Dopaminergic control over striatal targets appears to be retained in rats sustaining lesions of the nigrostriatal dopamine (DA) system as long as 5-10% of that projection remains. Similarly, during postnatal development, dopaminergic control over striatal neurons matures well before the innervation of striatum by the nigrostriatal bundle is attained. These observations suggest that enhanced efficacy of dopaminergic transmission may compensate for hypoinnervation of striatum after lesions or during development.To examine this hypothesis, striatal slices were superfused with Krebs bicarbonate buffer and effluent was collected and analyzed for endogenous DA. Electrical field stimulation (2 Hz) continuously delivered to slices prepared from intact adult rats increased DA efflux to 3-5 times the prestimulation rate within 10 min. Efflux then fell to approximately twice the basal rate over the next 20 min. DA efflux was also examined using slices prepared from adult animals given 6-hydroxydopamine 2-3 weeks earlier, and from 7-lo-d-old rat pups. In each group, striatal DA levels were 1 O-40% of adult control values. Nevertheless, stimulated DA efflux from these slices attained the same rate as that observed with intact, adult slices. Thus, fractional DA efflux from these slices was several times higher than the control rate by the end of the stimulation period. This increased DA efflux appeared to be a consequence of both increased release and decreased reuptake of DA, as the fractional DA efflux from control striatal slices could not be increased to the rate seen in hypoinnervated slices using nomifensine (10 PM), an inhibitor of DA efflux. Moreover, increased DA biosynthesis was indicated by the maintenance of DA stores in the hypoinnervated slices during stimulation.Thus, increased DA release, decreased reuptake, and increased synthesis may serve to compensate for hypoinnervation after injury or during development.The dopamine (DA)-containing neurons of the nigrostriatal bundle have significant influences on striatal function, as measured at both the cellular and behavioral levels (Ungerstedt, 197 1;Zigmond and Stricker, 1973;Marshall et al., 1974;

Neurohypophyseal secretion of oxytocin (OT) in response to dehydration, hypovolemia, restraint, and parturition in rats is known to be potentiated by the opioid antagonist naloxone. The present studies demonstrated that stimulation of OT secretion by systemic injections of cholecystokinin (CCK) and lithium chloride (LiCl) likewise are potentiated by naloxone pretreatment. Moreover, the inhibitory effects of CCK and LiCl on gastric motility and feeding similarly were enhanced by naloxone. Because neurohypophyseal hormone secretion and inhibition of gastric motility are known to be mediated by oxytocinergic neurons projecting from the paraventricular nucleus of the hypothalamus, this parallel potentiation by naloxone of CCK- and LiCl-induced effects on OT secretion, gastric motility, and food intake suggests that one of the pathways involved in the central control of feeding behavior also may be oxytocinergic. These findings therefore provide evidence in support of an important role of endogenous opioid peptides in regulating OT secretion in a diffuse neuronal system that mediates an integrated neuroendocrine, autonomic, and behavioral response to CCK, LiCl, and perhaps other treatments that similarly affect ingestive behavior in rats.

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STRICKER, E. M., AVD HAINSWORTH, F. R. 1970. Evaporative cooling in the rat: Effects of dehydration.Can. J. Physiol. Plaarmacol. 48,[18][19][20][21][22][23][24][25][26][27] Previous investigations dcmonstrrited that the water loss of rats associated with increased sajivary evaporation during heat stress is derived from both intracellular and intravascular sources. The present studies indicate that sufficient delaydration of either fluid compartment will impair temperature regulation. Salivary excretion from all dehydrated rats was virtually abolished at ambient temperatures below 38-40 "C, but temperature regulation was still possible if a large temperature gradient existed between the animals and the environment. Above these ambient temperatures, where increased evaporation is essential to survival, the rate of evaporative water loss returned to normal. However, body water reservoirs in dehydrated rats were rapidly depleted, salivary evaporation could not be maintained, and survival times were shortened. In contrast, access to drinking water significantly increased thermal tolerance. These results emphasize the importance of adequate body fluid hydration for evaporative cooling through saliva spreading by rats in the heat. In addition, they indicate that allocation of body water for evaporation takes precedence over conflicting demands for water conscrvation during heat stress.

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