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Biomedical subjects

P Alster

Publications and source records attributed to P Alster.

At least 37 records · Page 2Linked to original sources
PubMed1996

Effects of selective serotonin and dopamine agonists on plasma levels of glucose, insulin and glucagon in the rat.

Male Sprague-Dawley rats were given one of the 5-HT receptor agonists 8-OH-DPAT (0.5-2.0 mg kg-1), TFMPP (0.125-2.0 mg kg-1), DOI (0.125-2.0 mg kg-1), and m-CPBG (1.25-20.0 mg kg-1), selective for 5-HT1A, 5-HT1B, 5-HT2 and the 5-HT3 receptors, respectively, or one of the DA receptor agonists bromocriptine (2.0-32.0 mg kg-1), quinpirole (0.5-8.0 mg kg-1) and 7-OH-DPAT (0.2-3.2 mg kg-1), selective for DA D2, DA D2/D3 and DA D3 receptors, respectively. An additional group of animals was given buspirone (2.0-8.0 mg kg-1) a 5-HT1A receptor agonist and DA D2 receptor antagonist. Separate groups of rats were given both the 5-HT1A receptor antagonist pindolol and 8-OH-DPAT or both the DA D2/D3 receptor antagonist raclopride and 7-OH-DPAT. Blood samples were collected 30 min (in some cases 120 min) after drug administration and assayed for insulin, glucagon and glucose levels. The 5-HT1A receptor agonist 8-OH-DPAT produced a statistically significant decrease in plasma insulin levels and an increase in glucose, whereas glucagon levels were unaffected. The only effect observed after buspirone treatment was a small increase in plasma glucose levels. No significant effects on plasma insulin, glucagon or glucose were seen after treatment with the 5-HT1B, 5-HT2 or 5-HT3 agonists. The DA D3 receptor agonist 7-OH-DPAT produced a decrease in plasma insulin (3.2 mg kg-1, 120 min) and an increase in glucose levels. Administration of the DA D2/D3 receptor agonist quinpirole resulted only in increased plasma glucose, whereas the DA D2 receptor agonist bromocriptine had no effect. In support of a separate mediation of glucose secretion by 5-HT1A and DA D3 receptors, the effects of 8-OH-DPAT on glucose levels were antagonized by (-)pindolol pretreatment, and the 7-OH-DPAT-induced effects on glucose levels were antagonized by raclopride pretreatment. It is concluded that plasma glucose levels are under separate serotonergic and dopaminergic control, exerted via 5-HT1A and DA D3 receptors, respectively.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Suggestive evidence for a DA D3 receptor-mediated increase in the release of oxytocin in the male rat.

The dopamine (DA) D2/3 receptor agonists quinpirole (0.5-8.0 mg kg-1, s.c.) and 7-OH-DPAT (0.2-3.2 mg kg-1, s.c.), but not the preferential DA D2 receptor agonist bromocriptine (2.0-32.0 mg kg-1, s.c.), produced increased plasma oxytocin levels in the rat. In keeping with their affinity for the DA D2 receptor, all three compounds produced a marked suppression of plasma prolactin levels in their respective dose range. It is suggested that DA D3 receptors are involved in mechanisms regulating oxytocin secretion in the rat.

Animals↗
PubMed1994

High doses of oxytocin cause sedation and low doses cause an anxiolytic-like effect in male rats.

The aim of the present investigation was to explore dose relationships for effects of oxytocin on spontaneous motor activity in the rat. Oxytocin in doses from 1-1000 micrograms/kg was given SC to male Sprague-Dawley rats, and spontaneous motor behavior was measured by means of photocell-operated open-field observations. In the rats treated with low doses of oxytocin (1-4 micrograms/kg), there was a decrease in peripheral locomotor activity. With increasing doses (250-1000 micrograms/kg), there were clear signs of sedative effects as indicated by a suppression of locomotor activity and rearing. The time course for the effect of oxytocin on peripheral activity (1 microgram/kg) and rearing (1 mg/kg) was tested. A maximal effect was obtained within 1 h and, thereafter, the behavior gradually returned to normal within 24 h. This spectrum of effects caused by oxytocin was similar to that of midazolam but different from that induced by raclopride.

Animals↗
PubMed1994

Role of vagal nerve activity during suckling. Effects on plasma levels of oxytocin, prolactin, VIP, somatostatin, insulin, glucagon, glucose and of milk secretion in lactating rats.

The aim of this study was to investigate the role of vagal nerve activity for the release of oxytocin, prolactin and gastrointestinal (GI) hormones during suckling as well as for the secretion of milk in lactating rats. We have therefore performed experiments on vagotomized lactating rats. The animals were decapitated and trunk blood was collected from nonsuckling rats and from suckling rats in connection with milk ejection. Oxytocin, prolactin, vasoactive intestinal polypeptide (VIP), somatostatin, insulin, glucagon and glucose levels in plasma were measured by RIA-technique. In addition, maternal weight as well as the weight of the litters were recorded 7 d after vagotomy. As expected, oxytocin and prolactin levels rose in response to suckling in sham-operated controls. In vagotomized animals the suckling-induced increase of oxytocin was blocked and prolactin levels were significantly decreased. VIP levels in plasma increased following suckling in sham-operated animals and failed to respond after vagotomy. In contrast, somatostatin levels that rose significantly in sham-operated rats were even more significantly raised in vagotomized animals. In addition, insulin but not glucagon levels were increased by suckling. The insulin response, however, persisted after vagotomy. Interestingly, suckling was followed by a lowering of blood-glucose levels in vagotomized, but not in sham-operated animals. The vagotomized rats ate as much and increased in weight as sham-operated rats during the 7 d of vagotomy. The litters of vagotomized rats, however, gained significantly less weight in comparison with control litters. In conclusion, this study shows that vagal nerve activity is of importance for the release of oxytocin, prolactin, vasoactive intestinal polypeptide and somatostatin during suckling.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The antinociceptive effect of non-noxious sensory stimulation is mediated partly through oxytocinergic mechanisms.

The objective of the present study was to investigate whether oxytocinergic mechanisms may contribute to the antinociceptive effect of non-noxious, sensory stimulation. To test this hypothesis, oxytocin levels in plasma and cerebrospinal fluid (CSF) were measured in control rats as well as in rats exposed for 30 min to electro-acupuncture (2 Hz), thermal stimulation (40 degrees C) or vibration (100 Hz). All modes of stimulation induced significant elevations of oxytocin levels in plasma and/or in CSF, 30 or 90 min after the end of stimulation. Secondly, the antinociceptive effects of these treatments were investigated in the tail-flick test with and without prior administration of the oxytocin antagonist 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-oxytocin (1 mg kg-1 i.p.). All three modes of stimulation caused a significant delay of the tail-flick latency to the same degree as that caused by injection of oxytocin 1 mg kg-1 i.p. (electro-acupuncture P < 0.01, thermal stimulation and vibration P < 0.05). In all cases, the delay was reversed by administration of the oxytocin antagonist (1 mg kg-1 i.p.). These findings suggest that analgesic effects induced by non-noxious sensory stimulation may, in part, be mediated through activation of oxytocinergic mechanisms.

Acupuncture Therapy↗
PubMed1992

Amperozide and clozapine but not haloperidol or raclopride increase the secretion of oxytocin in rats.

The aim of the present study was to investigate whether amperozide, an antipsychotic drug which possesses anti-aggressive and anxiolytic-like properties, stimulates the secretion of oxytocin and if so, by which receptor mechanism. For this purpose, female or male Sprague Dawley rats were given amperozide (0.5, 2.5 and 5.0 mg/kg IP), ritanserin (5.0 mg/kg), raclopride (2.0 mg/kg) and prazosin (1.0 mg/kg) and were subsequently decapitated for collection of blood (30 and 120 min) after injection. Oxytocin levels were measured with radioimmunoassay. Amperozide 2.5 and 5 mg/kg increased plasma levels of oxytocin significantly (P < 0.05 and < 0.001). The effect appeared maximal about 30 min after injection of the drug and oxytocin levels were almost back to basal within 120 min. Similar effects were obtained in female and male rats as well as in animals that were freely fed or food deprived for 24 h. CSF levels of oxytocin were also increased. Ritanserin, a 5-HT2-receptor antagonist but not the D2 receptor antagonist raclopride or the alpha 1-adrenoceptor antagonist prazosin stimulated oxytocin release. In addition, clozapine, a neuroleptic with potent HT2-antagonistic properties, was a potent releaser of oxytocin, whereas haloperidol was without effect. A possible role for oxytocin in the behavioural effects of amperozide and clozapine remains to be explored.

Animals↗
PubMed1992

Vagally mediated release of gastrin and cholecystokinin following sensory stimulation.

The aim of the present study was to investigate whether gastrin, cholecystokinin (CCK) and somatostatin secretion can be influenced by sensory stimulation and if so, whether such effects are mediated via the vagal nerves. Male rats anaesthetized with chloral hydrate were exposed to three different stimuli, i.e. to low frequency (2 Hz) electrical stimulation of muscles via needles (electro-acupuncture), to thermal stimulation at 40 degrees C or to vibration at 100 Hz. The two former stimuli activate mainly small and medium sized myelinated fibres from muscles and skin respectively, whereas vibration activates large myelinated fibres from skin, subcutaneous tissue and muscles. Experiments were also performed on animals that were vagotomized or exposed to prior treatment with atropine (0.5 mg kg-1). Blood was collected at various time intervals and plasma levels of gastrin, CCK and somatostatin were measured with radioimmunoassay (RIA). All three stimuli, i.e. electro-acupuncture, vibration and thermal stimulation caused significant elevations of gastrin (103 +/- 11-151 +/- 16 pM, 105 +/- 8-140 +/- 12 pM and 105 +/- 14-162 +/- 4 pM) and cholecystokinin (9 +/- 0.8-15 +/- 2.8 pM, 8 +/- 0.5-10 +/- 1.5 pM and 8.0 +/- 0.5-10.5 +/- 1.5). Somatostatin was raised in response to electro-acupuncture (10 +/- 1-14 +/- 3 pM). Vagotomy and atropinization abolished the release of gastrin and CCK in response to all three stimuli. CCK levels were significantly reduced following electro-acupuncture in atropinized rats. In conclusion, gastrin and cholecystokinin release is stimulated by activation of sensory afferent, originating in skin, subcutaneous tissue as well as in muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1990

Quantitation of oncogene products by computer-assisted image analysis and flow cytometry.

The use of antibodies permits the study of oncogene product expression in cells and tissues. However, quantitation of the levels of expression in immunohistochemical preparations is beset by difficulties, and the available scoring system provide semiquantitative data at best. Here we describe the use of computer-assisted image analysis for determination of oncoprotein levels in a model system and compare the results with those generated by flow cytometric analysis. The oncogene products measured are located in the nucleus (c-myc p62 and c-fos p55), the inner surface of the membrane (c-ras p21), and both sides of the membrane (c-erbB-2 p185). In each instance, both analytic modalities yielded concordant results. Our data indicate that computer-assisted image analysis is a useful tool for quantitating cell components in immunohistochemical preparations.

Breast Neoplasms↗
PubMed1988

Interactions among red cell membrane proteins.

Interactions between human red band 2.1 with spectrin and depleted inside-out vesicles were studied by fluorescence resonance energy transfer and batch microcalorimetry. The band 2.1-spectrin binding isotherm is consistent with a one to one mole ratio. The association constant of 1.4 X 10(8) M-1 corresponds to the association free energy of -11.1 kcal/mol. Under our experimental conditions, the enthalpy of interaction of band 2.1-spectrin was found to be -10.8 kcal/mol and is independent of the protein mole ratio. The calculated entropic factor (-T delta S = 0.3 kcal/mol) strongly suggests a predominantly enthalpic character of the reaction. In addition, we investigated the role of band 2.1 on the binding of band 4.1 to spectrin [Podgorski, A., & Elbaum, D. (1985) Biochemistry 24, 7871-7876] and concluded that only small, if any, alterations of binding of band 4.1 to spectrin have taken place in the presence or absence of band 2.1. This suggests thermodynamic independence of the binding sites. Although the attachment of the cytoskeletal network to the membrane takes place through, at least, two different interactions, band 2.1-band 3 and 4.1-glycophorin, the relative enthalpy values suggest that band 2.1 contributes significantly more than band 4.1 to the energy of the interaction. In addition, we observed that polymerization of actin is modulated by the cytoskeletons as judged by their effect on the rate of actin polymerization.

Ankyrins↗
PubMed1986

Effect of nicotine on prostacyclin formation in human endocardium in vitro.

The effect of nicotine on the formation of prostacyclin by human endocardium was studied in vitro. Slices of cardiac valve cusps were incubated in a saline medium and the prostacyclin-like activity generated spontaneously by the tissue specimens was assessed in terms of its capacity to inhibit ex vivo platelet aggregation. In separate experiments supernatants of valvular tissue homogenates were incubated with [14C]arachidonate. This resulted in the appearance of labelled 6-keto-prostaglandin F1 alpha in the radiochromatograms, indicating the formation of prostacyclin in the homogenates. Nicotine inhibited dose-dependently the spontaneous generation of prostacyclin-like activity (I50 approximately equal to 2 X 10(-4) M), as well as the formation of 6-keto-prostaglandin F1 alpha (I50 approximately equal to 2 X 10(-5) M), indicating an inhibitory effect of the drug on endocardial prostacyclin production.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Effect of nicotine on the formation of prostacyclin-like activity and thromboxane in rabbit aorta and platelets.

The effect of nicotine on the bioformation of prostacyclin (PGI2) and of thromboxane (Tx)B2 in rabbit aorta and platelets, respectively, was investigated. Rabbit aortic rings were incubated with [14C]-arachidonic acid ( [14C]-AA) and the incubation products were separated with thin layer chromatography (t.l.c.). Alternatively, the aortic rings were incubated without substrate and their spontaneous formation of platelet anti-aggregatory activity was measured. Rabbit platelet microsomes were incubated with [14C]-AA and the products formed were separated with t.l.c. Rings of aorta were found to be incapable of converting added [14C]-AA to labelled 6-keto-PGF1 alpha (the stable hydrolysis product of PGI2). Rings of aorta incubated in saline medium spontaneously formed PGI2-like activity. This formation was dose-dependently inhibited by nicotine, with an I50 of about 10(-4) M. Platelet microsomes converted [14C]-AA to labelled TxB2. This formation was unaffected by nicotine. It is concluded that a true difference in sensitivity to nicotine exists between cyclo-oxygenase in rabbit aorta and platelets. The data also demonstrate a tissue difference between rabbit aorta and platelets concerning their utilization of exogenous AA as substrate in the formation of platelet active compounds.

Adenosine Deaminase↗
PubMed1983

Biosynthesis of prostaglandins in microsomes of human skeletal muscle and kidney.

The capacity of human skeletal muscle, renal cortical and renal medullary microsomes to synthesize prostaglandins (PGs) from exogenous precursor was investigated. The microsomal fractions were incubated with [1-14C]-labelled arachidonate ([14C]-AA) in the absence and in the presence of reduced glutathione (GSH). [14C]-PGs formed in the incubates were extracted, separated by thin-layer chromatography and quantified using liquid scintillation spectrometry. [14C]-labelled PGE2, PGF2 alpha and 6-keto-PGF1 alpha were found to be the principal products of microsomal PG formation and appeared in similar relative quantities in the incubates of all three tissues studied. In some incubates of renal cortical and renal medullary microsomes formation of smaller relative amounts of [14C]-PGD2 and thromboxane B2 was also noted. In addition, formation of substantial amounts of a polar, not yet identified compound was frequently observed in all incubates. In the absence of GSH, [14C]-6-keto-PGF1 alpha was the main PG formed by microsomes of all of the three tissues. At the expense of 6-keto-PGF, the addition of GSH resulted in an almost 2-fold stimulation of [14C]-PGF2 alpha formation in the skeletal muscle and renal cortical incubates, whereas in the renal medullary incubates an increase in the relative amounts of [14C]-PGE2 was observed. The PG synthetic capacity was highest in the skeletal muscle and lowest in the renal cortical microsomes. The results demonstrate a considerable capacity of human skeletal muscle and of the renal cortex and renal medulla to synthesize prostacyclin. Furthermore, the data reveal GSH-dependent differences in the expression of PG biosynthesis in these tissues. The GSH-dependent differentiation of PG synthesis may reflect a mechanism of adaptation of local PG production to the physiological processes.

Aged↗