A small dose of morphine increases intake of and preference for isotonic saline among rats (original) (raw)
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Psychopharmacology, 1990
Endogenous opioid peptides are thought to play a role in mediating the palatability or rewarding aspects of sweet tastes. There is also evidence, however, which suggests that opioids may influence the preference for the taste of salt as well. In the present studies, we measured the effects of central administration of naloxone and the mu agonist [D-Ala2,MePhe4,Gly-olS]enkephatin (DAGO) on the ingestion of salt solutions. In non-deprived rats given a choice of water and 0.6% saline, ICV injections of DAGO (1 and 3 nmol) significantly increased the intake of 0.6% saline; baseline water intake was minimal and was unaffected by DAGO. When rats were given a choice between water and 1.7% saline, DAGO stimulated both water and saline intake. Because 1.7% saline is a hypertonic solution, the increase in water intake may have been secondary to saline intake. In rats on a deprivation schedule in which water and 0.6% saline were available for only ~3 h/day, there was a tendency for DAGO to increase 0.6% saline intake and decrease water intake, though these effects were not significant. In rats given water and 1.7% saline, DAGO increased saline intake and had no effect on water intake. Natoxone was also tested in water-deprived rats. Naloxone (20 and 50 gg) significantly decreased 0.6% saline intake; baseline water intake was low (3-5 ml) and was unaffected by naloxone. When rats were given a choice between water and 1.7% saline, naloxone (50 pg) significantly reduced water intake, while intake of 1.7% saline was slightly increased. These results suggest a role for central mu opioid receptors in mediating the preference for salt solutions.
Psychopharmacology, 2002
Rationale: When paired with morphine, rats suppress their intake of saccharin solution, but not a less palatable salt solution. The reward comparison hypothesis argues that when a taste is paired with morphine, intake of the solution is expected to decrease as the palatability of the taste increases. Therefore, morphine should more effectively suppress intake of salt solution in rats that are conditioned in a sodium-deprived state than in rats that are conditioned in a sodium-replete state. Objectives: The present experiments evaluated the effect of furosemide-induced sodium deprivation on morphine and lithium-induced salt (experiment 1) and saccharin (experiment 2) avoidance and salt taste reactivity (experiment 4). Methods: Rats were injected with furosemide or saline 21 h prior to access to salt solution (experiments 1 and 3) or saccharin solution (experiment 2). Immediately following access to the solution, the rats were injected with saline, morphine or lithium chloride solution. In experiments 1 and 2, a two-bottle test measured the strength of the taste preference/avoidance. In experiments 3 and 4, the taste reactivity test evaluated the furosemide-induced unconditional palatability changes for salt solution (experiment 3) and the conditional palatability changes for salt previously paired with morphine or lithium (experiment 4). Results: Sodium depletion induced by furosemide pretreatment conditionally enhanced subsequent preference for salt solution using both the taste avoidance test (experiment 1) and the taste reactivity test (experiment 4). Salt-lithium associations, but not salt-morphine associations, suppressed salt preference. However, the salt-morphine (40 mg/kg) association enhanced salt preference (in both experiments 1 and 4) when rats were conditioned in a sodium-deprived state. In experiment 2, morphine-saccharin associations resulted in conditioned saccharin avoidance regardless of pretreatment condition. Conclusions: When the palatability of salt was enhanced by sodium depletion, morphine produced a mild conditioned salt preference in both a two-bottle preference test and enhanced ingestion reactions in the taste reactivity test, but morphine produced conditioned saccharin avoidance.
British Journal of Pharmacology, 1982
1 Rats are capable of consuming solutions of morphine sulphate in drinking water ad libitum in the absence of taste-masking chemicals and without the need for scheduled provision or prior parenteral administration of the drug. 2 The success of this method depends on the initial provision of a 0.1 mg/ml solution of morphine sulphate. 3 When the drug concentration is increased to 0.4 mg/ml, the rats achieve an average daily intake of 50 mg/kg body wt. each. 4 Daily intake of morphine may be increased by at least about three fold by increasing the drug concentration to 1.2 mg/ml. 5 Oral morphine administration causes only a moderate loss in body weight. 6 Rats whose daily intake of the drug is 50 mg/kg exhibit tolerance to the analgesic action of morphine and show a drastic loss in body weight at 24 h after withdrawal and most of the behavioural symptoms of the naloxone-precipitated withdrawal syndrome. 7 It is suggested that this simple method of morphine administration is suitable for further biochemical and behavioural studies of the actions of the drug.
Small doses of morphine enhance voluntary intake of a solution of only ethanol and water
Bulletin of the Psychonomic Society, 1988
Rats, subsequent to havin g an extensive hi story of intake of alcoholic beverages, were placed on a schedul e of water depr ivation . Each day , the y were given a 2-h opportunity to tak e either a 6% solution of ethanol (6 g of ethanol and 94 g of tap water for each 100 g of fluid) or wat er . Across daily opportuniti es, intakes of th e ethanol solution and water stabilized, with rats taking about 1.0 g/kg of ethanol. Then , immediately prior to some sessions, rats were given injection s of either placebo, or 1.0 or 2.0 mg/kg morphine. On days of administration of morphine, rats took considerably more etha nol than on days of placebo administ ration, with a mean increment of about 0.9 g/kg. This findin g supports results of similar exper iments and lend s credence to the idea that differential functioning of endogenous opioid systems may be a salient feature of differenti al intake of alcoholic bever ages.
Effects of preferential delta and kappa opioid receptor agonists on the intake of hypotonic saline
Physiology & Behavior, 1990
Effects of preferential delta and kappa opioid receptor agonists on the intake ofhypotonic saline. PHYSIOL BEHAV 47(3) 601-603, 1990.-A previous study has implicated central mu opioid receptors in the preference for salt solutions. Because mu, kappa and delta receptors are all thought to play a role in food intake and/or the mediation of palatability, we performed a series of experiments to determine whether preferential agonists at kappa and delta receptors might also stimulate the intake of salt solutions. When injected centrally into nondeprived rats, two selective agonists at delta receptors caused increases in the intake of 0.6% saline; the intake of concurrently available water was either unchanged or slightly increased. The selective kappa agonist U-50,488H had no effect on water or saline intake, whereas the preferential kappa agonist DAFPHEDYN caused a delayed increase in saline intake. These results indicate a role for central delta receptors in the preference for salt solutions, and are consistent with the suggestion that opioids play a role in the mediation of palatability.
Small doses of morphine and intake of water
Bulletin of the Psychonomic Society, 1988
Rats deprived of water for 19 h were given an opportunity to drink water for 30 min and for another 4.5 h. Prior to drinking, rats were injected with saline or morphine (1.0 mg/kg) to test whether morphine's effects persisted when given day after day . Surprisingly, we did not observe that morphine enhanced drinking. Subsequently, when rats were deprived of water for 23.5 h, morphine still did not increase intake. When we continued testing, with a demonstration replicating an experiment in which morphine increased dr inking and with other demonstrations, it became apparent that small doses of morphine do not always enhance intake of water.
Pharmacology, Biochemistry and Behavior, 1984
Brattleboro rats placed in metabolism cages were injected with morphine (Mor), naloxone (Nal), D-and L-aspartic acid (D-and L-Asp), D-phenylalanine (D-Phe), D-leucine (D-Leu) and prolyl-leucyl-glycinamide (PLG), alone and in suitable combinations. Food and fluid intake, urine outflow, faeces weight, rectal temperature and urinary osmolality were determined at the end of seven hours period of time. Mor, Nal, D-Asp and PLG alone caused a significant decrease in food and fluid intake, urine volume and faeces weight and a significant increase in urinary osmolality being the osmolality of the Mor, D-Asp and PLG injected groups higher than 300 mOsmol/kg. The combination of Nal with Mor, D-Asp and PLG appeared to intensify the changes induced by Mor, D-Asp and PLG whereas L-Asp antagonized the majority of changes caused by Mor or PLG. The results were discussed in the light of the previous experimental findings. DI Brattleboro rats Food intake Fluid intake Urine volume Faeces weight Rectal temperature Urine osmolality Morphine Naloxone D-and L-Aspartic acid D-Phenylalanine D-Leucine PLG
Blockade of central delta-opioid receptors inhibits salt appetite in sodium-depleted rats
Peptides, 2014
Various studies have investigated the role of central opioid peptides in feeding behavior; however, only a few have addressed the participation of opioids in the control of salt appetite. The present study investigated the effect of intracerebroventricular injections of the ␦-opioid antagonist, naltrindole (5, 10 and 20 nmol/rat) and the agonist, deltorphin II (2.5, 5, 10 and 20 nmol/rat) on salt intake. Two protocols for inducing salt intake were used: sodium-depletion and the central injection of angiotensin II. In addition, the effect of a central ␦-opioid receptor blockade on locomotor activity, on palatable solution intake (0.1% saccharin) and on blood pressure was also studied. The blockade of central ␦-opioid receptors inhibits salt intake in sodium-depleted rats, while the pharmacological stimulation of these receptors increases salt intake in sodium-replete animals. Furthermore, the blockade of central ␦-opioid receptors inhibits salt intake induced by central angiotensinergic stimulation. These data suggest that during sodium-depletion activation of the ␦-opioid receptors regulates salt appetite to correct the sodium imbalance and it is possible that an interaction between opioidergic and angiotensinergic brain system participates in this control. Under normonatremic conditions, ␦-opioid receptors may be necessary to modulate sodium intake, a response that could be mediated by angiotensin II. The decrease in salt intake following central ␦-opioid receptors blockade does not appear to be due to a general inhibition of locomotor activity, changes in palatability or in blood pressure.
Differential effects of morphine on food and water intake in food deprived and freely-feeding rats
Psychopharmacology, 1980
In two experiments the effects of a range of doses of morphine (1, 3, 10 and 30 mg/kg) on the food and water consumption of rats were studied. The results of the first experiment showed that in 24 h food-deprived rats, morphine reduced levels of food and water intake. The duration of these actions was dependent upon dose, with only the highest dose (30 mg/kg) producing any effect persisting for longer than 4 hr. In contrast a second experiment showed that morphine increased levels of food and water intake in non-deprived animals. The effect on food intake was most apparent when measurements were taken at 2 hr and after 4 h after drug administration, while water intake remained above control levels for over 6 h. This study shows that the actions of morphine on ingestion of food and water are affected by food deprivation, and the results are consistent with the hypothesised role of endogenous opiates in the mediation of such behaviour.