Abstract：
The objective of the present work is to examine from a new perspective the existence of causal factors not predicted by the classical theory that thirst and sodium appetite are two distinct motivations. For example, we ask why water deprivation induces sodium appetite, thirst is not \"water appetite\", and intracellular dehydration potentially causes sodium appetite. Contrary to the classical theory, we suggest that thirst first, and sodium appetite second, designate a temporal sequence underlying the same motivation. The single motivation becomes an \"intervenient variable\" a concept borrowed from the literature, fully explained in the text, between causes of dehydration (extracellular, intracellular, or both together), and respective behavioral responses subserved by hindbrain-dependent inhibition (e.g., lateral parabrachial nucleus) and forebrain facilitation (e.g., angiotensin II). A corollary is homology between rat sodium appetite and marine teleost thirst-like motivation that we name \"protodipsia\". The homology argument rests on similarities between behavior (salty water intake) and respective neuroanatomical as well as functional mechanisms. Tetrapod origin in a marine environment provides additional support for the homology. The single motivation hypothesis is also consistent with ingestive behaviors in nature given similarities (e.g., thirst producing brackish water intake) between the behavior of the laboratory rat and wild animals, rodents included. The hypotheses of single motivation and homology might explain why hyperosmotic rats, or eventually any other hyperosmotic tetrapod, shows paradoxical signs of sodium appetite. They might also explain how ingestive behaviors determined by dehydration and subserved by hindbrain inhibitory mechanisms contributed to tetrapod transition from sea to land.
摘要：
本工作的目的是从新的角度研究经典理论无法预测的因果因素的存在，即口渴和钠食欲是两种不同的动机。例如,我们问为什么缺水会引起钠食欲，口渴不是“水的食欲”，细胞内脱水可能导致钠食欲。与经典理论相反，我们建议先渴，其次是钠的食欲，指定相同动机的时间序列。单一动机成为一个“干预变量”，一个从文献中借用的概念，在文本中充分解释，在脱水原因之间(细胞外，细胞内，或两者一起)，和后脑依赖性抑制所保留的各自的行为反应(例如，臂旁核外侧)和前脑促进(例如，血管紧张素II）。推论是大鼠钠食欲与海洋硬骨鱼口渴样动机之间的同源性，我们将其称为“protopdipsia”。同源性论点基于行为（咸水摄入量）与各自的神经解剖学以及功能机制之间的相似性。海洋环境中的四足动物起源为同源性提供了额外的支持。单一动机假设也与自然界中的摄取行为一致，给定相似性(例如，产生微咸水摄入量的口渴）在实验大鼠和野生动物的行为之间，包括啮齿动物。单一动机和同源性的假设可能解释了为什么高渗大鼠，或者最终任何其他高渗四足动物，显示钠食欲的矛盾迹象。它们还可以解释由脱水决定的摄取行为和后脑抑制机制的抑制行为如何导致四足动物从海洋到陆地的过渡。
