Osmoregulatory thirst in rats after lateral preoptic lesions.

Abstract

In confirmation of previous observations, lesions of the lateral preoptic area in rats abolished water ingestion during a 4-hr test following an intraperitoneal injection of hypertonic NaCl solution. However, it was observed that these animals increased their water intakes when tests were prolonged to 24 hr and drank almost exactly what they needed for osmoregulation. Furthermore, they increased their water intakes normally when NaCl was given in their diet, when NaCl was administered intravenously, or when they were water deprived and given preloads of isotonic saline to remove hypovolemia. These findings indicate that rats with lateral preoptic lesions do experience osmoregulatory thirst, and consequently, they raise new doubts about whether osmoreceptors located in the lateral preoptic area mediate thirst following the administration of osmotic loads.In 1971, Blass and Epstein reported that lesions of the lateral preoptic area (LPO) of rats abolished water ingestion during a 4-hr test following an ip injection of hypertonic NaCl solution. Intact rats, in contrast, drank rapidly following this treatment and consumed 10-15 ml within the first 2 hr of the test. The specificity of the behavioral impairment was suggested by the additional finding (Blass & Epstein, 1971) that rats with LPO lesions drank normally in response to the other major stimulus for thirst, hypovolemia. These and other findings have been used to support the widespread view that osmoreceptors, located in the LPO, mediate thirst when the effective osmolarity of extracellular fluid is elevated (see review by Blass, 1973).Blass and Epstein used an ip injection of This work was supported, in part, by grants from the National Institute of Mental Health (MH-20620 and MH-25140). It includes portions of a dissertation presented by the first author to the University of Pittsburgh in partial fulfillment of the requirements for the master's degree. The technical assistance of Jen-Shew Yen and the helpful comments of Neil Rowland regarding this project are gratefully acknowledged. This report was presented in preliminary form at the meeting of the Society for Neurosciences, Toronto, November 1976.Requests for reprints should be sent to

Response to dipsogenic stimuli after abdominal vagotomy in rats

“…However, this experiment also provides evidence that neither reducing the osmotic load nor extending the measurement interval appreciably alters the weaker drinking response exhibited by vagally denervated rats in comparison with control rats. Extending the test duration to 24 h resulted only in a gradual diminution of the effect of the salt load, but no evidence of any sizable delayed drinking response to the osmotic load, such as that observed in brain-damaged rats (Coburn & Stricker, 1978;Grossman & Grossman, 1978;Stricker, 1976).…”

“…Numerous recent investigations have emphasized the importance of the stressfulness of experimental manipulations done to a denervated animal in determining its behavioral responsiveness. In certain circumstances, animals unresponsive to stressful regulatory challenges induced with high doses nonetheless exhibit regulatory capabilities when tested with a lower dose or in a much longer test period (Coburn & Stricker, 1978;Stricker, 1976;Stricker, Friedman, 0090-5046/81/020181-06$00.85/0 & Zigmond, 1975). In view of the potentially stressful properties of intraperitoneal administration of hypertonic saline (Giesler & Liebeskind, 1976), the first experiment evaluated the dipsogenic effect of several concentrations of saline, ranging from isotonic to .…”

Nucleus circularis and lateral preoptic regulation of osmotic thirst

“…The diffuse representation of osmoreceptor cells in the lateral preoptic area and the fact that rats with lesions restricted to the lateral preoptic show appropriate behavioral responses to dehydration raise questions about the functional significance of this area for the control of osmotic thirst (Coburn & Stricker, 1978). Also, deficits in thirst following large lesions of the lateral preoptic hypothalamus suggest not alterations of receptor mechanisms but, rather, second-order effects (Blass & Epstein, 1971;Malmo & Mundi, 1975;Tondat & Almli, 1976).…”

“…Another possible interpretation of the deficits produced following damage to the area of the nucleus circularis is that critical tracts enpassant were damaged. Coburn and Stricker (1978) proposed that the effect following lateral preoptic lesions might be due to damaging monaminergic pathways. In fact, our data demonstrate that deficits occur when the nucleus is only partially damaged.…”

“…The preoptic area was selected as the site for control lesions, even though many studies have shown deficits in osmotic thirst following lesions of both the preoptic and lateral hypothalamic areas (Blass & Epstein, 1971;Peck & Novin, 1971;Teitelbaum & Epstein, 1962). The lateral hypothalamus was not selected, because this area appears to be more involved with motor functions in drinking behavior than with osmoreception (Coburn & Stricker, 1978;Tondat&Almli, 1976).…”