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Biomedical subjects

L Ahtee

Publications and source records attributed to L Ahtee.

At least 91 records · Page 5Linked to original sources
PubMed1978

Effect of mecamylamine on the fate of dopamine in striatal and mesolimbic areas of rat brain; interaction with morphine and haloperidol.

1 The effects of the nicotinic cholinoceptor blocking drug, mecamylamine (alone or in combination with morphine or haloperidol) were investigated on the striatal homovanillic acid (HVA) concentration and on the alpha-methyl-p-tyrosine (AMPT)-induced depletion of striatal or mesolimbic dopamine content in the brain of rats. 2 Mecamylamine (2 mg/kg) alone did not alter the striatal HVA concentration, but it reduced the probenecid-induced accumulation of HVA. Mecamylamine pretreatment reduced the morphine- and haloperidol-induced elevation of striatal HVA concentrations. Hexamethonium did not alter the striatal HVA concentration when given alone or in probenecid- or morphine-treated rats, whereas pempidine (8 mg/kg) clearly reduced the probenecid-induced accumulation of HVA in the striatum. 3 Mecamylamine (2 and 8 mg/kg) slowed the rate of AMPT-induced depletion of dopamine from the striatum and mesolimbic area both in the brain of control rats treated with morphine or haloperidol. 4 Mecamylamine slightly prolonged the cataleptic effect of morphine. 5 The results indicate that mecamylamine inhibits the release of dopamine both from the striatal and mesolimbic dopaminergic neurones.

Animals↗
PubMed1977

Effect of muscarinic cholinergic drugs on morphine-induced catalepsy, antinociception and changes in brain dopamine metabolism.

The effects of drugs acting on muscarinic cholinergic receptors on the catalepsy, antinociception and changes in rectal temperature and in brain dopamine metabolism induced by morphine were studied in Wistar rats. Scopolamine (0.3 - 30 mg/kg) was about three times as potent as atropine (1 - 30 mg/kg) in potentiating the cataleptic effect of morphine. Methylscopolamine and methylatropine did not alter the cataleptic effect of morphine. Pilocarpine (100 mg/kg) and arecoline (10 mg/kg) slightly but significantly and RS86 (20 - 40 mg/kg) clearly antagonized the morphine-catalepsy. RS86 antagonized the atropine-induced potentiation of morphine catalepsy. The antinociceptive effect of pilocarpine was additive and that of RS86 less than additive with morphine. The antimuscarinic compounds did not alter the antinociceptive effect of morphine. Antimuscarinic compounds enhanced the hypothermic effect of morphine, but none of the compounds studied altered the hyperthermic effect of morphine. The antimuscarinic drugs reduced the concentration of striatal homovanillic acid (HVA) in about same proportion in control and morphine-treated rats. Both the muscarinic compounds and morphine increased the concentration of striatal HVA, but when combined their effects were not significantly different from those of morphine alone. Scopolamine antagonized and pilocarpine accelerated the morphine-induced increase in the rate of depletion of cerebral dopamine content. The present results show that the effects of muscarinic aand antimuscarinic cholinergic drugs on the cataleptic effect of morphine were opposite to their effects on the catalepsy induced by neuroleptic compounds.

Analgesia↗
PubMed1976

Effect of cholingeric drugs on methadone-induced catalepsy and stereotypies in rats treated chronically with methadone.

The effects of antimuscarinic (atropine, scopolamine, methylscopolamine), muscarinic (RS86, pilocarpine), antinicotinic (mecamylamine, hexamethonium) and nicotinic (nicotine) cholinergic drugs on the catalepsy and stereotypies induced by acute methadone in rats treated chronically with methadone were studied. The antimuscarinic drugs potentiated and the muscarinic drugs antagonized the cataleptic effect of methadone, whereas the antimuscarinic drugs tended to antagonize and the muscarinic drugs potentiated the methadone-induced stereotypies. Nicotine initially slightly potentiated, and mecamylamine antagonized the cataleptic effect of methadone. The actions of the cholinergic drugs on the extrapyramidal motor effects of methadone were most probably central, because methylscopolamine and hexamethonium had only very weak actions. These results show that the effects of antimuscarinic and muscarinic drugs on the catalepsy and stereotypies induced by methadone are opposite to their effects on the catalepsy and stereotypies produced by drugs which are thought to act on the postsynaptic dopaminergic receptors.

Animals↗
PubMed1976

Effect of ketamine anaesthesia on the content of monoamines and their metabolites in the rat brain.

The effects of ketamine anaesthesia (100 mg/kg i.p.) on the content of brain 5-hydroxytryptamine (5HT), 5-hydroxyindoleacetic acid (5HIAA), noradrenaline (NA), dopamine (DA) and homovanillic acid (HVA) were studied in male Wistar rats. Fifteen min after ketamine injection, when the rats were deeply anaesthetized, the 5HT content in many brain regions tended to be increased. An opposite tendency was found in the brain 5HIAA content. In rats treated with probenecid, which markedly lengthened ketamine anaesthesia, the accumulation of 5HIAA was significantly reduced by ketamine. In addition to ketamine anaesthesia, probenecid was found to lengthen thiopental anaesthesia. One hour after the ketamine administration, when the rats were no longer anaesthetized but were excited, the brain NA concentration was increased by 17% (P less than 0.02). The brain DA content was unchanged, but at 15 min and 1 hour after ketamine administration the striatal HVA content was increased by about 55% (P less than 0.05), suggesting an increased turnover of DA. The results suggest that during recovery from ketamine anaesthesia the increased NA content and the increased DA turnover may be associated with the postanaesthetic excitement of the rat, whereas the decreasamine anaesthesia.

Anesthesia, General↗
PubMed1976

Effect of narcotic analgesics on the striatal homovanillic acid content in mice; relation to antinociceptive effect.

The effects of various narcotic analgesics on striatal homovanillic acid (HVA) content, hot plate time and rectal temperature in mice were compared in relation to dose and time. The hypothermia induced by narcotic analgesics did not correlate with the striat"al HVA increase. Pentazocine, cyclazocine and thebaine had no effect on the hot plate time. The maximum prolongation of hot plate time induced by morphine, methadone or piminodine occurred before the highest HVA increase. The highest increase induced by narcotic analgesics in striatal HVA content was twice the original concentration. This occurred 2 hr after 40 mg/kg of morphine; 2 hr after 20 mg/kg of methadone; 1/2 hr after 20 mg/kg of piminodine; and 1 hr after 60 mg/kg of pentazocine. Cyclacozine (10 and 20 mg/kg) and thebaine (10 mg/kg) did not alter the HVA content. With the exception of pentazocine, those doses of narcotic analgesics that caused equal increases in striatal HVA content were also equianalgesic. These results suggest that there are similarities in the structural requirements for antinociceptive and striatal HVA-increasing effects of narcotic analgesics. The neuroleptic compound haloperidol (0.5 mg/kg) caused a fourfold increase in striatal HVA content making it twice as efficient as narcotic analgesics. This finding suggests that narcotic analgesics do not act on the same sites as neuroleptics when causing an increase in striatal HVA content.

Analgesics, Opioid↗
PubMed1975

Inhibition by apomorphine of the metoclopramide-induced catalepsy and increase in striatal homovanillic acid content.

1 The mechanism of the cataleptic effect of metoclopramide was analyzed by using drugs which alter the activity of dopaminergic or cholinergic neurones or the content of psi-aminobutyric acid in the central nervous system of rats. 2 The cataleptic effect of metoclopramide (20 mg/kg) was antagonized by apomorphine (10 mg/kg) and by atropine (50 mg/kg). Aminoxyacete acid (AOAA, 25-50 mg/kg) potentiated the catalepsy induced by metoclopramide (5 mg/kg). 3 Metoclopramide alone did not alter the rectal temperature of rats. It did not alter the AOAA-induced hypothermia, but it partially antagonized apomorphine-induced hypothermia. 4 Metoclopramide induced a six-fold increase in striatal homovanillic acid (HVA) concentration, but it did not change the dopamine or noradrenaline content in the brain of rats. Apomorphine decreased the striatal HVA concentration in control and in metoclopramide-treated rats. Atropine and AOAA did not alter the metoclopramide-induced increase in striatal HVA concentration. 5 The results suggest that metoclopramide produces catalepsy by blocking striatal dopamine receptors.

Animals↗
PubMed1975

Dextromethorphan inhibits 5-hydroxytryptamine uptake by human blood platelets and decreases 5-hydroxyindoleacetic acid content in rat brain.

The effect of dextromethorphan on the uptake and metabolism of 5-hydroxytryptamine (5-HT) was studied in human blood platelets and in rat brain. In the concentration of 120 nM dextromethorphan inhibited the uptake of 5-HT (1 mu-M) into platelets by 50%. The corresponding concentrations of imipramine and methadone under similar conditions were 22 and 590 nM, respectively. Dextromethorphan (20 to 40 mg kg-1) decreased the concentration of brain 5-hydroxyindoleacetic acid (5-HIAA) and the probenecid-induced accumulation of 5-HIAA time- and dose-dependently. However, dextromethorphan did not alter the pargyline-induced changes in brain 5-HT metabolism. Dextromethorphan-induced changes in brain 5-HT metabolism could arise from the inhibition of the re-uptake of 5-HT into neurons.

Animals↗
PubMed1974

Transport of taurine by normal human blood platelets.

1 Because normal human blood platelets contain higher concentrations of taurine than any other amino acid, and have a platelet: plasma concentration gradient exceeding 400: 1, we isolated the cells in vitro and incubated them with radioactively labelled taurine in order to investigate the existence of a metabolically-dependent accumulation process.2 Platelets incubated with taurine (1 to 100 nmol/ml) in autologous plasma or Krebs solution accumulated [(14)C]-taurine against the concentration gradient.3 The transport process was saturable at high concentrations, showed a requirement for sodium ions, and was temperature-dependent.4 The kinetics of transport fulfilled the criteria of Michaelis & Menten for saturable enzyme/substrate interactions, but the kinetic constants were influenced by the incubation medium.5 The metabolic inhibitors 2,4-dinitrophenol and iodoacetic acid in combination inhibited taurine transport in Krebs solution, but stimulated transport in autologous plasma. The latter result suggested the involvement of a sodium-dependent ATPase in taurine transport.6 We conclude that platelets actively transport taurine in vitro under experimental conditions closely resembling those likely to occur in vivo, and that this taurine transport process may be involved in the maintenance of the platelet: plasma concentration gradient.

Amino Acids↗