Total analysis for controlling mechanisms of drinking in seawater eels

通过腹膜内注射伊文思蓝，我们证明了三个核，即间脑中的大细胞视前核（PM）和前结节核（NAT）以及延髓（MO）中的最后区（AP），直接接触鳗鱼脑中的血流（Mukuda et al.，2005年）。在这些核团中，PM和NAT对致渴剂血管紧张素II（ANG II）和抗渴剂心钠素（ANP）有反应，但AP没有。两种肽分别抑制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）肌肉由MO中的舌咽-迷走运动复合体（GVC）胆碱能地支配（Mukuda & Ando，2003）。GVC中的自发活动被儿茶酚胺（CA）抑制（Ito等人，2006年）。酪氨酸羟化酶（TH）是一种合成儿茶酚胺的酶，在迷走神经叶（LX）、Cajal连合核（NCC）和迷走神经核（NCC）中均有表达。 关于我们 和Eel MO的AP（Ito等人，2006年）。然而，当AP被电刺激时，没有观察到GVC活动的反应。刺激LX和NCC可明显抑制GVC活性，刺激LX的抑制作用可被GABA_（B）受体拮抗剂阻断，刺激NCC的抑制作用可被CA受体拮抗剂阻断。鳗鱼迷走神经在鳃后分为10支，命名为X1-X10。其中，X2-X5支支配UES肌，刺激这些支后，UES收缩，尤以X5的作用最为显著。X5的作用被烟碱受体拮抗剂箭毒抑制，表明X5使用乙酰胆碱作为神经递质（制备中）。ACh和催产素（VT）使UES收缩，而异催产素（IT）使UES松弛。当静脉注射VT或IT时，前者降低饮酒率，后者增加饮酒率（准备中）。用TTX使神经元活动失活后，IT诱导的UES松弛仍然存在，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（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 Both peptides inhibited neuronal activity in the PM and the NAT separately (unpublished observation).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