Department of Physiology & Pathology, School of Dentistry, São Paulo State University (UNESP), 14801-903 Araraquara, São Paulo, Brazil.
CR2P, UMR 7207, CNRS/MNHN/SU, Muséum National d'Histoire Naturelle, Bâtiment de Géologie, CP 48, F-75231 Paris cedex 05, France.
Physiol Behav. 2024 Oct 1;284:114642. doi: 10.1016/j.physbeh.2024.114642. Epub 2024 Jul 18.
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.
本研究旨在从新的视角探讨经典理论无法预测的口渴和钠欲之间的因果关系。例如，我们会问为什么缺水会引起钠欲，口渴不是“水欲”，细胞内脱水可能会引起钠欲。与经典理论相反，我们认为口渴是第一，钠欲是第二，这是同一动机的时间顺序。单一的动机成为一个“干预变量”，这是一个从文献中借用的概念，在文本中进行了充分解释，将脱水的原因（细胞外、细胞内或两者同时）与由后脑抑制（例如，外侧臂旁核）和前脑促进（例如，血管紧张素 II）所支持的各自行为反应联系起来。一个推论是，大鼠的钠欲和海洋硬骨鱼的口渴样动机之间存在同源性，我们称之为“原口渴”。同源性论证基于行为（咸水摄入）和相应的神经解剖学以及功能机制之间的相似性。四足动物起源于海洋环境为同源性提供了额外的支持。单一动机假说也与自然摄食行为一致，因为实验室大鼠和野生动物（包括啮齿动物）的行为存在相似性（例如，口渴会产生咸水摄入）。单一动机和同源性的假设也可以解释为什么高渗性大鼠或最终任何其他高渗性四足动物都会出现钠欲的矛盾迹象。它们还可以解释为什么由脱水引起并由后脑抑制机制支持的摄食行为有助于四足动物从海洋到陆地的过渡。
