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P Södersten

Publications and source records attributed to P Södersten.

At least 19 recordsLinked to original sources
PubMed1997

Cholecystokinin, dopamine D2 and N-methyl-D-aspartate binding sites in the nucleus of the solitary tract of the rat: possible relationship to ingestive behavior.

Receptor autoradiography was used to investigate the distribution of brainstem binding sites for cholecystokinin, dopamine and N-methyl-D-aspartate with particular reference to the nucleus of the solitary tract of the rat, an area involved in the control of ingestive behavior. Binding sites for the A and B subtypes of the cholecystokinin receptor, labeled with [(125)I]cholecystokinin octapeptide sulfate in the presence or absence of antagonists for the devazepide (A) or L-365,260 (B) receptor, were present throughout the caudal rostral extent of the nucleus of the solitary tract, the A type predominating in the commissural, medial and gelatinous part and the B type in the lateral part. In the most rostral part of the medial nucleus of the solitary tract, both A and B receptors were present. Dopamine D2 receptors, labeled with [(125)I]NCQ-298, were found in all parts of the nucleus of the solitary tract. No binding to the dopamine D1 receptor, labeled with [(125)I]SCH-23982, was found in the brainstem. N-Methyl-D-aspartate receptors, labeled with [(3)H]dizocilpine maleate, were also present in the entire caudorostral extent of the nucleus of the solitary tract. Binding to cholecystokinin A receptors was co-distributed with [(125)I]NCQ-298 and [(3)H]dizocilpine maleate binding in the caudal and rostral parts of the nucleus of the solitary tract, and binding to cholecystokinin B receptors overlapped with [(125)I]NCQ-298 and [(3)H]dizocilpine maleate binding in the rostral nucleus of the solitary tract. These results are consistent with the hypothesis that cholecystokinin, dopamine and glutamate interact in the nucleus of the solitary tract in the control of ingestive behavior.

Animals↗
PubMed1997

Altered dopamine function in pathological gambling.

BACKGROUND: The possibility that monoaminergic neurotransmission is altered in pathological gambling was examined. METHODS: Monoamines and their metabolites were measured in CSF obtained at level L4-5 from ten pathological gamblers and seven controls. RESULTS: A decrease in dopamine and an increase in 3,4-dihydroxyphenylacetic acid and homovanilic acid was found. Noradrenaline and its metabolite 3-methoxy-4-hydroxyphenylglycol was also increased but 5-hydroxytryptamine and 5-hydroxyindoleacetic acid were unchanged. CONCLUSION: It is suggested that the function of the dopaminergic system, possibly mediating positive and negative reward, and the noradrenergic system, possibly mediating selective attention, is changed in pathological gambling.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Cholecystokinin octapeptide inhibits carbohydrate but not protein intake.

Male rats ingested about half as much of an intraorally infused (1 ml/min) carbohydrate solution compared with a protein solution. Blood levels of cholecystokinin octapeptide (CCK-8) had increased to 13.6 +/- 1.4 and 16.7 +/- 1.7 pmol/l when the rats stopped ingesting carbohydrate or protein and continued to increase to 35.6 +/- 3.2 pmol/l 30 min after the carbohydrate meal and 34.4 +/- 3.5 pmol/l 60 min after the protein meal. Intraperitoneal injection of CCK-8 (0.6-5.0 micrograms) inhibited and injection of the CCKA-receptor antagonist L-364, 718 (20-80 micrograms) facilitated carbohydrate intake, but neither CCK-8 nor L-364,718 affected protein intake. The results suggest that CCK-8 is not involved in regulating the duration of a protein meal but may be involved in regulating carbohydrate intake. The postprandial period of suppression of protein intake correlated with the disappearance of some amino acids, e.g., Arg, Tyr, and Trp, in the blood, and this may be of importance for protein ingestion, since these amino acids are neurotransmitter precursors.

Amino Acids↗
PubMed1996

Influence of peritoneal dialysis solutions with glucose and amino acids on ingestive behavior in rats.

Continuous ambulatory peritoneal dialysis (CAPD) is often associated with malnutrition; reduced intake of nutrients due to anorexia is an important factor. The glucose load from glucose-based peritoneal dialysis (PD) solutions and amino acids from amino acid-based solutions may favor suppression of the appetite. To study this matter we used a new experimental model in free-moving, unstressed male Wistar rats (300 to 350 g) with feeding catheters channeled from the top of the skull to the oral cavity. When the rats recovered from surgery they were tested under standardized conditions by giving them an intraoral infusion (1 ml/min) of a solution containing 342 g/liter of the sucrose or 97 g/liter protein solutions while recording the time (volume) of ingestion. Control rats consumed 18.8 +/- 0.9 ml of the sucrose and 39.8 +/- 0.8 ml of the protein solutions. Injections of PD solutions with 13.6, 22.7, and 38.6 g/liter of glucose reduced the ingestion of sucrose by 12.4%, 23.6% and 36.1%, respectively, but did not affect the ingestion of protein. Injections of 30 ml of PD solutions containing 11, 18 and 31 g/liter of amino acids reduced the ingestion of both sucrose by 9.7%, 17.1% and 33.2% and of protein by 13.5%, 25.9% and 33.1%, respectively. We conclude that in our experimental model, the inhibition of appetite caused by peritoneal solutions containing glucose or amino acids seems to be specific for each nutritional constituent and not simply an effect of hyperosmolality or large filling volumes.

Adaptation, Physiological↗
PubMed1996

Middle-sized molecule fractions isolated from uremic ultrafiltrate and normal urine inhibit ingestive behavior in the rat.

Uremic patients with suppressed food intake may regain appetite soon after starting dialysis, presumably because of the removal of one or more toxic factors that suppress appetite. To investigate this matter, this study used a new experimental model in free-moving, unstressed male Wistar rats (300 to 350 g) with feeding catheters channeled from the top of the skull to the oral cavity. When the rats recovered from surgery, they were tested under standardized conditions by being given an intraoral infusion (1 mL/min) of a 1 M sucrose solution or a 97 g/L protein solution or a mixed solution of carbohydrate, protein, and fat (Fortimel (Nutricia Nordica AB, Stockholm, Sweden)) while the time (volume) of ingestion was recorded. Solutions to be tested for their ability to inhibit ingestion were injected intraperitoneally (lp) and the intraoral infusion was started 20 min later. Plasma ultrafiltrate was collected from end-stage renal failure patients by isolated ultrafiltration at the beginning of their first hemodialysis and pooled. Ultrafiltrate was also obtained by filtering pooled plasma from healthy volunteers in vitro, using the same type of dialyzer and cellulose acetate membranes as those used in the uremic patients. Morning urine samples from healthy volunteers were pooled and subjected to the same in vitro filtration procedure as the normal plasma. Intraperitoneal injection of 20 mL normal ultrafiltrate had no effect on sucrose ingestion, whereas injection of 20 mL uremic ultrafiltrate reduced the ingestion of sucrose solution by 23% and the ingestion of Fortimel by 17%. Ten mL of ultrafiltrate from normal urine reduced the sucrose intake by 42%. The pooled ultrafiltrates from normal and uremic plasma and normal urine were subjected to molecular filtrations using a series of membranes with known cut-off points. The filtrations yielded four concentrated fractions with molecular weight ranges of 0.1 to 0.5 kilodaltons (kd), 0.5 to 1 kd, 1 to 5 kd, and 5 to 10 kd, respectively; the plasma fractions were concentrated a factor of about 25:1 and the urine fractions by about 15:1. After an ip injection of 2 mL of each concentrated plasma fraction, only the 1 to 5 kd fraction from the uremic ultrafiltrate inhibited sucrose intake, whereas the corresponding fraction from the normal ultrafiltrate had no effect. After injection of 1, 3, and 5 mL of the concentrated fractions of uremic ultrafiltrate, a dose-dependent inhibition of sucrose intake was achieved with the 1 to 5 kd fraction and, to a lesser extent, with the 5 to 10 kd fraction. Intraperitoneal injection of 0.5, 1.0, and 2 mL of the concentrated 1 to 5 kd fraction, but not of the other fractions from normal urine, also resulted in a dose-dependent inhibition of sucrose intake. The 1 to 5 kd fractions from the uremic ultrafiltrate and the normal urine ultrafiltrate also inhibited protein intake in a dose-dependent manner. These results suggest that one or more toxic compounds in the middle-molecule weight range, which are normally excreted in the urine, accumulate in uremia and suppress food intake.

Animals↗
PubMed1995

Mind mechanisms.

Explore the source record for details and available documents.

Consciousness↗
PubMed1995

Increased cerebrospinal fluid concentration of nitrite in Parkinson's disease.

The concentration of nitrite, a metabolite of nitric oxide (NO), was increased in the cerebrospinal fluid (CSF) of untreated patients with Parkinson's disease and in patients treated with L-DOPA in comparison with a group of patients without dopaminergic dysfunction. There was no difference in the concentration of L-arginine (ARG), a precursor of NO, between the groups. There was a highly significant, linear relationship between the concentration of nitrite and ARG in the CSF suggesting that the production of NO is dependent on the availability of ARG. The results support the possibility that production of NO is increased in the brain in Parkinson's disease.

Aged↗
PubMed1995

Inhibition of serotonin synthesis attenuates inhibition of ingestive behavior by CCK-8.

Ingestive behavior was activated in male rats by intraoral infusion of a 1-M solution of sucrose. Injection of cholecystokinin octapeptide (CCK-8; 1.6 or 5.0 micrograms) inhibited ingestion of the sucrose solution and increased the concentration of 5-hydroxytryptamine (5-HT) in the paraventricular hypothalamic nuclei. The inhibitory effect of the low, but not the high, dose of CCK-8 was attenuated by depleting 5-HT in the brain with p-chlorophenylalanine (PCPA; 100 mg/kg for 3 days). Treatment with 5-hydroxytryptophan (20 mg/kg) increased the concentration of 5-HT in the brain of rats pretreated with either NaCl or PCPA and enhanced the inhibitory effect of CCK-8 on ingestive behavior in the PCPA-, but not NaCl-, treated rats. 5-HT may play a role in the mechanism of action of CCK-8 but additional factors must be involved.

5-Hydroxytryptophan↗
PubMed1995

Diet-independent suppression of ingestive behavior by cholecystokinin octapeptide and amino acids.

Male rats consumed much more of an intraorally administered mixed protein, fat and carbohydrate solution than of a carbohydrate solution. Injection of cholecystokinin octapeptide (CCK-8, 0.6-5.0 microgram) suppressed intake of both solutions, but the CCK-A receptor antagonist L-364, 718 (20-40 micrograms) facilitated only carbohydrate intake. Blood levels of CCK-8 were higher after intake of the carbohydrate than the mixed solution. Blood levels of isoleucine, leucine, lysine, threonine, valine, and tryptophan increased only after intake of the mixed solution. Injection of these amino acids suppressed intake of both solutions. Blood levels of amino acids were also less after the seventh than after the first session ingesting the mixed solution. Treatment with CCK-8 or amino acids inhibits intake of any diet, but when secreted endogenously, these signals may terminate the meal in a diet-dependent manner.

Amino Acids↗
PubMed1995

Dopamine D1 or D2 antagonists enhance inhibition of consummatory ingestive behavior by CCK-8.

A dopamine D1 (SKF-38393, 1 mg)- or D2 (LY-171555, 0.1 mg)-receptor agonist inhibited intake of an intraorally infused solution of sucrose by male rats, a test of consummatory ingestive behavior. Treatment with a D1 (SCH-39166, 0.1 mg) or D2 (raclopride, 0.6 mg) antagonist reversed inhibition by the respective agonist but enhanced the inhibitory effect of cholecystokinin octapeptide (CCK-8; 1.8 micrograms). It was not possible to demonstrate specific effects of D1 and D2 agonists on intake of pellets, a test that does not discriminate consummatory ingestive behavior from appetitive ingestive behavior, i.e., behavior used to obtain food. The results demonstrate specific involvement of dopamine D1 and D2 receptors in inhibition of consummatory ingestive behavior.

Animal Feed↗
PubMed1994

Apomorphine suppresses ingestive behaviour in chronic decerebrate rats.

To determine whether dopamine receptors in the brain stem can mediate inhibition of feeding behaviour male rats in which the forebrain was disconnected from the brain stem were studied. Such decerebrate rats do not approach food but display ingestive responses if infused intraorally with a 1 M solution of sucrose at 0.6 ml min-1. Intraperitoneal injection of 5 micrograms cholecystokinin octapeptide, a physiological satiety peptide, or 400 micrograms apomorphine, a dopamine D1-D2 receptor agonist, suppressed intake of the sucrose solution. The results support a role of brain stem dopamine receptors in the control of ingestive behaviour.

Animals↗