Control of drinking behavior in eels neuronal circuit for swallowing reflex

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Intracranial administration of angiotensin II (ANG II), acetylcholine (Ach), isoproterenol, and substance P enhanced the drinking rate in a dose-dependent manner. Atrial natriuretic peptide, vasotocin (AVT), bradykinin, ghrelin, and phenylephrine inhibited the drinking rate dose-dependently (Kozaka, Fujii & Ando, 2003). These dipsogenic or antidipsogenic effects were also observed intravenous administration of these ligands (Ando et al., 2002). Similar effects by different administrations suggests that these ligands act on the brain. However, in general, most peptides can not pass through the blood-brain barrier (BBB). So some special sites which lack BBB are required to explain the above results. Such special sites are known as the circumventricular organs (CVOs) in mammals. To search for the CVOs in the eel, Evans blue (EB) was injected intraperitoneally and EB-positive nucleus was detected with fluorescent microscope. EB is well-known to bind serum albumin and the EB-albumin complex does not pass the BBB. The magnocellular preoptic nucleus (PM), anterior tuberal nucleus (ANT) and area postrema (AP) were stained with the EB. The PM was immunoreactive to the antibodies raised against ANG II and AVT, and the AP was stained with anti-tyrosine hydroxlase (TH) antibody (Mukuda, Matunaga & Ando, submitted). Swallowing is due to relaxation of the upper esophageal sphincter (UES) muscle. When EB was injected to the UES muscle, the glossopharyngeal vagal motor complex (GVC) in the medulla oblongate was labeled retrogradely and the GVC was immunoreactive to the antibody raised against choline acetyltransferase (Mukuda & Ando, 2003). Indeed, the UES muscle is innervated by cholinergic neurons (Kozaka and Ando, 2003). The neuronal activity of the GVC was inhibited by catecholamines, and the TH-immunoreactive fibers from the AP projected to the GVC (Mukuda & Ando, in preparation). Brain atlas of the eel was also constructed (Mukuda & Ando, 2003)