Some theoretical considerations in relation to innate appetite for salt

A central question in the study of instinctive behavior is the nature of the processes determining motivation or drive. The ethological concept of action-specific energy is discussed. The salt appetite of sodiumdeficient sheep has been examined as an instance of instinctive behaviour evoked by a chemical change in the body. Experimental analysis has included increasing the sodium concentration of the blood passing through the brain during the consummatory act of repairing sodium deficiency by rapid drinking of sodium bicarbonate solution. Also the effect on appetite of intraruminal and rapid intravenous infusion of sodium solutions, and of renal hypertension and nephrectomy are reported. A major problem presented by the remarkable capacity of the animals to satiate a large deficit with a rapid drinking act over 2–10 minutes, is how, following this, there is a precipitate decline of motivation before the sodium bicarbonate ingested could be absorbed and correct any extracellular or intracellular ionic deficit. The analysis has included experiments on animals with esophageal fistulae. A speculation on a possible nature of the intraneuronal chemical changes responsible for excitation of salt appetite is advanced, which is related to previous hypotheses on protein molecular basis of memory. It is proposed that within a specific population of cells in the neuraxis, which are not necessarily strictly localized, the development of sodium deficiency causing decrease of intracellular sodium concentration initiates a genetic propensity to induce a process of protein synthesis which sets in train the behavioral mechanisms of appetite. That is, structural nuclear DNA is released from inhibitor influence of regulator gene and initiates by messenger RNA the synthesis by ribosomes of a specific protein, and this induced enzyme may either alter the ionic or membrane characteristics of the neurocyton and hence its excitability or may increase the capacity of its transmitter generation at synapses; by either means excitation and transmission in naturally selected neuronal interconnections subserving salt appetite would be facilitated. The influence of these processes in the induction of central excitation and appetitive behavior may include a modulating effect on the midbrain reticular formation such as to bias attention to afferent sensory in-flow relevant to the releasing mechanisms of the consummatory act of the instinct. It is postulated that the process of satiation with the consummatory act is dependent on rapid or explosive degradation of the protein enzyme activating the instinctive pattern. The speculation is discussed in relation to other aspects of motivation, and it is suggested that the proposals, even if incorrect, may be useful in suggesting some avenues of investigation of salt appetite.