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Biomedical subjects

D Eccleston

Publications and source records attributed to D Eccleston.

At least 55 records · Page 3Linked to original sources
PubMed1981

Total and free serum haloperidol levels in schizophrenic patients and the effect of age thioridazine and fatty acid on haloperidol-serum protein binding in vitro.

1 Using radioimmunoassays, steady-state levels of total and free haloperidol (obtained by ultrafiltration and dialysis) have been determined in twenty-two patients on long term treatment receiving doses from 3 to 45 mg per day. 2 For the group, both total serum concentration and free drug concentration showed significant correlations (P less than 0.001) with daily dose. 3 No significant correlation was observed between age of the patient and percentage free haloperidol in serum. 4 In vitro experiments using sera from twenty-three healthy volunteers showed significant negative correlations (P less than 0.01) between age and percentage free haloperidol. 5 Thioridazine and oleic acid significantly enhanced the percentage of free haloperidol in normal human sera in vitro.

Adult↗
PubMed1979

Interactions between serotonergic and dopaminergic systems in rat brain demonstrated by small unilateral lesions of the raphe nuclei.

Unilateral lesions in the dorsal raphe (DR) resulted in decreased concentrations of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid and increases in homovanillic acid and 3,4-dihydroxyphenylacetic acid in the ipsilateral substantia nigra (SN). Unilateral lesions in the median raphe (MR) caused similar biochemical changes in the corpus striatim (CS). Apomorphine and amphetamine caused turning behaviour in the lesiond animals which was ipsiversive after DR lesions but contraversive after MR damage. The animals turned in the opposite direction to that induced by these drugs after treatment with 5-methoxy-N,N-dimethyltryptamine and in the same direction after treatment with phenelzine plus L-tryptophan. All the drug-induced turning behaviour was blocked by haloperidol. The turning induced by 5-methoxy-N,N-dimethyltryptamine and in the same direction after treatment with phenelzine plus L-tryptophan. All the drug-induced turning behaviour was blocked by haloperidol. The turning induced by 5-methoxy-N,N-dimethyltryptamine was blocked by methysergide. This work suggested that the DR and MR nuclei send projections differentially to SN and CS respectively. These projections may exert a tonically active inhibition of dopamine metabolism in their respective terminal areas.

Animals↗
PubMed1979

Tardive dyskinesia and dementia.

Seventeen schizophrenic patients with tardive dyskinesia (TD) and 33 schizophrenics without tardive dyskinesia were examined by psychological tests of intellectual function and EMI scans were performed. The group as a whole were found to be demented and 31 out of 45 had abnormalities on the scan. On a learning test the tardive dyskinesia group did significantly worse and using a measured parameter of the scan (the Ventricular Index) the tardive dyskinesia group had more abnormality. It is suggested that the higher incidence of pathology in the tardive dyskinesia group may be related to chronic neuroleptic toxicity.

Antipsychotic Agents↗
PubMed1978

The influence of L-tryptophan and monoamine oxidase inhibitors on catecholamine metabolism in rat brain.

1. L-Tryptophan (100 mg/kg) was administered to rats with or without pretreatment with a monoamine oxidase inhibitor and the concentration of 5-hydroxyindoleacetic acid, homovanillic acid, dihydroxyphenylacetic acid, 3-methoxy 4-hydroxyphenyl glycol, normetanephrine, noradrenaline and dopamine measured in whole brain one hour later. 2. L-Tryptophan increased the concentration of 5-hydroxyindoleacetic acid, homovanillic acid, dihydroxyphenylacetic acid, 3-methoxy 4-hydroxyphenyl glycol and normetanephrine. The concentration of noradrenaline did not change whilst that of dopamine increased significantly. 3. In animals pretreated chronically with a monoamine oxidase inhibitor, tryptophan increased the concentration of dihydroxyphenylacetic acid and homovanillic acid compared to monoamine oxidase alone. 4. The results suggest either a release of dopamine and noradrenaline by 5-hydroxytryptamine, with a compensatory increase in their synthesis, or an increase in the firing of dopaminergic and noradrenergic neurones after L-tryptophan.

Animals↗
PubMed1977

Immunohistochemical localization of cyclic GMP in rat cerebellum.

The technique of cyclic nucleotide fluorescence immunohistochemistry has been applied for the specific localization of cyclic GMP in rat cerebellum. We report immunofluorescence associated with fibres and membranes, contrasting with previously reported cytoplasmic localization of cyclic AMP in different cell populations, using a similar technique. We have been unable to detect changes in cyclic GMP staining in response to post-mortem changes, harmaline and pentobarbitone administration. A role of cyclic GMP is suggested in membrane ion transport.

Animals↗
PubMed1976

A comparison of D and L-tryptophan on the cerebral metabolism of 5-hydroxytryptamine and dopamine in the dog.

1 After D and L-tryptophan (50 mg/kg) were given intravenously in the dog, the concentration of the amino acid was increased in ventricular cerebrospinal fluid (CSF) during the subsequent 4 h or sampling, although the concentrations were significantly lower following the administration of the D-isomer. 2 There was no evidence that D-tryptophan increased the synthesis of 5-hydroxytryptamine (5-HT) in dog brain as judged by the failure to cause a change in 5-hydroxyindoleacetic acid (5-HIAA) concentrations in ventricular CSF different from that seen with controls. 3 There was no appreciable conversion of D-tryptophan to L-tryptophan in the dog. 4 D-tryptophan was cleared more rapidly from plasma than L-tryptophan. 5 No difference in plasma binding between D and L-tryptophan was detected.

Animals↗