Biomedical subjects

J Schulkin

Publications and source records attributed to J Schulkin.

At least 91 records · Page 5Linked to original sources

PubMed1991

Bed nucleus of the stria terminalis: site for the antinatriorexic action of tachykinins in the rat.

The present study investigated the sensitivity of the posterior part of the medial division of the bed nucleus of the stria terminalis (BNST) to the antinatriorexic action of the tachykinin eledoisin in the rat. Salt appetite was evoked by sodium depletion following furosemide-induced natriuresis. The results obtained show that bilateral injection of eledoisin into the BNST evokes a very potent antinatriorexic effect, a statistically significant inhibition being observed even at the dose of 3.1 ng/BNST. On the other hand, when eledoisin was injected into the lateral ventricle, just above the BNST, much larger doses were required to elicit comparable inhibition of salt appetite. The antinatriorexic effect of eledoisin into the BNST is apparently behaviorally selective, since the same doses, which inhibited salt appetite, did not significantly affect the intake of 10% sucrose solution in the sodium-depleted animal. Present results suggest that the BNST is a site of action for the effect of tachykinins on salt appetite.

Amino Acid Sequence↗

PubMed1991

Central gustatory lesions: II. Effects on sodium appetite, taste aversion learning, and feeding behaviors.

Intake and taste reactivity tests were used to determine the effects of bilateral lesions of the gustatory portions of the nucleus of the solitary tract (NST), the parabrachial nucleus (PBN), and the ventral posteromedial nucleus of the thalamus (VPMpc) on several complex ingestive behaviors. In the 1st experiment, lesions of the PBN and the NST blocked, and VPMpc lesions impaired, the behavioral expression of salt appetite. In the 2nd experiment, alanine was paired with injections of LiCl. Control rats as well as rats with NST and VPMpc lesions acquired the taste aversion, but rats with PBN lesions did not. In the 3rd experiment, all animals increased their food intake after injections of 2 U/kg insulin and 250 mg/kg 2-deoxy-D-glucose, and their food intake was suppressed after nutritive stomach loads.

Afferent Pathways↗

PubMed1991

Physiological consequences of NaCl ingestion by Na(+)-depleted rats.

We investigated the temporal relationships between NaCl intake, gastrointestinal Na+ content, and plasma concentrations of Na+, aldosterone, and plasma renin activity (angiotensin). Rats depleted of approximately 2.2 mmol Na+ by combined dietary Na+ restriction and furosemide injection (10 mg sc) drank a preload of 1, 2, or 3 mmol 0.5 M NaCl. Intake of a test 0.5 M NaCl solution given 15, 30, 60, or 120 min later was reduced by approximately 50% of the preload content, irrespective of the interval between preload and test. At 15 min after starting to drink, 61-71% of ingested Na+ remained in the stomach, 15-18% in the small intestine, approximately 5% was calculated to be in extracellular fluid, and less than 1% was excreted. Rates of gastric and gastrointestinal clearance of Na+ were related to the quantity of NaCl ingested. Whereas gastric emptying was initially very rapid (30-61 mumol/min) and decreased with time, gastrointestinal clearance was constant (16-39 mumol/min). Drinking 3 mmol NaCl reliably reduced plasma aldosterone concentrations within 15 min and renin activity within 30 min. Drinking 1 or 2 mmol NaCl reliably reduced levels of these hormones within 30-60 min. The results describe for the first time the distribution of Na+ after Na(+)-depleted rats drink NaCl. They suggest that the rat determines the quantity of Na+ it requires within the first 15 min of ingestion and thus does not depend on signals generated by the prolonged influence of Na+ in the gastrointestinal tract or the fall in plasma concentrations of aldosterone and angiotensin.

Administration, Oral↗

PubMed1990

Inhibition of salt appetite in the rat following injection of tachykinins into the medial amygdala.

The present study investigated the sensitivity of the medial region of the amygdala to the antinatriorexic action in the rat of the tachykinins eledoisin, substance P, neurokinin A and [Asp5,6, MePhe8] substance P(5-11) (also referred to as amino-senktide; NH2-SENK), which is a highly selective agonist for NK-3 receptors. The results obtained show that only the potent NK-3 agonists eledoisin and NH2-SENK inhibit salt appetite when injected into the medial region of the amygdala. Eledoisin and NH2-SENK inhibited salt appetite induced by sodium depletion, that has been proven to be governed by the synergism of angiotensin and aldosterone. They inhibited also salt appetite evoked by central renin injection, that is due to production of angiotensin II. On the other hand, eledoisin and NH2-SENK did not inhibit salt appetite evoked by subcutaneous deoxycorticosterone treatment. These findings suggest that the medial region of the amygdala is a site of action for the antinatriorexic effect of tachykinins and that their action at this site is mediated by NK-3 receptors. Moreover, our results show that in the medial amygdala, the antinatriorexic action of tachykinins appears to be directed toward the angiotensinergic component of the neural mechanism for salt appetite.

Amygdala↗

PubMed1990

Calcium deprivation increases salt intake.

Relative to rats fed chow or semisynthetic control diet, rats fed Ca2(+)-deficient diet increased daily "spontaneous" intake of 0.3 M NaCl solution by as much as eightfold. Intake of 0.3 M NaCl increased in monotonic relationship to the severity of Ca2+ deficiency, which was manipulated by both duration of depletion (0-32 days) and dietary Ca2+ content (0-50 mmol/kg Ca2+). The increased intake was specific to either Na+ or saltiness; relative to controls, Ca2(+)-deprived rats drank more of a wide range of NaCl solutions (0.05-0.50 M) but the same volume of 0.37 mM sucrose octaacetate (bitter), slightly more 2.5 mM citrate (sour), and significantly less 2.5 mM saccharin (sweet). Although urine volume of Ca2(+)-deprived rats was increased, total Na+ excretion was slightly decreased. Adrenal weights, hematocrit, and plasma concentrations of Na+, aldosterone, and angiotensin I were all normal. These results reveal that Ca2+ deficiency increases NaCl intake and thus challenge the notion that salt appetite is a specific response to perturbed Na+ homeostasis.

Animal Feed↗

PubMed1989

The medial amygdala is part of a mineralocorticoid-sensitive circuit controlling NaCl intake in the rat.

Damage in female rats to the medial region of the amygdala abolished the sodium appetite that is evoked by mineralocorticoids (both aldosterone and deoxycorticosterone) without preventing the sodium appetite induced by body sodium depletion. It also eliminated or reduced the daily-need free saline intake of the female rat. These results suggest that the medial region of the amygdala is part of a specifically mineralocorticoid-sensitive neural circuit subserving sodium appetite.

Aldosterone↗

PubMed1989

A role for the medial region of the amygdala in mineralocorticoid-induced salt hunger.

Damage to the medial region of the amygdala abolished aldosterone-induced salt hunger in the rat. In contrast, the salt hungers that are induced by adrenalectomy or by acute sodium depletion are left intact by the same brain damage. We suggest (a) that we have identified part of the neural circuit by which aldosterone participates in the genesis of salt hunger in the intact, sodium-depleted rat and (b) that these results provide further evidence for the hypothesis that there are separate receptive systems in the brain for the participation of aldosterone and angiotensin in the arousal of salt hunger.

Adrenalectomy↗

PubMed1989

Expression of salt hunger in hypophysectomized rats.

Hypophysectomized and pituitary-intact rats were tested for their expression of salt hunger under a variety of experimental conditions. The results show that hypophysectomized rats ingest less salt in response to salt hunger induced by sodium depletion, captopril or angiotensin in comparison to pituitary-intact rats. In contrast, both groups ingest the same amount of salt in response to mineralocorticoid-induced salt hunger. While sodium excretion and plasma sodium levels were comparable in the two groups, the angiotensinogen mRNA was reduced by hypophysectomy in several limbic brain regions as well as in the liver. These results suggest that reduced salt intake in response to manipulations of the body sodium and renin-angiotensin system in hypophysectomized rats may result from decreased angiotensinogen mRNA levels.

Angiotensin II↗

PubMed1989

Palatability shift of a salt-associated incentive during sodium depletion.

Previous studies of natural palatability-sensitive reactions, elicited from rats by tastes, have indicated that the taste of concentrated NaCl becomes more palatable during states of body sodium depletion. A training procedure based upon "sensory preconditioning" or "irrelevant incentive" designs was used here to establish gustatory conditioned labels (quinine or citric acid) for either NaCl or fructose while rats were in a normal physiological state. Experiment 1 replicated demonstrations by others that gustatory conditioned labels for salt can attract and act as independent incentives during the salt appetite induced by sodium depletion. Experiment 2 used the taste reactivity measure to show that the enhanced palatability of the taste of NaCl transfers to produce enhanced palatability of the taste of the isolated conditioned label for salt in a state-dependent fashion. These results offer further support for the proposition that conditioned incentives not only predict hedonic events to follow, but themselves become attributed with the hedonic properties of their reinforcers.

Animals↗

PubMed1987

Further evidence for hepatic control of salt intake in rats.

We examined the contributions of oral and hepatic factors to the control of salt intake in rats made "salt hungry" by combined dietary sodium restriction and furosemide treatment. A 7.5-ml preload of 0.5 M NaCl, which was either voluntarily ingested or slowly infused (7.5 ml/90 min) into the hepatic portal vein, decreased subsequent 0.5 M NaCl intake by approximately 7.5 ml in both cases. Hepatic portal infusions were probably acting in the liver because slow jugular infusions (7.5 ml/90 min) did not influence salt drinking, although rapid (7.5 ml/5 min) infusions by both routes reduced salt intake. If salt was ingested but drained through a gastric cannula, rats showed little sign of reducing salt in a 2-h test. These results suggest that the quantity of salt ingested by salt-hungry rats is regulated by a postabsorptive mechanism that is probably located in the liver.

Administration, Oral↗

PubMed1986

Sodium homeostasis in chronic decerebrate rats.

Physiological and behavioral concomitants of sodium need were studied in supracollicularly transected and pair-fed intact rats. Chronic decerebrate rats, like intact rats, reduced their urine sodium output when placed on a sodium-deficient diet. Similarly, 24 hr after sodium loading, decerebrate and intact rats excreted comparable levels of the excess sodium. In the 2 hr immediately following the loading, decerebrate rats excreted less sodium. In contrast, behavioral aspects of sodium homeostasis were completely absent in chronic decerebrate rats. In separate experiments, intraoral intake, and taste-reactivity responses, elicited by intraoral infusions of NaCl were measured during sodium-replete and sodium-deficient conditions. In response to oral infusions of NaCl, intact rats consumed significantly more and produced greater numbers of ingestive taste-reactivity responses when they were sodium deficient than when they were sodium replete. The same sodium-depletion treatments in chronic decerebrate rats, however, altered neither the intraoral intake of NaCl nor the frequency of NaCl-elicited ingestive taste-reactivity responses. These results suggest that the behavioral compensatory responses that follow changes in the internal sodium state are dependent upon forebrain mechanisms.

Afferent Pathways↗

PubMed1986

Hepatic contribution to satiation of salt appetite in rats.

We examined the influence of hepatic-portal vein infusion of NaCl and of hepatic vagotomy on 3% NaCl solution drinking by sodium-deficient rats. Combined dietary sodium restriction and administration of the natriuretic agent, furosemide (5 mg), produced a vigorous appetite for 3% NaCl solution that was attenuated by portal infusion of NaCl. Whereas infusions (1 ml/30 min) of NaCl into the hepatic-portal vein in concentrations as low as 0.15 M (isotonic) significantly reduced 3% NaCl consumption, a higher concentration (0.6 M) infused into the jugular vein, or portal infusions of KCl (0.6 M) or sucrose (1.2 M), were ineffective. Rats with selective hepatic vagotomy displayed an attenuated appetite for salt whether or not they received hepatic-portal NaCl. This was not due to altered excretion of sodium. Taken together, these results suggest that the liver or portal vein can provide a sodium-specific neural signal capable of attenuating the appetite for salt and this information is transferred to the brain by fibers in the hepatic vagus that fire in reciprocal relationship with portal sodium concentration.

Animals↗

PubMed1985

Running to the taste of salt in mineralocorticoid-treated rats.

In the present series of studies, the running speed of rats in a runway was used to measure appetitive motivation for different concentrations of salt solutions. We found that when rats were thirsty, they were not interested in running for concentrated salt solutions; when they were rendered salt hungry by mineralocorticoid treatment in addition to the thirst, or even without thirst, they ran vigorously for salty tasting solutions, as high as 24% NaCl. The running speed is correlated with the degree of the mineralocorticoid treatment and the salt concentration. Moreover, drinking 5 cc of a 3% NaCl solution before the runway test decreases the running speed of the mineralocorticoid-treated rat. The experiments are discussed in the context of the effects of hormonal events on the movitation to ingest salt solutions.

Animals↗

PubMed1985

Brief preoperative exposure to saline protects rats against behavioral impairments in salt appetite following central gustatory damage.

Adult rats who receive large electrolytic lesions at the level of the thalamic taste relay display impairments in taste related behavior, specifically the appetite for salt that results from changes in sodium balance. However, if the rats are given preoperative experience of ingesting a salty taste they are protected against these impairments in salt appetite that result from the lesion. In the present study we found that a brief (30 s) preoperative exposure to saline is sufficient to protect adult rats against expected deficits in salt appetite that normally result from central gustatory damage at the level of the thalamic taste relay. It is becoming increasingly clear that preoperative events can lessen the severity of the effects of brain damage. The results are discussed in the context of the appetite for salt, and preoperative immunization from behavioral deficits that result from brain damage.

Animals↗

PubMed1985

Further studies on salt appetite following lateral hypothalamic lesions: effects of preoperative alimentary experiences.

Lateral hypothalamic lesions impair salt appetite, but rats with lesions show enhanced saline ingestion following natrorexigenic treatments if given preoperative salt drive experiences. In this study, the preoperative drive to ingest salt (without the consummatory experience of saline ingestion) was found to be necessary for this effect. Exposure to saline, or the treatments of water deprivation or insulin-induced feeding, when given preoperatively were not protective.

Animals↗

PubMed1985

Circadian wheel-running activity of rats under schedules of limited daily access to salt.

Schedules of limited daily access to food result in 'anticipatory' activity preceding each daily feeding. It is well-established that such food-anticipatory activity depends on a food-entrainable circadian timing mechanism. In the present study, we sought to extend the generality of these results by maintaining rats in running wheels under schedules which provided access to salt solutions or to salty food for 2 hr each day. The animals were subjected to dietary, pharmacological and surgical treatments that promote salt appetite. However, we found no evidence for daily salt-anticipatory wheel running activity in any condition.

Administration, Oral↗

PubMed1984

Preoperative latent place learning preserves salt appetite following damage to the central gustatory system.

Rats given the experience of tasting saline before receiving lesions in the region of the thalamic taste relay are protected from the usual lesion-induced deficits in salt appetite. In this study, the location of the saline during postoperative testing was varied from the location during preoperative training for some rats, and it was kept the same for others. A clear protective effect was evident when the preoperative and postoperative location was the same but not when it was different. This protective effect may be due to place learning, because it is known that rats can remember tasting saline in a particular place and then return there when in a state of sodium need.

Animals↗

PubMed1984

Sodium depletion enhances salt palatability in rats.

Sterotyped fixed action patterns (FAPs) are elicited in rats by oral infusions of taste solutions. These taste-elicited FAPs can be classified as either ingestive or aversive. They reflect the palatability of the taste and can be modified by learning and by the physiological state of the animal. These studies demonstrated that when the physiological state of the rat is altered by sodium depletion, the pattern of FAPs elicited by oral infusions of 0.5 M NaCl shifts from a mixture of ingestive and aversive components (while sodium replete) to exclusively ingestive ones (while sodium deplete). This shift in taste reactivity occurred the first time the rats were made sodium deplete. A similar shift was not observed to accompany infusions of 0.01 M HCl, a taste solution that also elicited mixed ingestive and aversive FAPs. This result suggests that the shift in response to NaCl is not due to a general change in ingestive bias or to a general taste deficit. On the basis of the change in FAPs, it is concluded that the palatability of highly concentrated salt solutions increases in sodium-deplete rats. Such a shift in salt palatability may be instrumental in directing the appetitive behavior of the animal.

Animals↗