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Biomedical subjects

A Carlsson

Publications and source records attributed to A Carlsson.

At least 343 records · Page 19Linked to original sources
PubMed1979

Bone mass in primary coxarthrosis.

The bone mineral content was measured by gamma absorptiometry at two levels on the forearms, proximally on the shafts and distally close to the wrist, in 53 cases of primary coxarthrosis. The bone mineral content at the distal measuring site, representing trabecular bone, was increased in coxarthrosis cases as compared with normal controls; the difference was significant only in women. At the proximal measuring site, representing cortical bone, there was no significant difference. The findings support the concept of impairment of the resilience of the juxta-articular trabecular bone as one factor contributing to the pathogenesis of arthrosis.

Adult↗
PubMed1979

The inhibition of rat brain monoamine oxidase-B by J-508 (N-methyl-N-propargyl-(1-indanyl)-ammonium hydrochloride), and its use for the titration of this enzyme form.

The interaction between rat brain monoamine oxidase-B and J-508, an analogue of L-deprenil, has been investigated. J-508 inhibits rat brain monoamine oxidase-B in a manner consistent with a 'suicide' reaction, and is so potent an inhibitor that it produces inhibition at concentrations of the same order as those of the enzyme. This property has been used to determine the nature of the changed monoamine oxidase-B activity in the corpus striatum after hemitransection of rat brain.

Alkynes↗
PubMed1978

Monoamine metabolism during bicuculline-induced epileptic seizures in the rat.

Brain levels of tyrosine, dopamine (DA), noradrenaline (NA), tryptophan, 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) were measured after 30, 60 and 120 min of sustained seizure activity, induced in paralyzed, artificially ventilated and anaesthetized (70% N2O) rats by administration of bicuculline (1.2 mg/kg i.v.). In separate animals the rates of accumulation of DOPA and 5-hydroxytryptophan (5-HTP) were estimated in three different brain regions after blockage of the aromatic L-amino acid decarboxylase with NSD 1015 (100 mg/kg). The tissue level of NA was markedly reduced at 30 min and remained low during 120 min of sustained epileptic seizures. In contrast, the DA concentration, being essentially unaffected at 30 min, continuously increased during the following 90 min. 5-HT decreased significantly after 30 min but returned to control levels following 60 and 120 min of seizure activity. The 5-HIAA concentration progressively increased. In all three brain regions (striatum, limbic forebrain and hemispheres) the rate of tyrosine hydroxylation increased. Tryptophan hydroxylation showed a significant increase only in the limbic forebrain. The results suggest that bicuculline-induced seizures lead to an increased functional activity in NA neurons and, at least initially, also in 5-HT neurons. In contrast, DA neurons appear to be inhibited.

5-Hydroxytryptophan↗
PubMed1978

Influence of transient ischemia on monoamine metabolism in the rat brain during nitrous oxide and phenobarbitone anaesthesia.

Cerebral ischemia was induced in normothermic, artificially ventilated rats, anesthetized with 70% N2O or 150 mg/kg of phenobarbitone, by bilateral occlusion of the common carotid arteries and by simultaneous depression of the mean arterial blood pressure to 50 mm Hg. The levels of tyrosine, dopamine (DA), noradrenaline (NA), tryptophan, 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were measured after 15 min of ischemia as well as after 30 min of recirculation. In separate experiments (70% N2O) the rate of accumulation of DOPA and 5-hydroxytryptophan (5-HTP) was determined in three different brain regions (striatum, limbic forebrain and hemispheres) during recirculation. During ischemia, the monoamine pattern was unaffected. Following recirculation, increases in DA, 5-HIAA, tyrosine and tryptophan were found irrespective of the type of anesthesia used. Pronounced postischemic decreases in NA and 5-HT were observed in animals anesthetized with nitrous oxide but not in those given phenobarbitone. During recirculation the rate of tyrosine hydroxylation increased in all three brain regions while tryptophan hydroxylation was reduced. It is tentatively concluded that following transient, global cerebral ischemia, neuronal activity is low or eliminated in dopaminergic and serotoninergic neurons and high in noradrenergic neurons.

5-Hydroxytryptophan↗
PubMed1978

Effect of intraperitoneally administered GABA on the locomotor activity of mice.

Gammaaminobutyric acid (GABA) was injected intraperitoneally (i.p.) into mice at doses from 25--2000 mg/kg, and spontaneous locomotor activity was recorded for the following 20 min. A slight but significant decrease in the spontaneous locomotor activity was noted only with the highest dose. The stimulation of motor activity induced by ethanol (2.4 g/kg i.p.) was significantly counteracted by GABA (100 mg/kg i.p. and upwards). A further suppression of ethanol-induced hyperactivity was reached by pretreatment with aminooxyacetic acid (AOAA, 15 mg/kg i.p.). The stimulation of motor activity induced by morphine (10 mg/kg i.p.) remained unaffected by even high doses of i.p. GABA. Motility produced by activation of postsynaptic catecholamine receptors, i.e., by apomorphine (3 mg/kg i.p.) and clonidine (3 mg/kg i.p.) following reserpine (10 mg/kg i.p.) and alpha-methyltyrosine (250 mg/kg i.p.) pretreatment, was not affected by i.p. GABA injections, whereas hypomotility caused by a low dose of haloperidol (150 microgram/kg i.p.) was enhanced. In conjunction with earlier biochemical data, these results suggest a certain access of blood-borne GABA to the CNS, leading to inhibition of dopaminergic neurons involved in motility regulation.

Aminooxyacetic Acid↗
PubMed1978

On the mode of action of diazepam on brain catecholamine metabolism.

Intraperitoneal injection of diazepam in moderate dosage (1--10mg/kg) to rats caused a decrease in dopa and 5-hydroxytryptophan (5-HTP) formation, measured as the accumulation of these intermediates induced by inhibition of the aromatic L-aminoacid decarboxylase by means of NSD 1015 (3-hydroxybenzylhydrazine (HCl), in limbic forebrain, striatum and the remaining hemisphere portion. These effects are opposite to those induced by gamma-aminobutyric acid (gaba) and gamma-butyrolactone (100 and 750 mg/kg i.p. respectively), and the effects of the latter agents were significantly counteracted by diazepam. The effect of diazepam on dopa formation persisted after the acute transection of dopaminergic axons (transverse cerebral hemisection at the level of the caudal hypothalamus). The elevation of dopamine following hemisection was also significantly counteracted on the hemisected side of the brain, the intact side remaining unchanged. The data do not support the hypothesis that benzodiazepines act by enhancing gabaergic transmission. They rather suggest that these agents exert an inhibitory action on transmitter synthesis and utilization at the synaptic level, i.e. an action not necessarily bearing any direct relationship to gaba.

4-Butyrolactone↗
PubMed1978

Neurotensin and its amide analogue [Gln4]-neurotensin: effects on brain monoamine turnover.

Intracerebroventricularly administered neurotensin and [Gln4]-neurotensin (50-200 microgram) increased the formation of Dopa in different brain regions of rats after inhibition of the aromatic L-amino acid decarboxylase. For both neuropeptides these increases were dose dependent (20-150%). In the corpus striatum [Gln4]-neurotensin was twice as active as neurotensin and it tended to be more active also in other brain regions. The brain tyrosine concentrations were also increased. [Gln4]-neurotensin (100-200 microgram) following inhibition of the aromatic L-amino acid decarboxylase, increased the accumulation of 5-hydroxytryptophan in all brain regions by 30-60%. In contrast, neurotensin was completely inactive. In both cases the brain tryptophan concentrations were increased. Both neurotensin and [Gln4]-neurotensin also accelerated the disappearance of dopamine, noradrenaline and 5-hydroxytryptamine after inhibition of monoamine synthesis. These results show an increased brain monoamine turnover induced by both neuropeptides.

Animals↗
PubMed1978

Effects of antidepressant agents on the synthesis of brain monoamines.

The effect of seventeen established or possible antidepressant agents on the synthesis of 5-HT, noradrenaline and dopamine in rat brain has been investigated by measuring the accumulation of 5-hydroxytryptophan and DOPA induced by an inhibitor of the aromatic L-aminoacid decarboxylase (3-hydroxybenzylhydrazine hydrochloride, 100 mg/kg i.p.). All the established inhibitors of 5-HT, noradrenaline and dopamine uptake were found to inhibit the synthesis of the respective monoamines, presumably by influencing a receptor-mediated feedback mechanism. A close correlation appears to exist between blockade of transmitter uptake and inhibition of transmitter synthesis. The results support current ideas on the mode of action of antidepressant agents.

5-Hydroxytryptophan↗
PubMed1978

The effect of beta-alanine on motor behaviour, body temperature and cerebral monoamine metabolism in rat.

Intracerebroventricular (ICV) injection of beta-alanine produced a decrease in rectal temperature, inhibition of exploratory behaviour and motility, and changes in the metabolism of cerebral monoamines. Dopa and 5-HTP accumulation after inhibition of L-aromatic amino acid decarboxylase, NSD 1015 (3-hydroxybencylhydrazine HCl, 100 mg/kg i.p.) was found to be significantly increased in all the dissected cerebral regions of animals treated with beta-alanine, as compared to the controls. Levels of tyrosine and tryptophan did not show any significant change. Endogenous levels of dopamine (DA), noradrenaline (NA), serotonin (5-HT) and 5-hydroxyindolacetic acid (5-HIAA), did not change. After inhibition of the catecholamines synthesis with alpha-methyltryrosine (alpha-MT), dopamine depletion was retarded and noradrenaline accelerated, but without reaching statistical significance. After intraperitoneal (i.p.) injection of beta-alanine, significant changes in motor behaviour were found. Body temperature and metabolism of brain catecholamine were unchanged. This lack of effect could be explained by poor penetration through the blood-brain barrier.

Alanine↗
PubMed1978

Potentiation by neuroleptic agents of the inhibitory action of intraperitoneally administered GABA on the locomotor activity of mice.

The ability of several neuroleptics to potentiate the inhibitory action of IP administered GABA on the motor activity of mice has been investigated. Haloperidol, chlorpromazine, thioridazine, and clozapine, but not the apparently selective dopamine receptor-blocking agent spiperone, were found to possess such activity. Phenoxybenzamine also proved active in potentiating GABA. Thus blockade of dopamine receptors as well as alpha-adrenergic receptors may be responsible for neuroleptic-induced potentiation of GABA actions.

Animals↗
PubMed1978

Pivaloyl esters of N,N-dialkylated dopamine congeners. Central dopamine-receptor stimulating activity.

In order to test for dopamine-receptor stimulating activity a new, sensitive biochemical screening method was designed. For behavioral studies and for determination of the duration of action on the compounds, motor activity measurements were used. O,O'-Dipivaloyl-N,N-dipropyldopamine (4) was the only derivative of a series of dipivaloyl-N,N-dialkyldopamines studied that showed any significant activity. However, the monopivaloyl ester 2-(3-pivaloyloxyphenyl)-N,N-dipropylethylamine (8) seemed to be more potent. The same relationship was found for the corresponding phenols, N,N-dipropyldopamine (3) and 2-(3-hydroxyphenyl)-N,N-dipropylethylamine (7), although both were more active than their pivaloyl esters.

Administration, Oral↗
PubMed1978

On the disulfiram-like effect of coprine, the pharmacologically active principle of Coprinus atramentarius.

Coprine or disulfiram was given to rats in various doses at various time intervals before the administration of 2 g/kg ethanol. The ratio acetaldehyde/ethanol in the alveolar air was measured by gas chromatography and was taken as an index of the aldehyde dehydrogenase (ALDH) activity. The activity of dopamine beta-hydroxylase (DBH) was estimated in the same animals by measuring the amount of 14C-octopamine formed from 14C-tyramine in the heart. Coprine and disulfiram both caused an increase in the acetylaldehyde/ethanol ratio, coprine being more potent than disulfiram. Disulfiram, but not coprine, reduced the net yield of 14C-octopamine. In rats pretreated with either coprine or disulfiram, blood-pressure and heart-rate were recorded before and after intraperitoneal injections of 0.4 g/kg ethanol. In both cases ethanol caused a marked and rapid fall in blood-pressure. However, this effect was accompanied by tachycardia only in animals treated with coprine. It is concluded that coprine like disulfiram inhibits ALDH, but only disulfiram causes an additional inhibition of DBH. This difference may account for differences in the cardiovascular response to ethanol.

Agaricales↗