Total analysis for controlling mechanisms of drinking in seawater eels

通过腹腔注射Evans蓝，我们证明了三个核，即中脑的大细胞视前核（PM）和结节前核（NAT）以及延髓的后脑区（AP），直接与鳗鱼脑中的血流接触（Mukuda等，2005）。在这些核中，PM和NAT对didiogen血管紧张素II （angii）和抗didiogen心房钠肽（ANP）有反应，但AP没有。两种多肽分别抑制PM和NAT中的神经元活性（未发表的观察结果）。另一方面，鳗鱼的上食管括约肌（UES）受舌咽部-迷走神经运动复合体（GVC）的胆碱能神经支配（Mukuda & Ando, 2003）。儿茶酚胺（catecholamines, CAs）抑制了GVC的自发活性（Ito et al., 2006）。酪氨酸羟化酶（TH）是一种儿茶酚胺合成酶，在鳗鱼MO的迷走神经叶（LX）、Cajal的联合核（NCC）、More和AP中检测到（Ito et al, 2006）。然而，当AP受到电刺激时，GVC活性没有反应。当LX和NCC受到刺激时，GVC活性明显受到抑制，且LX刺激的抑制作用被GABA_B受体拮抗剂阻断，而NCC刺激的抑制作用被CA受体拮抗剂（制剂）阻断。鳗鱼MO的迷走神经在鳃后分为10支，命名为X1-X10。在这些分支中，X2-X5支配UES肌，因为刺激这些分支后UES收缩，尤其是X5的作用最为突出。X5的作用被尼古丁受体拮抗剂curare抑制，提示X5使用乙酰胆碱作为神经递质（在制剂中）。乙酰胆碱和催产素使鳗鱼UES肌收缩，而异肽催产素使其松弛。静脉注射VT或IT时，前者的饮酒率降低，后者的饮酒率增加（准备中）。用TTX灭活神经元活动后，IT诱导的UES松弛仍然存在，这表明IT作用于肌肉，而不是神经末梢。此外，IT还增强了神经刺激的UES收缩（在准备中）。少

By injecting Evans blue intraperitoneally, we demonstrated that three nuclei, the magnocellular preoptic nucleus (PM) and the anterior tuberal nucleus (NAT) in the diencephalon and the area postrema (AP) in the medulla oblongata (MO), contact directly to the blood stream in the eel brain (Mukuda et al., 2005). Among these nuclei, the PM and the NAT responded to a dipsogen, angiotensin II (ANG II), and an antidipsogen, atrial natriuretic peptide (ANP), but the AP did not. Both peptides inhibited neuronal activity in the PM and the NAT separately (unpublished observation). On the other hand, the upper esophageal sphincter (UES) muscle of the eel is innervated cholinergically by the glossopharyngeal-vagal motor complex (GVC) in the MO (Mukuda ＆ Ando, 2003). The spontaneous activity in the GVC was inhibited by catecholamines (CAs) (Ito et al., 2006). Tyrosine hydroxylase (TH), a catecholamine synthesizing enzyme, was detected in the vagal lobe (LX), the commissural nucleus of Cajal (NCC) a … More nd the AP of the eel MO (Ito et al., 2006). However, when the AP was stimulated electrically, no response was observed in the GVC activity. When the LX and the NCC were stimulated, the GVC activity was inhibited remarkably, and the inhibition by the LX stimulation was blocked by GABA_B receptor antagonist and that by NCC stimulation was blocked by CA receptor antagonist (in preparation). The vagal nerve from the eel MO was divided into 10 branches, named as X1-X10, behind the gills. Among these branches, X2-X5 innervated the UES muscle, since the UES was contracted after stimulating these branches, especially effect of X5 was most prominent. The effect of X5 was inhibited by curare, a nicotinic receptor antagonist, suggesting that X5 uses acetylcholine as a neurotransmitter (in preparation). Although the eel UES muscle was contracted by ACh and vasotocin (VT), it was relaxed by isotocin (IT). When VT or IT was injected intravenously, the drinking rate was decreased by the former and increased by the latter (in preparation). The IT-induced relaxation of the UES was still remained after inactivating neuronal activity with TTX, suggesting that IT acts on the muscle, not on the nerve terminals. Furthermore, IT also enhanced nerve-stimulated UES contraction (in preparation). Less