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Biomedical subjects

E M Stricker

Publications and source records attributed to E M Stricker.

At least 127 records · Page 7Linked to original sources
PubMed1984

Thirst and sodium appetite after colloid treatment in rats with septal lesions.

Previous experiments in which angiotensin II (AII) and mineralocorticoids were administered to rats have suggested that these hormones play a natural role in mediating thirst and sodium appetite. This hypothesis was examined by making use of rats with septal lesions, which have an apparent sensitivity to the central effects of AII, and studying their behavioral response to subcutaneous colloid treatment, which produces hypovolemia and thereby stimulates the secretions of renin and aldosterone. The induced thirst and sodium appetite both were markedly enhanced in the brain-damaged animals. However, water intake was not increased when the hypovolemia was moderate, and sodium appetite was augmented only when animals had been sodium deprived, a procedure known to potentiate aldosterone secretion. These findings support previous suggestions that whereas AII normally contributes little to thirst, it may help to mediate sodium appetite in rats when aldosterone is abundant. Finally, the two drives were not elicited uniformly; those animals that drank the most water after colloid treatment consumed the least saline. These findings suggest that whereas septal lesions may sensitize the rat's brain to the sodium-appetite-eliciting effects of AII as well as to its dipsogenic effects, sodium appetite emerges only if the induced thirst is not too pronounced.

Aldosterone↗
PubMed1984

Food intake and gastric emptying in rats with streptozotocin-induced diabetes.

Recent studies suggest that the rate of nutrient transit through the upper gastrointestract may provide cues that are important to the control of food intake. We examined gastrointestinal function in rats with streptozotocin-induced diabetes and related these findings to concomitant changes in food intake. Control and diabetic rats were adapted to one of two isocaloric diets either high in carbohydrate or fat. Control rats ate similar amounts of each diet. In contrast, diabetic animals fed high-carbohydrate diet were hyperphagic, whereas those fed low-carbohydrate diet ate normal amounts of food. Gastric emptying, intestinal mass, disaccharidase activity, and glucose absorption were increased in normophagic diabetic rats fed a low-carbohydrate diet. Feeding diabetic rats high-carbohydrate diet potentiated each of these effects, and food intake was highly correlated with rate of gastric emptying. These and other results indicate that diabetes enhances gastric emptying and intestinal carbohydrate digestion and absorption, even in the absence of hyperphagia. Consequently, the hyperphagia of diabetic rats may be in part a behavioral response to a greatly accelerated clearance of nutrients from the upper gastrointestinal tract that occurs when these animals are fed diets rich in carbohydrate.

Animals↗
PubMed1984

Brain catecholamines and the central control of food intake.

Analysis of motivated behaviors indicates the presence of two components, a component that is specific to a particular behavior and a nonspecific component that they all share. Thus, feeding and drinking may be readily differentiated from each other, yet behavioral arousal is a feature of both. Accumulating evidence now suggests that brain catecholamines are involved in the nonspecific aspects of behavior. For example, a variety of sensory stimuli have been shown to increase activity in central catecholaminergic systems measured by electrophysiological, biochemical and electrochemical techniques. Conversely, destruction of these systems leads to a profound decrease in sensory responsiveness. We have been studying the role of the dopamine-containing neurons of the nigrostriatal bundle in motivated behavior. Studies in which dopaminergic activity was monitored in striatum indicate that dopamine release is markedly, though briefly, elevated in response to a variety of intense environmental stimuli, including cold and tail shock. On the other hand, lesions of this pathway impair sensorimotor integration and, thereby, lead to akinesia, sensory neglect and the virtual elimination of all voluntary activities. Moreover, although there is a gradual recovery of function in these brain-damaged animals, they remain less sensitive to stimulation than control animals. For example, they eat but maintain body weight at a level considerably lower than controls, presumably because it takes a greater stimulus of hunger to provoke feeding and less food intake to cause that stimulus to slip below threshold levels of activation. These, and other findings, suggest an important role of brain catecholamines in behavioral arousal, that is, in permitting animals to remain alert and to respond appropriately to relevant sensory stimuli.

Animals↗
PubMed1983

Environmental stimuli but not homeostatic challenges produce apparent increases in dopaminergic activity in the striatum: an analysis by in vivo voltammetry.

Using in vivo voltammetry in rats, we examined the relationship between the electrochemical signal measured in the striatum and the behavioral responses associated with various types of stimulation. Three patterns emerged. First, a series of homeostatic challenges, including abrupt decreases in glucose utilization, blood volume, or arterial blood pressure, were ineffective in altering the electrochemical signal despite the sympathoadrenal response produced by each. Second, intense exteroceptive stimuli, such as an electric shock applied to the tail or placing animals in a shallow ice-water bath, provoked large and abrupt rises in the signal which decayed rapidly. Third, rats eating after a 24-h fast, drinking after a period of dehydration, or presented with novel olfactory or visual stimuli, exhibited much smaller and more gradual rises in the electrochemical signal which were more long-lasting. In each case, the magnitude of the change in electrochemical signal was generally related to the level of behavioral activation, being most prominent when treatments produced a startle response. Those large increases in signal were markedly attenuated by pretreatment with alpha-methyl-p-tyrosine or gamma-butyrolactone, drugs known to decrease the release of dopamine, suggesting that the signal observed was associated with an increase in the activity of central dopaminergic neurons.

Animals↗
PubMed1983

Short- and long-term changes in adrenal tyrosine hydroxylase activity during insulin-induced hypoglycemia and cold stress.

Insulin-induced hypoglycemia increases the capacity for catecholamine biosynthesis in the rat adrenal medulla by two temporally distinct processes: a rapid increase in the affinity of tyrosine hydroxylase (TH) for cofactor and a more gradual increase in the maximal TH activity. Cold exposure leads to comparable long-term increases in adrenal TH activity, apparently without causing a prior activation of TH.

Adrenal Medulla↗
PubMed1983

Subtotal destruction of central noradrenergic projections increases the firing rate of locus coeruleus cells.

The intraventricular administration of 6-hydroxydopamine was used to destroy 80-90% of the noradrenergic terminals in the forebrain of male rats with little apparent damage to the cells of origin in locus-coeruleus. Both 36 h and 21 days later the basal firing rate of these cells was elevated 4-fold above control levels. Moreover, microiontophoretic application of norepinephrine was significantly less effective in inhibiting the spontaneous activity of locus coeruleus cells in these rats relative to control animals. The increased firing may represent a compensatory response to the injury, leading to increased transmitter release release from terminals spared by the lesion.

Animals↗
PubMed1983

Thirst and sodium appetite after colloid treatment in rats: role of the renin-angiotensin-aldosterone system.

Recent experiments indicated that rats usually develop sodium appetite 5 hr after subcutaneous injection of polyethylene glycol (PEG) solution. However, sodium appetite appeared within 30 to 60 min if the rats had been maintained on sodium-deficient diet instead of Purina chow for 2-4 days previously. Elevated levels of aldosterone paralleled the appearance of NaCl consumption in both circumstances. In the present experiments, sodium appetite was no longer potentiated by pretreatment maintenance on sodium-deficient diet when the hypersecretion of aldosterone after PEG administration was prevented by prior hypophysectomy. Conversely, sodium appetite was enhanced in PEG-treated rats when angiotensin II (AII) was produced in unusually large amounts in the brain, owing to the systemic administration of captopril. This latter effect occurred even when drinking water was withheld and plasma sodium concentrations were markedly elevated. These and other findings raise the possibility that the normal secretion of aldosterone in rats after PEG treatment might permit physiological amounts of AII to be effective in stimulating sodium appetite. Such actions would complement the accepted physiological role of the renin-angiotension-aldosterone system in the maintenance of blood pressure and sodium balance.

Aldosterone↗
PubMed1982

Effects of dopamine-depleting brain lesions on experimental hyperphagia in rats.

Dopamine (DA)-depleting brain lesions of various sizes were produced in rats either by intracerebroventricular injections of 6-hydroxydopamine (6-HDA) or by electrolytic lesions of the lateral hypothalamic (LH) area. Among 30 animals that became aphagic and adipsic for at least four days after large LH or 6-HDA-induced brain lesions, only three developed hyperphagia after electrolytic lesions of the ventromedial hypothalamus (VMH) or daily injections of long-acting protamine-zinc insulin (PZI). In 20 rats with smaller LH or 6-HDA-induced lesions, which had not shown marked initial behavioral dysfunctions, only three gained as much weight after VMH lesions as the control animals. Similarly, 6 of 10 rats with smaller LH lesions could not tolerate a 15-day series of PZI treatments, although 14 of 17 rats with smaller 6-HDA-induced lesions increased their food intake and gained weight during the PZI treatments as did control animals. These results indicate that hypothalamic hyperphagia can be blocked by DA-depleting brain lesions that neither produce an initial period of aphagia and adipsia nor involve hypothalamic tissue. They further indicate that even small LH lesions may prevent the development of hyperphagia elicited by PZI, whereas only very large 6-HDA-induced lesions consistently have this effect.

Animals↗
PubMed1981

Water intake in hypovolemic sheep: effects of crushing the left atrial appendage.

Sheep increased their water intake in proportion to the amount of protein-free, isosmotic fluid that was removed from their blood by ultrafiltration. This behavioral response to hypovolemia was eliminated by crushing the left atrial appendage of the heart. The surgical maneuver had no effect on basal water intake or on the drinking response to a salt load. These findings suggest that left atrial stretch receptors, which influence secretion of antidiuretic hormone when stimulated, may also play an important role in mediating thirst during hypovolemia.

Animals↗
PubMed1981

Impaired drinking responses of rats with lesions on the subfornical organ.

electrolytic lesions of the subfornical organ (SFO) in rats are known to abolish their drinking response to intravenous infusion of angiotensin II (AII). Such lesions also attenuate drinking after 20% polyethylene glycol solution (PEG) is given subcutaneously, which suggests that AII may play an important role in mediating thirst during hypovolemia. However, the present studies show that such rats with SFO lesions may drink normal amounts when larger plasma volume deficits are caused by 30% PEG treatment. They also may drink normal amounts in response to 20% PEG when pretreated either with caffeine or hypertonic NaCl solution. Furthermore, they may not drink in response to relatively low doses of hypertonic saline but drink normal amounts when given larger doses. These and other results suggest that the SFO is involved in a control system for thirst and that after damage to it, greater stimulation than usual may be required for drinking to be initiated. From this perspective, drinking would be expected following either suprathreshold stimulation or drug-induced lowering of the activation threshold in these animals, as was observed, with the loss of putative AII receptors in the SFO also contributing to their particularly severe deficits in thirst induced by AII.

Angiotensin II↗
PubMed1981

Thirst and sodium appetite after colloid treatment in rats.

Subcutaneous injection of polyethylene glycol (PEG) solution produced a progressive sequestration of extracellular fluid at the injection site. Appropriately, PEG-treated rats showed both thirst and sodium appetite. However, water intake began within 1 to 2 hr after the injections, whereas consumption of NaCl solution did not start until 3-4 hr later. Then rats ingested both fluids alternately until plasma volumes were restored, whereupon saline intake became even more prominent while water was consumed due to induced osmoregulatory needs. These three phases were seen regardless of the dose of PEG that was administered or the concentration of saline that was available. In contrast, after maintenance on a sodium-deficient diet for 2-4 days, or after bilateral adrenalectomy, rats increased their intake of saline immediately after PEG treatment. These and other findings suggest that the delayed onset of sodium appetite after PEG treatment that occurs when rats are maintained on standard sodium-rich chow results from the buffer provided by surplus extracellular fluid in those animals. They further suggest that sodium appetite is not directly associated with decreases in plasma volume or sodium concentration but instead may be stimulated by decreased availability of sodium in the brain.

Animals↗
PubMed1980

Compensatory increase in tyrosine hydroxylase activity in rat brain after intraventricular injections of 6-hydroxydopamine.

The neurotoxin 6-hydroxydopamine produced a permanent loss of endogenous norepinephrine and of 3H-labeled norepinephrine uptake sites in the hippocampus within 5 days. These losses were initially accompanied by parallel decreases in tyrosine hydroxylase activity and synaptosomal norepinephrine synthesis. Within 21 days, however, hippocampal tyrosine hydroxylase activity and norepinephrine synthesis rate increased three- to fivefold. These data suggest a novel form of plasticity in brain-damaged animals characterized by an increase in the capacity for transmitter biosynthesis in residual neurons.

Animals↗