要细胞外信号调节激酶 1-2（ERK1-2）磷酸化。然而，味觉刺激引起的磷酸化 ERK1-2（pERK）反应的分布模式尚不清楚。本研究在麻醉和清醒大鼠的岛叶中研究了味觉刺激驱动的 pERK 表达的分布模式。在戊巴比妥麻醉和清醒大鼠中，味觉刺激（10%蔗糖）诱导了所有 IC 细分部分（颗粒前岛叶，DI 和颗粒岛叶，GI）的锥体细胞中 pERK 样免疫反应。与麻醉大鼠相比，麻醉前和清醒的大鼠在蔗糖应用时表现出约 10 倍更多的 pERK 样免疫阳性（pERK-LI）细胞。大多数 pERK-LI 细胞位于 II/III 层，但不在更深的层中，几乎没有表达 pERK 的 Parvalbumin/somatostatin-免疫阳性细胞。在 AI 中，喙侧区域比尾侧区域表现出更多的 pERK-LI 细胞，而大多数 pERK-LI 细胞存在于 rhinal fissure 和 middle cerebral artery（MCA）交界处周围的 DI/GI 中，在活体光学成像中，除了腹侧初级和次级体感皮层外，在蔗糖应用期间还发现了激活。味觉体验影响 IC 中 pERK-LI 细胞的数量：与蔗糖暴露大鼠相比，蔗糖刺激在 AI/GI 中诱导了更多的 pERK-LI 细胞，而蔗糖暴露大鼠在 1 周内接受了蔗糖溶液。这些结果表明，味觉区上层的锥体细胞对味觉刺激引起的 ERK1-2 磷酸化高度敏感，这可能会引起 IC 中的神经可塑性变化。
