Hypertonic saline and sucrose, but not urea, induced drinking when injected (2 /A. in 1 min.) directly into the lateral preoptic area (LPO) near the anterior commissure. In contrast, local cellular dehydration was not a stimulus in the dorsal (DHA) and lateral hypothalamus (LHA) where hypertonic saline nonspecifically excited neurons to induce drinking or eating. Rabbits allowed isotonic saline and water chose water immediately following either intravenous injections of hypertonic saline or intracranial injections into LPO, but not following injections into DHA or LHA. Electrolytic lesions, including the osmosensitive portion of LPO, abolished the drinking that normally follows intravenous injections of hypertonic saline although ad-lib water intake was normal and not dependent upon the intake of dry food.1 A preliminary account of these experiments was given by D.

Normal adult rats lived on powdered diets adulterated to contain as much as 1.6% quinine sulfate, on a palatable high-fat diet, or in Skinner boxes with 45-mg Noyes pellets available on fixed-ratio (FR) schedules as high as FR 256. They maintained lower body weights over periods of months in proportion to the percentage of quinine adulteration or the fixed ratio. Rats exposed to the high-fat diet overate as much and gained weight as rapidly as rats recovering from food deprivation, and became moderately obese. Rats having become lean or obese contingent on the palatability or accessibility of their diet defended body weight by eating more in the cold, less when force-fed by gavage, and more to restore weight after food deprivation. Yet on chow they restored and defended body weights typical of rats whose diet had been confined to commercially prepared chow. These results are interpreted to be inconsistent with motivational models that rigidly distinguish drive from incentive, that treat body weight changes as evidence for failure to regulate energy balance or body weight, or that rely exclusively on deprivation of food or reduction of body weight for definitions of need for calories. Instead, caloric homeostasis in rats may incorporate ecological constraints.Deprivation of food unambiguously establishes a biological need for food on the assumption that homeostatic regulation tends to restore the same caloric steady state in all circumstances to which the animal subsequently might be exposed, e.g., different diets or schedules of reinforcement. Yet adult laboratory rats feeding ad lib maintain different body weights on different nutritionally adequate diets (e.g.,

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A portion of jejunum in C3H/HeJ mice was irradiated in situ with 250 kV X rays, and the resulting elastic stiffness increase was used as an assay of chronic fibrotic injury. With data from this assay dose-response curves were evaluated with early- and late-appearing chronic intestinal injuries in two experiments. (1) After split-dose treatment with an interfraction interval of 0.0, 0.25, 0.5, 1.0, 2, 4 or 24 h, the asymptotic dose-recovery ratios in assays at 2-3 weeks and at 4 months were statistically similar, R = 1.34 (95% confidence limits: 1.29-1.39) with t1/2 = 0.75 h (0.48-1.17), and R = 1.36 (1.31-1.42) with t1/2 = 0.49 h (0.21-0.86), respectively, although the slopes of the dose-response curves for the early and late assays differed significantly. (2) Mice received 2, 3, 4, 5, 10 or 15 equal X-ray fractions in 5 days with interfraction intervals of at least 5.5-6 h. The data from the dose responses were used in either of two analyses of variance for calculating alpha/beta values. Using slopes in transformed Fe plots, alpha/beta was 8.5 Gy (6.1-12.5) for the assay at 2-3 weeks and 3.6 Gy (2.4-5.4) at 4 months. Using these and other data we argue that assay at the two times measured separate fibrotic responses to injuries to the small intestine, namely, a rapidly appearing consequential late effect that had the same alpha/beta value as for crypt microcolony assays because it was a sequela of acute inflammation after transient loss of mucosal epithelial integrity after crypt sterilization, and a lower-threshold primary or true late effect with a lower alpha/beta value, which progressively masked the consequential injury.

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