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Biomedical subjects

R Rodnight

Publications and source records attributed to R Rodnight.

At least 73 records · Page 4Linked to original sources
PubMed1981

Ontogeny of membrane-bound protein phosphorylating systems in the rat.

The ontogeny of the major intrinsic phosphoproteins in membrane fractions prepared from cerebral cortex was studied in the rat. The apparent membrane content of 4 phosphoproteins increased markedly over the period 10-15 days after birth, i.e. coinciding with the onset of synaptogenesis. Two of these proteins (molecular weights 79,000 and 86,000) were phosphorylated in cyclic AMP-dependent reactions, and two (molecular weights 50,000 and 162,000) were phosphorylated in reactions dependent on Ca2+ + cytosol extract. The apparent content of other acceptor proteins phosphorylated in analogous reactions increased more gradually from birth to adulthood. In contrast the apparent membrane content of a protein of 47,000 daltons, which was phosphorylated in a reaction requiring Ca2+ only, was relatively very high at birth and until 15 days of age, but then declined 6-fold until adulthood was reached. The relative distribution of the intrinsic phosphoproteins in several particulate fractions was also compared in 1- and 19-day-old rats. In 1-day-old animals the phosphoprotein of 47,000 daltons was found predominantly in a light membrane fraction, but at 19 days it was only just discernible in the equivalent fraction and was found instead in heavier fractions.

Aging↗
PubMed1980

A longitudinal study of urinary excretion of N,N,-dimethyltryptamine in psychotic patients.

The excretion of N,N,-dimethyltryptamine (DMT) has been measured in longitudinal studies of five patients with schizophrenic illnesses and in four patients with rapidly or slowly cycling manic-depressive illness. The excretion of DMT was frequently raised in patients when they were psychotic but was usually normal when they had recovered. However, rapid changes in the severity of illness or sudden switches from one mood state to another were not accompanied by changes in the excretion of DMT. These findings contrast with the immediate hallucinogenic effects of an injection of DMT, and suggest that the extracerebral production of DMT (as measured by its urinary excretion) does not provoke the experience of hallucinations in psychotic patients.

Bipolar Disorder↗
PubMed1979

Increased excretion of dimethyltryptamine and certain features of psychosis: a possible association.

The excretion of the hallucinogen dimethyltryptamine (DMT) and its precursor N-methyltryptamine (NMT) was studied among 74 recently admitted psychiatric patients and 19 normal persons. Both compounds were detected in 24-hour urine samples from all subjects. Dimethyltryptamine excretion was greatest in schizophrenia, mania, and "other psychosis" and tended to decline as clinical state improved. Psychotic depressives excreted smaller amounts of DMT more akin to those excreted by neurotic and normal subjects. Urinary NMT excretion was unrelated to psychiatric diagnosis. Ratings on the Present State Examination (PSE) also indicated that increased excretion of DMT was associated with psychotic rather than neurotic psychopathology. Forty-three percent of the variance in urinary DMT levels could be explained in terms of six of the 38 PSE syndromes. Syndromes suggesting elation, perceptual abnormalities, and difficulty in thinking and communicating were most correlated with raised urinary DMT excretion.

Adolescent↗
PubMed1979

Urinary excretion of dimethyltryptamine in liver disease.

The urinary excretion of N,N-dimethyltryptamine (DMT) was higher in patients with severe liver disease than in normal subjects. This difference remained significant when patients with all grades of hepatic encephalopathy were excluded. Patients with liver disease whose mental states were normal excreted amounts of DMT similar to those of patients with a hospital diagnosis of schizophrenia.

Acute Disease↗
PubMed1977

Factors affecting the urinary excretion of endogenously formed dimethyltryptamine in normal human subjects.

The hallucinogenic substance N',N'-dimethyltryptamine and its precursor N-methyltryptamine were found in 24-h specimens of urine from 19 normal human subjects; the mean excretion rates were 386 ng 24 h(-1) and 856 ng 24 h(-1) respectively. The urinary excretion of both compounds was unrelated to age, sex, urinary volume, or creatinine, nor was any consistent diurnal pattern observed. Rates for the mono and dimethylated compounds were not correlated. Diet and the intestinal flora were excluded as a source of urinary dimethyltryptamine. Administration to 4 subjects of sufficient ammonium chloride to increase the H ion concentration of the urine caused a transient increase in dimethyltryptamine excretion but no consistent increase in the rate for N-methyltryptamine. Acidification of the urine did not appear to be the determining factor in this result since in one subject the same drop in urinary pH was achieved by feeding methionine without any increase in dimethyltryptamine excretion.

Adult↗
PubMed1977

Phosphorylation of synaptic-membrane proteins from ox cerebral cortex in vitro. Preparation of fractions enriched in phosphorylated proteins by using extraction with detergents and urea, and gel filtration.

Synaptic-membrane fragments from ox cerebral cortex contain basal and cyclic AMP-stimulated protein kinase(s) that transfer 32P from [gamma-32P]ATP to hydroxyl groups of serine and threonine residues in membrane-protein substrates. In the present work, labelled membrane fragments were partitioned into soluble and insoluble fractions with Triton X-100, Nonidet P. 40, sodium deoxycholate and urea, and the distribution of 32P-labelled protein in the fractions was determined by polyacrylamide-gel electrophoresis and radioautography. A high percentage of phosphorylated protein sustrates remained insoluble, including those whose phosphorylation was most highly stimulated by cyclic AMP. Whole membrane fragments and samples prepared by detergent extraction were fractionated on Sepharose 6B columns in the presence of low concentrations of sodium dodecyl sulphate and pooled fractions were analysed by polyacrylamide-gel electrophoresis and radioautography. Phosphorylated proteins were fractionated on the basis of their molecular weight, but homogeneous protein was not obtained. The results are discussed in relation to the techniques used and the results obtained in other laboratories.

Animals↗
PubMed1977

Effects of electroshock and drugs administered in vivo on protein kinase activity in rat brain.

The effect of electroshock and treatment with reserpine, amphetamine or lithium chloride on protein kinase activity in synaptic membrane fragments prepared from rat brain was investigated. Naive rats subjected to electroshock procedures showed significant increases in both basal and cyclic AMP-stimulated activity irrespective of whether the treatment was sham, acute or chronic. These increases did not occur in animals which had been tamed by daily handling for 15 days prior to treatment, suggesting that the response was induced by the stress of an unfamiliar situation. Administration of lithium chloride and reserpine caused a small but significant increase in the stimulated activity. Doses of d-amphetamine of 5 mg/kg had no effect on either basal or stimulated activity, but higher doses (up to 15 mg/kg) resulted in a pronounced increase in both activities, which may have been related to drug-induced stress.

Animals↗
PubMed1976

Phosphorylation of synaptic-membrane proteins from ox cerebral cortex in vitro. Partition of substrates and protein kinase activities with triton X-100.

Synaptic-membrane fragments from ox cerebral cortex contain basal and cyclic AMP-stimulated protein kinase activity catalysing the phosphorylation of endogenous substrates. Extraction of membrane fragments with Triton X-100 solubilized less than 20% of the kinase activity and left the major part of the endogenous substrates in the insoluble fraction.

Animals↗
PubMed1976

Protein phosphorylation in respiring slices of guinea-pig cerebral cortex. Evidence for a role for noradrenaline and adenosine 3':5'-cyclic monophosphate in the increased phosphorylation observed on application of electrical pulses.

1. Exposure of slices of cerebral cortex from guinea pigs to electrical pulses for 10s or to noradrenaline, 5-hydroxytryptamine or histamine increases the rate of phosphorylation of unidentified proteins in the tissue; the increases in protein phosphorylation due to electrical pulses and noradrenaline were non-additive, whereas the increases due to pulses and 5-hydroxytryptamine or histamine were additive. 2. The stimulating effects of electrical pulses and noradrenaline on protein phosphorylation were antagonized by the beta-adrenergic blocking agents L-propranolol, dichloroisoprenaline, practolol and ICI 66082, but not by the alpha-adrenergic blocking agents, phentolamine and phenoxybenzamine. 3. The increase in protein phosphorylation associated with electrical pulses was antagonized by 10 mum-trifluoperazine and 0.5 mum-prostaglandin E1. 4. It is postulated that under the experimental conditions used the action of electrical pulses on protein phosphorylation is mediated by noradrenaline acting through a beta-adrenergic receptor mechanism probably involving adenylate cyclase.

Adrenergic alpha-Antagonists↗
PubMed1976

Urinary dimethyltryptamine and psychiatric symptomatology and classification.

The excretion of dimethyltryptamine (DMT) was studied amongst 122 recently admitted psychiatric patients and 20 normal subjects. DMT was detected in the urine of 47% of those diagnosed by their psychiatrists as schizophrenic, 38% of those with other non-affective psychoses, 13% of those with affective psychoses, 19% of those with neurotic and personality disorders and 5% of normal subjects. Ninety-nine patients were interviewed in a semi-standardized fashion, and also categorized according to a variety of operational definitions of the psychoses. The operational definitions failed to reveal any group significantly more correlated with urinary DMT than a hospital diagnosis of schizophrenia, but a discriminant function analysis of symptomatology could be used to define a group of 21 patients of whom 15 (71%) excreted detectable DMT. There was a general relationship between psychotic symptoms and urinary DMT, but specifically schizophrenic symptoms did not appear to be major determinants of DMT excretion.

Adolescent↗
PubMed1975

Observations on the binding of adenosine 3':5'-monophosphate to cell membrane fragments from ox cerebral cortex.

Microsomal or synaptosome membrane fragments from ox brain bind cyclic AMP with a pH optimum of 7.0. Scatchard analysis shows the presence of at least two binding sites. Cyclic GMP and cyclic IMP only inhibit binding at concentrations 5000 times that of cyclic AMP and even higher concentration ratios of ATP and AMP have no effect. Membrane fragments saturated with cyclic [3-H]AMP lost less than 7% of bound nucleotide on incubation at 0 degrees C for 45 min but lost 25 % in the same period in the presence of 10 muM non-radioactive cyclic AMP.

Acetylcholine↗