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Biomedical subjects

A D Sherman

Publications and source records attributed to A D Sherman.

At least 37 records · Page 2Linked to original sources
PubMed1984

Variable clinical response to choline in tardive dyskinesia.

Tardive dyskinesia is widely believed to be a state of relative hyperdopaminergic and hypocholinergic imbalance in the striatum of patients chronically treated with neuroleptics. However, not all patients with tardive dyskinesia respond to cholinergic drugs, which theoretically should restore the balance and improve the symptoms. We report a controlled, double-blind, crossover study of choline chloride in 11 patients with persistent tardive dyskinesia. Seven patients showed partial or minimal improvement, while two did not change and two deteriorated. The results are discussed in the light of other similar findings in the literature, and the implications for pharmacological subtypes of tardive dyskinesia using cholinergic probes are explored.

Acetylcholine↗
PubMed1983

Plasma serine to cysteine ratio as a biological marker for psychosis.

In a study of plasma amino acids in psychiatric patients, serine to cysteine (S/C) ratio was higher (S/C = 1.57 +/- 0.28) in 57 psychotics compared to 27 nonpsychotics (S/C = 1.06 +/- 0.23). This difference was highly significant at P less than 0.001. Psychotic patients were given a psychosis score (p score) of 1-4. The S/C ratios of individual patients were significantly correlated to their p scores (r = 0.65, P less than 0.001). S/C ratios were not related to diagnosis, age, sex, food intake and medications. When the initial S/C ratio and p scores of 22 patients were compared to their S/C ratio and p score at the time when they were improved and ready to be discharged, there was a concomitant fall both in S/C ratios and p scores suggesting the high S/C ratios may be indicative of a state rather than a trait characteristic. Our findings lead us to the conclusion that S/C ratios may provide a marker for the presence of psychosis and an index of its severity.

Adolescent↗
PubMed1982

Regional aspects of the delay of acquisition conditioned avoidance responding by chlorpromazine.

Chlorpromazine injected into the amygdala, septum, or caudate delayed the acquisition of a one-way active avoidance response. Injections into nine other brain areas were inactive. Following a standard dose of chlorpromazine at its ED50 for delaying avoidance acquisition, tissue levels of chlorpromazine from those animals displaying reduced acquisition were significantly higher in the caudate and amygdala than from animals not demonstrating a drug effect.

Amygdala↗
PubMed1982

Tricyclic antidepressant drug action correlates with its tissue levels in anterior neocortex.

In the behavioral reversal of learned helplessness in the rat by imipramine, a strong correlation is found between "cure" of helplessness and drug level in anterior neocortex, the locus of drug action in this model of depression. This suggests that the delayed onset of therapeutic action of antidepressant drugs is due to the time required to achieve adequate drug levels at the site of their action.

Animals↗
PubMed1982

Specificity of the learned helplessness model of depression.

The learned helplessness model of depression was tested for its responsiveness to several types of antidepressant therapies, and to a number of psychoactive drugs which are not effective in treating depression in humans. Chronic administration of tricyclic antidepressants (imipramine, desipramine, amitryptyline, nortryptyline, or doxepin), atypical antidepressants (iprindole or mianserin), monoamine oxidase inhibitors (iproniazid or pargyline), or electroconvulsive shock was effective in reversing learned helplessness. Chronic treatment with anxiolytics (diazepam, lorazepam, or chlordiazepoxide), neuroleptics (chlorpromazine or haloperidol) stimulants (amphetamine or caffeine), or depressants (phenobarbital or ethanol) was not. Thus, this model provides a reasonable degree of specificity toward therapies which are successful in humans.

Animals↗
PubMed1981

GABAergic modulation of learned helplessness.

Previous studies have demonstrated the GABAergic system in the hippocampus to be a major controlling factor in the reversal of learned helplessness by antidepressants. In the present work, animals in which learned helplessness (LeH) was induced by exposure to uncontrollable electric shock demonstrated a decreased depolarization-induced release of GABA relative to controls, and an increased release of hippocampal glutamate. Injection of bicuculline but not glutamate into the hippocampus produced a behavioral state identical to that induced by uncontrollable shock, but had no influence on pain sensitivity. When flux through the "small" hippocampal pool of GABA was determined, chronic treatment with imipramine or iprindole, but lorazepam or chlorpromazine elevated this measure. These three findings along with those of prior experiments, suggest a controlling role for GABA in the learned helplessness model of depression.

Amino Acids↗
PubMed1981

A pharmacologically pertinent animal model of mania.

Intraventricular injection of 6-hydroxydopamine (HDA) produces rats which are irritable and hyperresponsive to environmental stimuli. Chronic administration of lithium was found to prevent the development of hyperreactivity to mild footshock, while chronic electroconvulsive shock effected a return toward normal behavior. HDA-induced hyperreactivity is proposed as a pharmacological model of mania.

Affective Disorders, Psychotic↗
PubMed1980

L-kynurenine: its synthesis and possible regulatory function in brain.

One pathway by which tryptophan is metabolized in the brain as well as in the periphery is through cleavage of the indole ring to formylkynurenine and then kynurenine. Indoleamine-2,3-dioxygenase, the enzyme that catalyzes this cleavage, and kynurenine are distributed all across the different anatomic regions of brain. Approximately 40% of the kynurenine in brain is synthesized there, the remainder having come from plasma. Tryptophan loading, which has been used both experimentally and therapeutically as a means of increasing tryptophan conversion to serotonin, also increases kynurenine formation in the brain and in the periphery. Because of the formation of kynurenine, which competes for cerebral transport and cellular uptake of L-tryptophan, and because of substrate inhibition on tryptophan hydroxylase, excessively high doses of tryptophan may actually decrease the production of cerebral serotonin and 5-hydroxyindoleacetic acid.

Animals↗
PubMed1979

Biopterin. VI. Purification and primary amino acid sequence of mammalian D-erythro-7,8-dihydroneopterin triphosphate synthetase.

An enzyme that catalyzes the conversion of 2-amino-6-(5'-triphosphoribosyl)amino-5- or 6-formamido-6-hydroxypyrimidine, but not of guanosine triphosphate, to quinonoid 6-(D-erythro-1'-2'-3'-trihydroxypropyl)dihydropterin triphosphate and formic acid has been purified to homogeneity from some mammalian brain and liver. The enzyme of a single strand is a basic protein of 9177 daltons consisting of 68 amino acid residues--except the enzyme from rat brain, which has one additional aspartic acid as residue 7. The enzyme possesses three free SH groups and, in its most active form, 1 mol of phosphate per mole of enzyme. Peptides isolated after hydrolysis with trypsin, chymotrypsin, or weak acid were separated by thin-layer chromatography and sequenced manually by Edman degradation. The complete sequence of the molecule was established as follows: (formula: see text)

Amino Acid Sequence↗