| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Research Abstract |
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 Both peptides inhibited neuronal activity in the PM and the NAT separately (unpublished observation).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
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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
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