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Biomedical subjects

A Argiolas

Publications and source records attributed to A Argiolas.

At least 109 records · Page 6Linked to original sources
PubMed1983

Facilitation of phospholipase A2 activity by mastoparans, a new class of mast cell degranulating peptides from wasp venom.

The effect of mastoparan, Ile-Asn-Leu-Lys-Ala-Leu-Ala-Ala-Leu-Ala-Lys-Lys-Ile-LeuNH2, and related peptides on the release of arachidonic acid from egg yolk lecithin liposomes, rat peritoneal mast cells, and cultured human fibroblasts was studied. In unsonicated liposomes, labeled with 1-stearoyl-2[1-14C]arachidonyl-sn-glycero-3-phosphocholine, 5 X 10(-5) M mastoparan caused a 12-, 15-, and 50-fold increase in the production of arachidonic acid catalyzed by phospholipase A2 from bee venom, eastern diamondback rattlesnake and porcine pancreas, respectively. The stimulant effect of mastoparan and related peptides was dose-dependent and further enhanced by sonication of liposomes. In contrast, melittin, while stimulating the production of arachidonic acid by phospholipase from bee venom, was inactive with the rattlesnake and pancreatic enzymes. Melittin was also only weakly active with liposomes containing stearic acid in place of arachidonic acid. Like melittin, mastoparans stimulated phospholipase activity in tissue homogenates and caused a dose-dependent release of arachidonic acid from rat peritoneal mast cells and cultured human fibroblasts prelabeled with [14C]arachidonic acid. The heptapeptide fragments mastoparan 1-7 and mastoparan 8-14, and succinylated mastoparan were ineffective. The results suggest that mastoparan and related peptides in insect venoms act, at least in part, by stimulating phospholipase activity.

Amino Acid Sequence↗
PubMed1983

Bradykinin reverses the effect of opiates in the gut by enhancing acetylcholine release.

Four naturally occurring peptides of the kinin family, bradykinin, lysylbradykinin, methionyllysylbradykinin, and polisteskinin reverse the inhibitory effect of morphine, metenkephalin, and epinephrine on the electrically stimulated guinea pig ileum longitudinal muscle myenteric plexus preparation. Bradykinin, the most potent kinin, enhances the release of acetylcholine in the gut, and its reversal of the opiate inhibitory effect is blocked by the anticholinergic drug, hyoscine.

Acetylcholine↗
PubMed1983

Suppression of voluntary ethanol consumption in rats by gamma-butyrolactone.

The effect of gamma-butyrolactone (GBL) on voluntary ethanol intake was studied in a group of Wistar rats in which a stable preference had been induced by exposure to increasing ethanol concentrations. These rats drank 60% of their daily fluid intake as 15% ethanol solution, corresponding to about 6 g ethanol/kg/day. GBL, injected intraperitoneally at the dose of 200 mg/kg, twice daily for 3 consecutive days, decreased ethanol intake by about 80% on the days of treatment, but did not reduce total fluid intake. Ethanol intake remained significantly reduced up to the 5th day following cessation of GBL administration. GBL, up to a concentration of 10(-3) M, inhibited neither alcohol-dehydrogenase nor aldehyde-dehydrogenase in rat liver homogenates, nor dopamine-beta-hydroxylase in homogenates of adrenal medulla or hypothalamus of rats. It is suggested that inhibition of firing in dopaminergic neurons mediates the suppressant effect of GBL on ethanol preference.

4-Butyrolactone↗
PubMed1983

Effect of (-)-cathinone, a khat leaf constituent, on dopaminergic firing and dopamine metabolism in the rat brain.

The effect of (-)-cathinone (CAT), an alkaloid from khat leaves, on brain dopamine (DA) metabolism and on the firing rate of nigral DA neurons was studied in rats, in comparison with that of d-amphetamine. Like d-amphetamine, CAT (8-40 mg/kg i.p.) decreased DOPAC levels in the caudate nucleus, nucleus accumbens and frontal cortex, without modifying DA concentrations. CAT showed approximately one fifth of the potency of d-amphetamine in this effect. CAT, injected i.v. to unanesthetized, paralyzed rats, inhibited the firing rate of DA neurons in the substantia nigra, pars compacta, showing a similar potency to that of d-amphetamine in this respect. CAT-induced inhibition of dopaminergic firing was reversed by haloperidol.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Delayed inhibition of dopamine synthesis by gamma-butyrolactone and baclofen: dopamine autoreceptor supersensitivity?

The administration of gamma-butyrolactone (GBL) (750 mg . kg-1 i.p.) and baclofen (20 mg . kg-1 i.p.) to rats caused a transient increase followed by a long-lasting decrease in striatal dopamine (DA) synthesis, as measured by DOPA accumulation after decarboxylase inhibition. DA synthesis was reduced to 40-50% of the control value for 2-12 h following either treatment. The GBL- and baclofen-induced inhibition of DN synthesis was reversed by haloperidol (2-5 mg . kg-1 i.p.) and by a second dose of baclofen or GBL. The subcutaneous dose of 15 mg . kg-1 of apomorphine, insufficient to decrease DA synthesis in control rats, produced a further decrease in DA synthesis in animals pretreated with baclofen. These results suggest that the delayed DA synthesis inhibition following GBL or baclofen treatment was due to stimulation of supersensitive DA autoreceptors.

4-Butyrolactone↗
PubMed1982

Evidence for dopamine autoreceptors controlling dopamine synthesis in the substantia nigra.

The effect of apomorphine and haloperidol on DOPA accumulation after inhibition of DOPA decarboxylase activity with NSD 1015 was compared in the substantia nigra (SN) and caudate nucleus (CN) of normal rats and rats deprived of nigral afferences from the striatum by means of intrastriatal kainic acid. In normal rats apomorphine decreased DOPA accumulation to the same extent in both the SN and CN. However, haloperidol produced a more pronounced increase in DOPA accumulation in the CN than in the SN. The effect of both drugs still persisted in the SN and CN after destruction of the neuronal strionigral feedback loop with kainic acid. The results provide evidence for the existence of nigral dopamine autoreceptors controlling dopamine synthesis in the SN.

Animals↗
PubMed1982

N-n-propyl-norapomorphine: an extremely potent stimulant of dopamine autoreceptors.

N-n-propyl-norapomorphine (NPA) is 10-20 times more potent than apomorphine in producing hypomotility and inhibiting both striatal and limbic dopamine (DA) synthesis and the firing rate of nigral dopaminergic cells in rats. The threshold subcutaneous doses of NPA and apomorphine to significantly inhibit motor activity or DA synthesis are 1.25 and 24 microgram/kg, respectively. The intravenous ED 50 of NPA to inhibit dopaminergic firing is 0.36 microgram/kg and that for apomorphine is 9.1 microgram/kg. The above effects of NPA, as those of apomorphine, are antagonized by haloperidol and, stereospecifically by (--) sulpiride.

Animals↗
PubMed1982

Effect of dopamine agonists and antagonists on DOPA formation in the substantia nigra.

The effect of different psychotropic drugs on the rate of DOPA accumulation after administration of a decarboxylase inhibitor (NSD 1015) was compared in the substantia nigra (SN) and caudate nucleus (CN) by a new radioenzymatic method. Inhibition of monoamine oxidase with pargyline or stimulation of dopamine (DA) receptors with apomorphine, N-n-propylnorapomorphine or D-amphetamine reduced DOPA formation in the CN and SN to the same extent. Vice versa, both inhibition of DA receptors with haloperidol or (-)sulpiride and depletion of DA concentration with reserpine enhanced DOPA formation to a greater extent in the CN than in the SN. Apomorphine antagonized not only the effect of haloperidol and (-)sulpiride, but also, and even more effectively, that of reserpine. The results indicate that DA synthesis in the SN is controlled by both end-product inhibition and DA receptor-mediated mechanisms.

Animals↗
PubMed1981

Repeated electroconvulsive shock prevents the sedative effect of small doses of apomorphine.

Repeated electroconvulsive shock (ECS) (one shock daily for 8 days), but not single ECS, eliminates the sedative response to small doses of apomorphine (25--1000 microgram/kg) and potentiates the stimulant response to high doses (200 microgram/kg) of the drug in rats. This effect is observed 1 and 4 days after the last ECS. However, repeated ECS does not prevent the inhibitory effect of apomorphine on dopamine (DA) synthesis. The results suggest that repeated ECS may lead to the development of subsensitivity in DA receptors that mediate sedation and that these receptors are differentiated from those controlling DA synthesis.

Animals↗
PubMed1981

A simple radioenzymatic method to measure picogram amounts of DOPA in brain and biological fluids.

A simple radioenzymatic method for the determination of DOPA is described. The method is based on the conversion of DOPA to 3-O-[methyl-3H]DOPA by catechol-O-methyltransferase in the presence of S-adenosyl-[methyl-3H]methionine and purification of the labelled product by Sephadex G10 and Dowex 50 W x 4 ion exchange resin. The method has been applied to the assay of endogenous DOPA in different brain area and to measuring DOPA accumulation after inhibition of aromatic amino acid DOPA decarboxylase.

Animals↗
PubMed1980

Effect of acute and chronic ethanol on dopamine synthesis in the caudate nucleus, substantia nigra and frontal cortex.

A single oral administration of 3.2 g/kg ethanol to normal rats increased 3,4-dihydroxyphenylacetic acid (DOPAC) content and DOPA formation in the caudate nucleus but had no effect in frontal cortex and substantia nigra and did not modify dopamine (DA) levels in any of the brain regions analyzed. Complete tolerance to the stimulant effect on DOPA formation developed after chronic ethanol-treatment (3.2 g/kg daily for 60 days). However ethanol administration to ethanol dependent rats produces a marked DA depletion and increases DOPAC concentration in the brain areas studied. The present results show that acute and chronic ethanol release DA stores, but only in the acute conditions DA depletion is compensated by enhanced synthesis.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1980

Effect of ethanol on the metabolism of regional brain dopamine.

Acute oral administration of ethanol (3.2g/kg) to rats increased (DOPAC) levels in the caudate nucleus, but had no effect on DOPAC levels in the substantia nigra and frontal cortex and failed to modify dopamine content in any of the above areas. On the other hand, the administration of the same dose of ethanol to rats which had been chronically treated with ethanol (3.2g/kg daily for 60 days), produced a decrease of DA content and a parallel increase of DOPAC levels in all areas studied. In chronically treated rats, 24 hrs after last ethanol administration dopamine levels in the frontal cortex were 60% higher than in controls. The results suggest that ethanol administration causes dopamine release in different brain areas.

3,4-Dihydroxyphenylacetic Acid↗